Endocrinology and Metabolism

Original Articles

Diabetes, obesity and metabolism Big Data Articles (National Health Insurance Service Database)
Impact of Glucose Metabolism Status on the Association between Apolipoprotein A-I and Ischemic Risk in Patients with Coronary Artery Disease: A Large-Sample Cohort Study: Kailun Yan, Jiawen Li, Kexin Zhang, Menglu Liu, Pei Zhu, Xiaofang Tang, Deshan Yuan, Yuejin Yang, Runlin Gao, Jinqing Yuan, Xueyan Zhao; Endocrinol Metab. 2025;40(6):904-915. Published online November 7, 2025; DOI: https://doi.org/10.3803/EnM.2025.2407

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Abstract PDF Supplementary Material PubReader ePub: Background
Apolipoprotein A-I (ApoA-I) is a key cardioprotective lipoprotein. Nevertheless, it remains unclear how ApoA-I relates to ischemic risk across glucose metabolism statuses in patients with coronary artery disease (CAD). This study investigated whether glucose metabolism status influences the association between ApoA-I and ischemic risk in CAD patients.
Methods
This cohort study included 10,724 consecutive CAD patients undergoing percutaneous coronary intervention, who were classified into diabetes mellitus (DM), pre-DM, and normal glucose regulation (NGR) groups. The primary clinical endpoint was major adverse cardiac and cerebrovascular event (MACCE), defined as a composite of all-cause death, myocardial infarction, revascularization, and stroke.
Results
Of the 10,232 patients ultimately included, 2,139 (20.9%) experienced MACCE over 5 years. A significant interaction was observed between ApoA-I levels and glucose metabolism status (P for interaction=0.041). In the DM group, an L-shaped association between ApoA-I and MACCE was found, with lower ApoA-I levels linked to a higher risk of MACCE (P for non-linearity= 0.044). Multivariate Cox regression analysis showed that patients in the lowest quintile of ApoA-I had a 1.327-fold increased risk of MACCE compared to those at the lowest risk (hazard ratio, 1.327; 95% confidence interval, 1.097 to 1.604). However, no significant association was observed in the pre-DM or NGR groups (both P>0.05).
Conclusion
This large-scale, 5-year follow-up study is the first to demonstrate that lower ApoA-I levels are associated with increased MACCE risk in CAD patients with DM, highlighting the potential value of ApoA-I in risk stratification and as a therapeutic target.

Diabetes, obesity and metabolism
Antilipolytic Insulin Sensitivity Indices Measured during an Oral Glucose Challenge: Associations with Insulin-Glucose Clamp and Central Adiposity in Women without Diabetes: Foued Naimi, Christophe Richer dit Laflèche, Marie-Claude Battista, André C. Carpentier, Jean-Patrice Baillargeon; Endocrinol Metab. 2025;40(4):561-573. Published online March 18, 2025; DOI: https://doi.org/10.3803/EnM.2024.2129

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Background
Tissue overexposure to non-esterified fatty acids (NEFA) contributes to the development of metabolic conditions, with insulin-mediated suppression of lipolysis being an important mechanism in limiting this overexposure. We investigated which dynamic NEFA insulin-suppression indices derived from the oral glucose tolerance test (OGTT) were best associated with those derived from the insulin-glucose clamp, as well as with central adiposity and glucoregulatory parameters.
Methods
This cross-sectional study recruited 29 women without diabetes, 15 healthy women, and 14 women with polycystic ovary syndrome. The OGTT indices of NEFA insulin-suppression were the decremental NEFA area under the curve, negative log-linear NEFA slope, percentage of NEFA suppression (%NEFA_supp) and time to suppress NEFA levels by 50% (T50_NEFA). The indices derived from the two-step euglycemic-hyperinsulinemic clamp (low-dose insulin step) were delta NEFA and %NEFA_supp.
Results
Among the OGTT and clamp indices, T50_NEFA[OGTT] and %NEFA_supp[clamp] showed the closest associations in both subgroups (r=–0.58). Additionally, T50_NEFA correlated significantly in all women with waist circumference (r=0.64), body fat percentage (r=0.60), fasting insulinemia (r=0.53), and M-value insulin sensitivity index (r=–0.45). Similarly, %NEFA_supp[clamp] correlated significantly in all women with waist circumference (r=–0.57), body fat percentage (r=–0.54), fasting insulinemia (r=–0.55), and M-value insulin sensitivity index (r=0.51). T50_NEFA and %NEFA_supp[clamp] also correlated with other anthropometric and metabolic parameters associated with lipotoxicity.
Conclusion
For dynamic testing of NEFA insulin-suppression in women, T50_NEFA was the OGTT-derived index best correlated with a clamp index (%NEFA_supp). These indices were also the most closely associated with anthropometric and glucoregulatory parameters. Thus, the OGTT-derived T50_NEFA appears valid for assessing dynamic antilipolytic insulin action.

Citations

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Impact of a high dietary fiber cereal meal intervention on the progression of liver fibrosis in T2DM with MASLD
Xi-Shuang Chen, Hui-Zhen Liu, Fang Huang, Jian Meng, Jing-Xian Fang, Yu Han, Hui-Ming Zou, Qing Gu, Xue Hu, Qian-Wen Ma, Yue-Xia Han, Sui-Jun Wang
Frontiers in Endocrinology.2025;[Epub] CrossRef

Review Articles

Diabetes, obesity and metabolism
Regulation of Energy and Glucose Homeostasis by the Nucleus of the Solitary Tract and the Area Postrema: Kyla Bruce, Ameth N. Garrido, Song-Yang Zhang, Tony K.T. Lam; Endocrinol Metab. 2024;39(4):559-568. Published online August 1, 2024; DOI: https://doi.org/10.3803/EnM.2024.2025

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The central nervous system regulates feeding, weight and glucose homeostasis in rodents and humans, but the site-specific mechanisms remain unclear. The dorsal vagal complex in the brainstem that contains the nucleus of the solitary tract (NTS) and area postrema (AP) emerges as a regulatory center that impacts energy and glucose balance by monitoring hormonal and nutrient changes. However, the specific mechanistic metabolic roles of the NTS and AP remain elusive. This mini-review highlights methods to study their distinct roles and recent findings on their metabolic differences and similarities of growth differentiation factor 15 (GDF15) action and glucose sensing in the NTS and AP. In summary, future research aims to characterize hormonal and glucose sensing mechanisms in the AP and/or NTS carries potential to unveil novel targets that lower weight and glucose levels in obesity and diabetes.

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Eriko Furube, Rena Fujii, Yuri Nambu, Daishi Hiratsuka, Ryoichi Yoshimura, Seiji Miyata
Stem Cell Reviews and Reports.2026; 22(1): 222. CrossRef
Adipocyte-derived extracellular vesicles are key regulators of central leptin sensitivity and energy homeostasis
Jin Wang, Xuhong Zhang, Ye Zhu, Haixiang Sun, Xuetao Chen, Zhicong Zhao, Nina Zhang, Chenyu Zhang, Liang Li, Yan Bi
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Mineral, Bone & Muscle
Osteocalcin: Beyond Bones: Jakub Krzysztof Nowicki, Elżbieta Jakubowska-Pietkiewicz; Endocrinol Metab. 2024;39(3):399-406. Published online May 28, 2024; DOI: https://doi.org/10.3803/EnM.2023.1895

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Apart from basic roles such as supporting the body, protecting internal organs, and storing calcium, the skeletal system also performs hormonal functions. In recent years, several reports have been published on proteins secreted by bones and their impact on the homeostasis of the entire body. These proteins include fibroblast growth factor 23, sclerostin, lipocalin 2, and osteocalcin. Osteocalcin, the most abundant non-collagenous protein in bone tissue, is routinely measured as a clinical marker for diagnosing bone metabolism disorders. Its molecule undergoes numerous transformations, with decarboxylation being the critical process. Decarboxylation occurs in the acidic environment typical of bone resorption, facilitating the release of the molecule into the bloodstream and enabling its hormonal action. Decarboxylated osteocalcin promotes insulin secretion and stimulates the proliferation of pancreatic islet β-cells. It also plays a role in reducing the accumulation of visceral fat and decreasing fat storage in the liver. Furthermore, decarboxylated osteocalcin levels are inversely correlated with fasting serum glucose levels, total body fat, visceral fat area, and body mass index. Apart from its role in energy metabolism, osteocalcin affects testosterone production and the synthesis of glucagon-like peptide-1. It is also actively involved in muscle-bone crosstalk and influences cognitive function.

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Namgok Lecture 2023

Diabetes, obesity and metabolism
Hypothalamic AMP-Activated Protein Kinase as a Whole-Body Energy Sensor and Regulator: Se Hee Min, Do Kyeong Song, Chan Hee Lee, Eun Roh, Min-Seon Kim; Endocrinol Metab. 2024;39(1):1-11. Published online February 14, 2024; DOI: https://doi.org/10.3803/EnM.2024.1922

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5´-Adenosine monophosphate (AMP)-activated protein kinase (AMPK), a cellular energy sensor, is an essential enzyme that helps cells maintain stable energy levels during metabolic stress. The hypothalamus is pivotal in regulating energy balance within the body. Certain neurons in the hypothalamus are sensitive to fluctuations in food availability and energy stores, triggering adaptive responses to preserve systemic energy equilibrium. AMPK, expressed in these hypothalamic neurons, is instrumental in these regulatory processes. Hypothalamic AMPK activity is modulated by key metabolic hormones. Anorexigenic hormones, including leptin, insulin, and glucagon-like peptide 1, suppress hypothalamic AMPK activity, whereas the hunger hormone ghrelin activates it. These hormonal influences on hypothalamic AMPK activity are central to their roles in controlling food consumption and energy expenditure. Additionally, hypothalamic AMPK activity responds to variations in glucose concentrations. It becomes active during hypoglycemia but is deactivated when glucose is introduced directly into the hypothalamus. These shifts in AMPK activity within hypothalamic neurons are critical for maintaining glucose balance. Considering the vital function of hypothalamic AMPK in the regulation of overall energy and glucose balance, developing chemical agents that target the hypothalamus to modulate AMPK activity presents a promising therapeutic approach for metabolic conditions such as obesity and type 2 diabetes mellitus.

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Review Article

Miscellaneous
Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer: Aliya Lakhani, Da Hyun Kang, Yea Eun Kang, Junyoung O. Park; Endocrinol Metab. 2023;38(6):619-630. Published online November 21, 2023; DOI: https://doi.org/10.3803/EnM.2023.1814

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Metabolism is a dynamic network of biochemical reactions that support systemic homeostasis amidst changing nutritional, environmental, and physical activity factors. The circulatory system facilitates metabolite exchange among organs, while the endocrine system finely tunes metabolism through hormone release. Endocrine disorders like obesity, diabetes, and Cushing’s syndrome disrupt this balance, contributing to systemic inflammation and global health burdens. They accompany metabolic changes on multiple levels from molecular interactions to individual organs to the whole body. Understanding how metabolic fluxes relate to endocrine disorders illuminates the underlying dysregulation. Cancer is increasingly considered a systemic disorder because it not only affects cells in localized tumors but also the whole body, especially in metastasis. In tumorigenesis, cancer-specific mutations and nutrient availability in the tumor microenvironment reprogram cellular metabolism to meet increased energy and biosynthesis needs. Cancer cachexia results in metabolic changes to other organs like muscle, adipose tissue, and liver. This review explores the interplay between the endocrine system and systems-level metabolism in health and disease. We highlight metabolic fluxes in conditions like obesity, diabetes, Cushing’s syndrome, and cancers. Recent advances in metabolomics, fluxomics, and systems biology promise new insights into dynamic metabolism, offering potential biomarkers, therapeutic targets, and personalized medicine.

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Original Article

Diabetes, obesity and metabolism
Association between Serum Amyloid A Levels and Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis: Ting Liu, Meng Li, Chunying Cui, Jielin Zhou; Endocrinol Metab. 2023;38(3):315-327. Published online June 7, 2023; DOI: https://doi.org/10.3803/EnM.2023.1621

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Background
To date, consistent data have not been reported on the association between serum amyloid A (SAA) levels and type 2 diabetes mellitus (T2DM). The purpose of this study was to systematically summarize their relationship.
Methods
Databases including PubMed, Cochrane Library, Embase, Web of Science, and MEDLINE were searched until August 2021. Cross-sectional and case-control studies were included.
Results
Twenty-one studies with 1,780 cases and 2,070 controls were identified. SAA levels were significantly higher in T2DM patients than in healthy groups (standardized mean difference [SMD], 0.68; 95% confidence interval [CI], 0.39 to 0.98). A subgroup analysis showed that the mean age of participants and the continent that participants were from were related to differences in SAA levels between cases and controls. Furthermore, in T2DM patients, SAA levels were positively associated with body mass index (r=0.34; 95% CI, 0.03 to 0.66), triglycerides (r=0.12; 95% CI, 0.01 to 0.24), fasting plasma glucose (r=0.26; 95% CI, 0.07 to 0.45), hemoglobin A1c (r=0.24; 95% CI, 0.16 to 0.33), homeostasis model assessment for insulin resistance (r=0.22; 95% CI, 0.10 to 0.34), C-reactive protein (r=0.77; 95% CI, 0.62 to 0.91), and interleukin-6 (r=0.42; 95% CI, 0.31 to 0.54), but negatively linked with highdensity lipoprotein cholesterol (r=–0.23; 95% CI, –0.44 to –0.03).
Conclusion
The meta-analysis suggests that high SAA levels may be associated with the presence of T2DM, as well as lipid metabolism homeostasis and the inflammatory response.

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Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis
Yixin Chang, Yezhou Liu, Yuanrui Zou, Richard D. Ye
International Journal of Molecular Sciences.2025; 26(3): 987. CrossRef
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Praveen Papareddy, Heiko Herwald
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Review Article

Miscellaneous
Brown Adipose Tissue: Activation and Metabolism in Humans: Imane Hachemi, Mueez U-Din; Endocrinol Metab. 2023;38(2):214-222. Published online March 27, 2023; DOI: https://doi.org/10.3803/EnM.2023.1659

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Brown adipose tissue (BAT) is a thermogenic organ contributing to non-shivering thermogenesis. BAT becomes active under cold stress via sympathetic nervous system activation. However, recent evidence has suggested that BAT may also be active at thermoneutrality and in a postprandial state. BAT has superior energy dissipation capacity compared to white adipose tissue (WAT) and muscles. Thus, it has been proposed that the recruitment and activation of additional BAT may increase the overall energy-expending capacity in humans, potentially improving current whole-body weight management strategies. Nutrition plays a central role in obesity and weight management. Thus, this review discusses human studies describing BAT hyper-metabolism after dietary interventions. Nutritional agents that can potentially recruit brown adipocytes via the process of BAT-WAT transdifferentiation are also discussed.

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Original Articles

Thyroid
Metabolite Changes during the Transition from Hyperthyroidism to Euthyroidism in Patients with Graves’ Disease: Ho Yeop Lee, Byeong Chang Sim, Ha Thi Nga, Ji Sun Moon, Jingwen Tian, Nguyen Thi Linh, Sang Hyeon Ju, Dong Wook Choi, Daiki Setoyama, Hyon-Seung Yi; Endocrinol Metab. 2022;37(6):891-900. Published online December 26, 2022; DOI: https://doi.org/10.3803/EnM.2022.1590

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Background
An excess of thyroid hormones in Graves’ disease (GD) has profound effects on systemic energy metabolism that are currently partially understood. In this study, we aimed to provide a comprehensive understanding of the metabolite changes that occur when patients with GD transition from hyperthyroidism to euthyroidism with methimazole treatment.
Methods
Eighteen patients (mean age, 38.6±14.7 years; 66.7% female) with newly diagnosed or relapsed GD attending the endocrinology outpatient clinics in a single institution were recruited between January 2019 and July 2020. All subjects were treated with methimazole to achieve euthyroidism. We explored metabolomics by performing liquid chromatography-mass spectrometry analysis of plasma samples of these patients and then performed multivariate statistical analysis of the metabolomics data.
Results
Two hundred metabolites were measured before and after 12 weeks of methimazole treatment in patients with GD. The levels of 61 metabolites, including palmitic acid (C16:0) and oleic acid (C18:1), were elevated in methimazole-naïve patients with GD, and these levels were decreased by methimazole treatment. The levels of another 15 metabolites, including glycine and creatinine, were increased after recovery of euthyroidism upon methimazole treatment in patients with GD. Pathway analysis of metabolomics data showed that hyperthyroidism was closely related to aminoacyl-transfer ribonucleic acid biosynthesis and branched-chain amino acid biosynthesis pathways.
Conclusion
In this study, significant variations of plasma metabolomic patterns that occur during the transition from hyperthyroidism to euthyroidism were detected in patients with GD via untargeted metabolomics analysis.

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Genetic associations of plasma metabolites with immune cells in hyperthyroidism revealed by Mendelian randomization and GWAS-sc-eQTLs xQTLbiolinks analysis
Yutong Li, Xingyu Song, Yuyang Huang, Sifan Zhou, Linkun Zhong
Scientific Reports.2025;[Epub] CrossRef
Butyrate Ameliorates Graves’ Orbitopathy Through Regulating Orbital Fibroblast Phenotypes and Gut Microbiota
Pingbo Ouyang, Jia Qi, Boding Tong, Yunping Li, Jiamin Cao, Lujue Wang, Tongxin Niu, Xin Qi
Investigative Ophthalmology & Visual Science.2025; 66(3): 5. CrossRef
Serum metabolome analysis in hyperthyroid cats before and after radioactive iodine therapy
Molly A. Bechtold, Yimei Lin, Meredith L. Miller, Jennifer M. Prieto, Carol E. Frederick, Lucinda L. Bennett, Mark E. Peterson, Kenneth W. Simpson, John P. Loftus, Anu Sayal
PLOS ONE.2024; 19(6): e0305271. CrossRef
Evaluation of the Dysregulation of Cholesterol and Glucose Levels in Graves' Disease Using Clinical Data Analysis
Zainab Razaq Kareem, Fatin Fadhel Al-Kazazz, Ahmed Mahdi Rheima, Ameer Radhi Sultan
Reports of Biochemistry and Molecular Biology.2024; 13(2): 159. CrossRef
Associations of serum keratin 1 with thyroid function and immunity in Graves’ disease
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PLOS ONE.2023; 18(11): e0289345. CrossRef

Thyroid Big Data Articles (National Health Insurance Service Database)
Repeated Low High-Density Lipoprotein Cholesterol and the Risk of Thyroid Cancer: A Nationwide Population- Based Study in Korea: Jinyoung Kim, Mee Kyoung Kim, Ki-Hyun Baek, Ki-Ho Song, Kyungdo Han, Hyuk-Sang Kwon; Endocrinol Metab. 2022;37(2):303-311. Published online April 6, 2022; DOI: https://doi.org/10.3803/EnM.2021.1332

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Background
High-density lipoprotein cholesterol (HDL-C) plays an important role in the reverse cholesterol transport pathway and prevents atherosclerosis-mediated disease. It has also been suggested that HDL-C may be a protective factor against cancer. However, an inverse correlation between HDL-C and cancer has not been established, and few studies have explored thyroid cancer.
Methods
The study participants received health checkups provided by the Korean National Health Insurance Service from 2009 to 2013 and were followed until 2019. Considering the variability of serum HDL-C level, low HDL-C level was analyzed by grouping based on four consecutive health checkups. The data analysis was performed using univariate and multivariate Cox proportional hazard regression models.
Results
A total of 3,134,278 total study participants, thyroid cancer occurred in 16,129. In the crude model, the hazard ratios for the association between repeatedly measured low HDL-C levels and thyroid cancer were 1.243, 1.404, 1.486, and 1.680 (P for trend <0.01), respectively, which were significant even after adjusting for age, sex, lifestyle factors, and metabolic diseases. The subgroup analysis revealed that low HDL-C levels likely had a greater impact on the group of patients with central obesity (P for interaction= 0.062), high blood pressure (P for interaction=0.057), impaired fasting glucose (P for interaction=0.051), and hyperlipidemia (P for interaction=0.126).
Conclusion
Repeatedly measured low HDL-C levels can be considered a risk factor for cancer as well as vascular disease. Low HDL-C levels were associated with the risk of thyroid cancer, and this correlation was stronger in a metabolically unhealthy population.

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Namgok Lecture 2021

Diabetes, Obesity and Metabolism
The Influence of Obesity and Metabolic Health on Vascular Health: Eun-Jung Rhee; Endocrinol Metab. 2022;37(1):1-8. Published online February 28, 2022; DOI: https://doi.org/10.3803/EnM.2022.101

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The prevalence of obesity is rapidly increasing worldwide. Obesity should not be understood only as the accumulation of fat in the body, but instead as a phenomenon that exerts different effects on our health according to the place of fat deposition and its stability. Obesity is the starting point of most metabolic diseases, such as diabetes, hypertension, metabolic syndrome, sleep apnea, and eventually cardiovascular disease. There are different kinds of obesity, ranging from simple obesity to sarcopenic obesity. The main purpose of intervening to address obesity is to decrease the ultimate consequence of obesity—namely, cardiovascular disease. The main mechanism through which obesity, especially abdominal obesity, increases cardiovascular risk is the obesity-induced derangement of metabolic health, leading to the development of metabolic diseases such as diabetes, non-alcoholic fatty liver disease, and metabolic syndrome, which are the main initiators of vascular damage. In this review, I discuss the influence of various types of obesity on the risk of metabolic diseases, and how these diseases increase cardiovascular disease risk.

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Review Article

Diabetes, Obesity and Metabolism
Homeostatic Regulation of Glucose Metabolism by the Central Nervous System: Jong Han Choi, Min-Seon Kim; Endocrinol Metab. 2022;37(1):9-25. Published online February 28, 2022; DOI: https://doi.org/10.3803/EnM.2021.1364

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Evidence for involvement of the central nervous system (CNS) in the regulation of glucose metabolism dates back to the 19th century, although the majority of the research on glucose metabolism has focused on the peripheral metabolic organs. Due to recent advances in neuroscience, it has now become clear that the CNS is indeed vital for maintaining glucose homeostasis. To achieve normoglycemia, specific populations of neurons and glia in the hypothalamus sense changes in the blood concentrations of glucose and of glucoregulatory hormones such as insulin, leptin, glucagon-like peptide 1, and glucagon. This information is integrated and transmitted to other areas of the brain where it eventually modulates various processes in glucose metabolism (i.e., hepatic glucose production, glucose uptake in the brown adipose tissue and skeletal muscle, pancreatic insulin and glucagon secretion, renal glucose reabsorption, etc.). Errors in these processes lead to hyper- or hypoglycemia. We here review the current understanding of the brain regulation of glucose metabolism.

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Original Articles

Adrenal Gland
Metabolic Subtyping of Adrenal Tumors: Prospective Multi-Center Cohort Study in Korea: Eu Jeong Ku, Chaelin Lee, Jaeyoon Shim, Sihoon Lee, Kyoung-Ah Kim, Sang Wan Kim, Yumie Rhee, Hyo-Jeong Kim, Jung Soo Lim, Choon Hee Chung, Sung Wan Chun, Soon-Jib Yoo, Ohk-Hyun Ryu, Ho Chan Cho, A Ram Hong, Chang Ho Ahn, Jung Hee Kim, Man Ho Choi; Endocrinol Metab. 2021;36(5):1131-1141. Published online October 21, 2021; DOI: https://doi.org/10.3803/EnM.2021.1149

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Background
Conventional diagnostic approaches for adrenal tumors require multi-step processes, including imaging studies and dynamic hormone tests. Therefore, this study aimed to discriminate adrenal tumors from a single blood sample based on the combination of liquid chromatography-mass spectrometry (LC-MS) and machine learning algorithms in serum profiling of adrenal steroids.
Methods
The LC-MS-based steroid profiling was applied to serum samples obtained from patients with nonfunctioning adenoma (NFA, n=73), Cushing’s syndrome (CS, n=30), and primary aldosteronism (PA, n=40) in a prospective multicenter study of adrenal disease. The decision tree (DT), random forest (RF), and extreme gradient boost (XGBoost) were performed to categorize the subtypes of adrenal tumors.
Results
The CS group showed higher serum levels of 11-deoxycortisol than the NFA group, and increased levels of tetrahydrocortisone (THE), 20α-dihydrocortisol, and 6β-hydroxycortisol were found in the PA group. However, the CS group showed lower levels of dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEA-S) than both the NFA and PA groups. Patients with PA expressed higher serum 18-hydroxycortisol and DHEA but lower THE than NFA patients. The balanced accuracies of DT, RF, and XGBoost for classifying each type were 78%, 96%, and 97%, respectively. In receiver operating characteristics (ROC) analysis for CS, XGBoost, and RF showed a significantly greater diagnostic power than the DT. However, in ROC analysis for PA, only RF exhibited better diagnostic performance than DT.
Conclusion
The combination of LC-MS-based steroid profiling with machine learning algorithms could be a promising one-step diagnostic approach for the classification of adrenal tumor subtypes.

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An Analysis of Post-Adrenalectomy Dynamics in MACS (Mild Autonomous Cortisol Secretion)-Positive Adrenal Tumours: The Biomarkers and Clinical Impact
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Machine learning in endocrinology: current applications and future perspectives
Magdalena Kamińska, Małgorzata Trofimiuk-Müldner, Grzegorz Sokołowski, Alicja Hubalewska-Dydejczyk
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Clinical Utility of Salivary Steroid Profiling for the Differential Diagnosis of Adrenal Diseases
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Nathan Mullen, James Curneen, Padraig T Donlon, Punit Prakash, Irina Bancos, Mark Gurnell, Michael C Dennedy
Endocrine Reviews.2024; 45(1): 125. CrossRef
Steroid profiling in adrenal disease
Danni Mu, Dandan Sun, Xia Qian, Xiaoli Ma, Ling Qiu, Xinqi Cheng, Songlin Yu
Clinica Chimica Acta.2024; 553: 117749. CrossRef
Plasma Steroid Profiling Combined With Machine Learning for the Differential Diagnosis in Mild Autonomous Cortisol Secretion From Nonfunctioning Adenoma in Patients With Adrenal Incidentalomas
Danni Mu, Xia Qian, Yichen Ma, Xi Wang, Yumeng Gao, Xiaoli Ma, Shaowei Xie, Lian Hou, Qi Zhang, Fang Zhao, Liangyu Xia, Liling Lin, Ling Qiu, Jie Wu, Songlin Yu, Xinqi Cheng
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Alessandro Prete, Irina Bancos
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Plasma Steroid Profiling Between Patients With and Without Diabetes Mellitus in Nonfunctioning Adrenal Incidentalomas
Yui Nakano, Maki Yokomoto-Umakoshi, Kohta Nakatani, Hironobu Umakoshi, Hiroshi Nakao, Masamichi Fujita, Hiroki Kaneko, Norifusa Iwahashi, Tatsuki Ogasawara, Tazuru Fukumoto, Yayoi Matsuda, Ryuichi Sakamoto, Yoshihiro Izumi, Takeshi Bamba, Yoshihiro Ogawa
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Serum and hair steroid profiles in patients with nonfunctioning pituitary adenoma undergoing surgery: A prospective observational study
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The Journal of Steroid Biochemistry and Molecular Biology.2023; 230: 106276. CrossRef
Recent Updates on the Management of Adrenal Incidentalomas
Seung Shin Park, Jung Hee Kim
Endocrinology and Metabolism.2023; 38(4): 373. CrossRef
LC-MS based simultaneous profiling of adrenal hormones of steroids, catecholamines, and metanephrines
Jongsung Noh, Chaelin Lee, Jung Hee Kim, Seung Woon Myung, Man Ho Choi
Journal of Lipid Research.2023; 64(11): 100453. CrossRef
2023 Korean Endocrine Society Consensus Guidelines for the Diagnosis and Management of Primary Aldosteronism
Jeonghoon Ha, Jung Hwan Park, Kyoung Jin Kim, Jung Hee Kim, Kyong Yeun Jung, Jeongmin Lee, Jong Han Choi, Seung Hun Lee, Namki Hong, Jung Soo Lim, Byung Kwan Park, Jung-Han Kim, Kyeong Cheon Jung, Jooyoung Cho, Mi-kyung Kim, Choon Hee Chung
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Aliya Lakhani, Da Hyun Kang, Yea Eun Kang, Junyoung O. Park
Endocrinology and Metabolism.2023; 38(6): 619. CrossRef
Prevalence and Characteristics of Adrenal Tumors in an Unselected Screening Population
Ying Jing, Jinbo Hu, Rong Luo, Yun Mao, Zhixiao Luo, Mingjun Zhang, Jun Yang, Ying Song, Zhengping Feng, Zhihong Wang, Qingfeng Cheng, Linqiang Ma, Yi Yang, Li Zhong, Zhipeng Du, Yue Wang, Ting Luo, Wenwen He, Yue Sun, Fajin Lv, Qifu Li, Shumin Yang
Annals of Internal Medicine.2022; 175(10): 1383. CrossRef

Diabetes, Obesity and Metabolism
Role of TRPV4 Channel in Human White Adipocytes Metabolic Activity: Julio C. Sánchez, Aníbal Valencia-Vásquez, Andrés M. García; Endocrinol Metab. 2021;36(5):997-1006. Published online October 14, 2021; DOI: https://doi.org/10.3803/EnM.2021.1167

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Background
Intracellular calcium (Ca²⁺) homeostasis plays an essential role in adipocyte metabolism and its alteration is associated with obesity and related disorders. Transient receptor potential vanilloid 4 (TRPV4) channels are an important Ca²⁺ pathway in adipocytes and their activity is regulated by metabolic mediators such as insulin. In this study, we evaluated the role of TRPV4 channels in metabolic activity and adipokine secretion in human white adipocytes.
Methods
Human white adipocytes were freshly cultured and the effects of the activation and inhibition of TRPV4 channels on lipolysis, glucose uptake, lactate production, and leptin and adiponectin secretion were evaluated.
Results
Under basal and isoproterenol-stimulated conditions, TRPV4 activation by GSK1016709A decreased lipolysis whereas HC067047, an antagonist, increased lipolysis. The activation of TRPV4 resulted in increased glucose uptake and lactate production under both basal conditions and insulin-stimulated conditions; in contrast HC067047 decreased both parameters. Leptin production was increased, and adiponectin production was diminished by TRPV4 activation and its inhibition had the opposite effect.
Conclusion
Our results suggested that TRPV4 channels are metabolic mediators involved in proadipogenic processes and glucose metabolism in adipocyte biology. TRPV4 channels could be a potential pharmacological target to treat metabolic disorders.

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Namgok Lecture 2020

Obesity and Metabolism
Cellular and Intercellular Homeostasis in Adipose Tissue with Mitochondria-Specific Stress: Min Jeong Choi, Saet-Byel Jung, Joon Young Chang, Minho Shong; Endocrinol Metab. 2021;36(1):1-11. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2021.956

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Paracrine interactions are imperative for the maintenance of adipose tissue intercellular homeostasis, and intracellular organelle dysfunction results in local and systemic alterations in metabolic homeostasis. It is currently accepted that mitochondrial proteotoxic stress activates the mitochondrial unfolded protein response (UPR^mt) in vitro and in vivo. The induction of mitochondrial chaperones and proteases during the UPR^mt is a key cell-autonomous mechanism of mitochondrial quality control. The UPR^mt also affects systemic metabolism through the secretion of cell non-autonomous peptides and cytokines (hereafter, metabokines). Mitochondrial function in adipose tissue plays a pivotal role in whole-body metabolism and human diseases. Despite continuing interest in the role of the UPR^mt and quality control pathways of mitochondria in energy metabolism, studies on the roles of the UPR^mt and metabokines in white adipose tissue are relatively sparse. Here, we describe the role of the UPR^mt in adipose tissue, including adipocytes and resident macrophages, and the interactive roles of cell non-autonomous metabokines, particularly growth differentiation factor 15, in local adipose cellular homeostasis and systemic energy metabolism.

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Review Article

Miscellaneous
Systems Biology: A Multi-Omics Integration Approach to Metabolism and the Microbiome: Jang Won Son, Saeed Shoaie, Sunjae Lee; Endocrinol Metab. 2020;35(3):507-514. Published online September 22, 2020; DOI: https://doi.org/10.3803/EnM.2020.303

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The complex and dynamic nature of human physiology, as exemplified by metabolism, has often been overlooked due to the lack of quantitative and systems approaches. Recently, systems biology approaches have pushed the boundaries of our current understanding of complex biochemical, physiological, and environmental interactions, enabling proactive medicine in the near future. From this perspective, we review how state-of-the-art computational modelling of human metabolism, i.e., genome-scale metabolic modelling, could be used to identify the metabolic footprints of diseases, to guide the design of personalized treatments, and to estimate the microbiome contributions to host metabolism. These state-of-the-art models can serve as a scaffold for integrating multi-omics data, thereby enabling the identification of signatures of dysregulated metabolism by systems approaches. For example, increased plasma mannose levels due to decreased uptake in the liver have been identified as a potential biomarker of early insulin resistance by multi-omics approaches. In addition, we also review the emerging axis of human physiology and the human microbiome, discussing its contribution to host metabolism and quantitative approaches to study its variations in individuals.

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Original Article

Endocrine Research
Liver X Receptor β Related to Tumor Progression and Ribosome Gene Expression in Papillary Thyroid Cancer: Seonhyang Jeong, In-Kyu Kim, Hyunji Kim, Moon Jung Choi, Jandee Lee, Young Suk Jo; Endocrinol Metab. 2020;35(3):656-668. Published online August 20, 2020; DOI: https://doi.org/10.3803/EnM.2020.667

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Background
Intracellular lipid deposition has been reported in thyroid glands in obese animal and human. To understand the regulatory mechanism of lipid metabolism in thyroid cancer, we investigated the expression status of liver X receptor (LXR) and analyzed its clinicopathological characteristics and molecular biological features.
Methods
Expression status of LXR and its transcriptional targets in human cancers were analyzed using The Cancer Genome Atlas (TCGA). The gene-sets related to high LXRβ expression was investigated by gene set enrichment analysis (GSEA) using Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways and gene ontology biologic process. Quantitative reverse transcription polymerase chain reaction was performed in thyroid cancer samples using our validation cohort.
Results
In contrast to low expression of LXRα, LXRβ was highly expressed in thyroid cancer compared to the other types of human cancers. High LXRβ expression was correlated with the expression of LXRβ transcriptional targets genes, such as apolipoprotein C1 (APOC1), APOC2, apolipoprotein E (APOE), ATP binding cassette subfamily G member 8 (ABCG8), sterol regulatory elementbinding protein 1c (SREBP1c), and SPOT14. Furthermore, High LXRβ expression group indicated poor clinicopathological characteristics and aggressive molecular biological features independently from the drive mutation status. Mechanistically, high LXRβ expression was coordinately related to ribosome-related gene sets.
Conclusion
The mechanistic link between LXRβ and ribosomal activity will be addressed to develop new diagnostic and therapeutic targets in thyroid cancers.

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Review Articles

Miscellaneous
Machine Learning Applications in Endocrinology and Metabolism Research: An Overview: Namki Hong, Heajeong Park, Yumie Rhee; Endocrinol Metab. 2020;35(1):71-84. Published online March 19, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.1.71

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Machine learning (ML) applications have received extensive attention in endocrinology research during the last decade. This review summarizes the basic concepts of ML and certain research topics in endocrinology and metabolism where ML principles have been actively deployed. Relevant studies are discussed to provide an overview of the methodology, main findings, and limitations of ML, with the goal of stimulating insights into future research directions. Clear, testable study hypotheses stem from unmet clinical needs, and the management of data quality (beyond a focus on quantity alone), open collaboration between clinical experts and ML engineers, the development of interpretable high-performance ML models beyond the black-box nature of some algorithms, and a creative environment are the core prerequisites for the foreseeable changes expected to be brought about by ML and artificial intelligence in the field of endocrinology and metabolism, with actual improvements in clinical practice beyond hype. Of note, endocrinologists will continue to play a central role in these developments as domain experts who can properly generate, refine, analyze, and interpret data with a combination of clinical expertise and scientific rigor.

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Obesity and Metabolism
Recent Progress on Branched-Chain Amino Acids in Obesity, Diabetes, and Beyond: Md Abu Bakkar Siddik, Andrew C. Shin; Endocrinol Metab. 2019;34(3):234-246. Published online September 26, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.3.234

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Branched-chain amino acids (BCAAs) are essential amino acids that are not synthesized in our body; thus, they need to be obtained from food. They have shown to provide many physiological and metabolic benefits such as stimulation of pancreatic insulin secretion, milk production, adipogenesis, and enhanced immune function, among others, mainly mediated by mammalian target of rapamycin (mTOR) signaling pathway. After identified as a reliable marker of obesity and type 2 diabetes in recent years, an increasing number of studies have surfaced implicating BCAAs in the pathophysiology of other diseases such as cancers, cardiovascular diseases, and even neurodegenerative disorders like Alzheimer's disease. Here we discuss the most recent progress and review studies highlighting both correlational and potentially causative role of BCAAs in the development of these disorders. Although we are just beginning to understand the intricate relationships between BCAAs and some of the most prevalent chronic diseases, current findings raise a possibility that they are linked by a similar putative mechanism.

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Obesity and Metabolism
Implications of Mitochondrial Unfolded Protein Response and Mitokines: A Perspective on Fatty Liver Diseases: Hyon-Seung Yi; Endocrinol Metab. 2019;34(1):39-46. Published online March 21, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.1.39

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The signaling network of the mitochondrial unfolded protein response (UPR^mt) and mitohormesis is a retrograde signaling pathway through which mitochondria-to-nucleus communication occurs in organisms. Recently, it has been shown that the UPR^mt is closely associated with metabolic disorders and conditions involving insulin resistance, such as alcoholic and non-alcoholic fatty liver and fibrotic liver disease. Scientific efforts to understand the UPR^mt and mitohormesis, as well as to establish the mitochondrial proteome, have established the importance of mitochondrial quality control in the development and progression of metabolic liver diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). In this review, we integrate and discuss the recent data from the literature on the UPR^mt and mitohormesis in metabolic liver diseases, including NAFLD/NASH and fibrosis.

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Mineral, Bone & Muscle
Regulation of Osteoblast Metabolism by Wnt Signaling: Megan C. Moorer, Ryan C. Riddle; Endocrinol Metab. 2018;33(3):318-330. Published online August 14, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.3.318

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Wnt/β-catenin signaling plays a critical role in the achievement of peak bone mass, affecting the commitment of mesenchymal progenitors to the osteoblast lineage and the anabolic capacity of osteoblasts depositing bone matrix. Recent studies suggest that this evolutionarily-conserved, developmental pathway exerts its anabolic effects in part by coordinating osteoblast activity with intermediary metabolism. These findings are compatible with the cloning of the gene encoding the low-density lipoprotein related receptor-5 (LRP5) Wnt co-receptor from a diabetes-susceptibility locus and the now well-established linkage between Wnt signaling and metabolism. In this article, we provide an overview of the role of Wnt signaling in whole-body metabolism and review the literature regarding the impact of Wnt signaling on the osteoblast's utilization of three different energy sources: fatty acids, glucose, and glutamine. Special attention is devoted to the net effect of nutrient utilization and the mode of regulation by Wnt signaling. Mechanistic studies indicate that the utilization of each substrate is governed by a unique mechanism of control with β-catenin-dependent signaling regulating fatty acid β-oxidation, while glucose and glutamine utilization are β-catenin-independent and downstream of mammalian target of rapamycin complex 2 (mTORC2) and mammalian target of rapamycin complex 1 (mTORC1) activation, respectively. The emergence of these data has provided a new context for the mechanisms by which Wnt signaling influences bone development.

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Miscellaneous
Evidence of the Possible Harm of Endocrine-Disrupting Chemicals in Humans: Ongoing Debates and Key Issues: Duk-Hee Lee; Endocrinol Metab. 2018;33(1):44-52. Published online March 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.1.44

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Evidence has emerged that endocrine-disrupting chemicals (EDCs) can produce adverse effects, even at low doses that are assumed safe. However, systemic reviews and meta-analyses focusing on human studies, especially of EDCs with short half-lives, have demonstrated inconsistent results. Epidemiological studies have insuperable methodological limitations, including the unpredictable net effects of mixtures, non-monotonic dose-response relationships, the non-existence of unexposed groups, and the low reliability of exposure assessment. Thus, despite increases in EDC-linked diseases, traditional epidemiological studies based on individual measurements of EDCs in bio-specimens may fail to provide consistent results. The exposome has been suggested as a promising approach to address the uncertainties surrounding human studies, but it is never free from these methodological issues. Although exposure to EDCs during critical developmental periods is a major concern, continuous exposure to EDCs during non-critical periods is also harmful. Indeed, the evolutionary aspects of epigenetic programming triggered by EDCs during development should be considered because it is a key mechanism for developmental plasticity. Presently, living without EDCs is impossible due to their omnipresence. Importantly, there are lifestyles which can increase the excretion of EDCs or mitigate their harmful effects through the activation of mitohormesis or xenohormesis. Effectiveness of lifestyle interventions should be evaluated as practical ways against EDCs in the real world.

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Diabetes-Related Cardiac Dysfunction: Lamario J. Williams, Brenna G. Nye, Adam R. Wende; Endocrinol Metab. 2017;32(2):171-179. Published online June 23, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.2.171

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The proposal that diabetes plays a role in the development of heart failure is supported by the increased risk associated with this disease, even after correcting for all other known risk factors. However, the precise mechanisms contributing to the condition referred to as diabetic cardiomyopathy have remained elusive, as does defining the disease itself. Decades of study have defined numerous potential factors that each contribute to disease susceptibility, progression, and severity. Many recent detailed reviews have been published on mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors. As such, the focus of the current review is to highlight aspects of each of these topics and to provide specific examples of recent advances in each area.

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Obesity and Metabolism
Brain Regulation of Energy Metabolism: Eun Roh, Min-Seon Kim; Endocrinol Metab. 2016;31(4):519-524. Published online December 20, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.4.519

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In healthy individuals, energy intake is in balance with energy expenditure, which helps to maintain a normal body weight. The brain's inability to control energy homeostasis underlies the pathology of hyperphagia and obesity. The brain detects body energy excess and deficit by sensing the levels of circulating metabolic hormones and nutrients and by receiving metabolic information from the periphery via the autonomic nervous system. A specialized neuronal network coordinates energy intake behavior and the metabolic processes affecting energy expenditure. Here, we briefly review neuronal mechanisms by which our body maintains energy balance.

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Obesity and Metabolism
Connecting Myokines and Metabolism: Rexford S. Ahima, Hyeong-Kyu Park; Endocrinol Metab. 2015;30(3):235-245. Published online August 4, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.3.235

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Abstract PDF PubReader

Skeletal muscle is the largest organ of the body in non-obese individuals and is now considered to be an endocrine organ. Hormones (myokines) secreted by skeletal muscle mediate communications between muscle and liver, adipose tissue, brain, and other organs. Myokines affect muscle mass and myofiber switching, and have profound effects on glucose and lipid metabolism and inflammation, thus contributing to energy homeostasis and the pathogenesis of obesity, diabetes, and other diseases. In this review, we summarize recent findings on the biology of myokines and provide an assessment of their potential as therapeutic targets.

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Thyroid
Mitochondrial Energy Metabolism and Thyroid Cancers: Junguee Lee, Joon Young Chang, Yea Eun Kang, Shinae Yi, Min Hee Lee, Kyong Hye Joung, Kun Soon Kim, Minho Shong; Endocrinol Metab. 2015;30(2):117-123. Published online June 30, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.2.117

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Primary thyroid cancers including papillary, follicular, poorly differentiated, and anaplastic carcinomas show substantial differences in biological and clinical behaviors. Even in the same pathological type, there is wide variability in the clinical course of disease progression. The molecular carcinogenesis of thyroid cancer has advanced tremendously in the last decade. However, specific inhibition of oncogenic pathways did not provide a significant survival benefit in advanced progressive thyroid cancer that is resistant to radioactive iodine therapy. Accumulating evidence clearly shows that cellular energy metabolism, which is controlled by oncogenes and other tumor-related factors, is a critical factor determining the clinical phenotypes of cancer. However, the role and nature of energy metabolism in thyroid cancer remain unclear. In this article, we discuss the role of cellular energy metabolism, particularly mitochondrial energy metabolism, in thyroid cancer. Determining the molecular nature of metabolic remodeling in thyroid cancer may provide new biomarkers and therapeutic targets that may be useful in the management of refractory thyroid cancers.

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Obesity and Metabolism
Roles of Protein Arginine Methyltransferases in the Control of Glucose Metabolism: Hye-Sook Han, Dahee Choi, Seri Choi, Seung-Hoi Koo; Endocrinol Metab. 2014;29(4):435-440. Published online December 29, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.4.435

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Glucose homeostasis is tightly controlled by the regulation of glucose production in the liver and glucose uptake into peripheral tissues, such as skeletal muscle and adipose tissue. Under prolonged fasting, hepatic gluconeogenesis is mainly responsible for glucose production in the liver, which is essential for tissues, organs, and cells, such as skeletal muscle, the brain, and red blood cells. Hepatic gluconeogenesis is controlled in part by the concerted actions of transcriptional regulators. Fasting signals are relayed by various intracellular enzymes, such as kinases, phosphatases, acetyltransferases, and deacetylases, which affect the transcriptional activity of transcription factors and transcriptional coactivators for gluconeogenic genes. Protein arginine methyltransferases (PRMTs) were recently added to the list of enzymes that are critical for regulating transcription in hepatic gluconeogenesis. In this review, we briefly discuss general aspects of PRMTs in the control of transcription. More specifically, we summarize the roles of four PRMTs: PRMT1, PRMT 4, PRMT 5, and PRMT 6, in the control of hepatic gluconeogenesis through specific regulation of FoxO1- and CREB-dependent transcriptional events.

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Obesity and Metabolism
Role of Autophagy in the Control of Body Metabolism: Wenying Quan, Myung-Shik Lee; Endocrinol Metab. 2013;28(1):6-11. Published online March 25, 2013; DOI: https://doi.org/10.3803/EnM.2013.28.1.6

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Autophagy plays a crucial role in the maintenance of cellular nutrient balance and the function of organelles such as mitochondria or the endoplasmic reticulum, which are important in intracellular metabolism, insulin release, and insulin sensitivity. In the insulin-producing pancreatic β-cells, autophagy is important in the maintenance of β-cell mass, structure, and function. Mice with deficiencies in β-cell-specific autophagy show reduced β-cell mass and defects in insulin secretion that lead to hypoinsulinemia and hyperglycemia but not diabetes. However, these mice developed diabetes when bred with ob/ob mice, suggesting that autophagy-deficient β-cells have defects in dealing with the increased metabolic stress imposed by obesity. These results also imply that autophagy deficiency in β-cells could be a factor in the progression from obesity to diabetes. Another important function of autophagy is in hypothalamic neurons for the central control of energy expenditure, appetite, and body weight. In addition, mice with autophagy deficiencies in the target tissues of insulin have yielded diverse phenotypes. Taken together, these results suggest that autophagy is important in the control of whole body energy and nutrient homeostasis, and its dysregulation could play a role in the development of metabolic disorders and diabetes.

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Changes in Growth Hormone-Axis Function in Nutrient Excess or Deprivation.: Seungjoon Park; Endocrinol Metab. 2011;26(4):279-284. Published online December 1, 2011; DOI: https://doi.org/10.3803/EnM.2011.26.4.279

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Abstract PDF: Growth hormone (GH) is produced in a select population of cells, somatotropes, located in the anterior pituitary gland. GH is released into the general circulation where it interacts with multiple peripheral tissues through its receptor, GH receptor, to regulate growth and metabolic function. GH-releasing hormone (GHRH) and somatostatin are the primary positive and negative regulators of GH secretion, respectively. More recently, ghrelin has emerged as an additional stimulatory hormone for GH release. In humans, GH levels decrease in states of nutrient excess, such as obesity, and increase in response to nutrient deprivation, such as fasting, type 1 diabetes, and anorexia nervosa. Considering that GH regulates metabolism of carbohydrate, lipid, and protein, clarifying the mechanisms by which metabolic changes alter pituitary GH synthesis and secretion will increase our knowledge on the pathophysiology and treatment of metabolic diseases. In this review, the effect of nutrient excess and nutrient deficiency on GH-axis function in humans and other mammals will be summarized, with particular emphasis on studies exploring the direct effects of systemic signals, including insulin-like growth factor 1 (IGF-1) and insulin, on somatotrope function. Additionally, new mouse models with somatotrope-specific knockout of IGF-1 and insulin receptors generated by using the Cre/loxP system will be discussed.

Original Articles

The Effects of Combined Treatment of Alendronate Plus Active or Plain Vitamin D on the Vitamin D Metabolism and Bone Turnover Markers in Patients with Osteoporosis.: Jee Hoon Koo, Hyun Kyung Kim, In Sung Kim, Eun Kyung Kim, Yoon Sok Chung; Endocrinol Metab. 2010;25(4):305-309. Published online December 1, 2010; DOI: https://doi.org/10.3803/EnM.2010.25.4.305

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BACKGROUND
The purpose of this study was to evaluate the effects of combined treatment with alendronate plus active or plain vitamin D on the vitamin D metabolism and bone turnover markers in patients with osteoporosis. METHODS: We investigated 297 osteoporosis outpatients who were treated with Maxmarvil(R) (alendronate 5 mg plus calcitriol 0.5 microg) daily or Fosamax Plus(R) (alendronate 70 mg plus cholecalciferol 2,800 IU) weekly for 1 year. The serum levels of 25(OH)D, parathyroid hormone (PTH), calcium, phosphorus, osteocalcin and N-telopeptide were measured at baseline and after 3, 6, and 12 months of treatment. RESULTS: The data of 72 of the 297 patients were analyzed. In the Maxmarvil(R) group (n = 45), the serum PTH significantly decreased by 17% from baseline at 6 months (microd = -6.10; +/- 0.85 SE; P < 0.05) and it remained suppressed to 12 months. The serum 25(OH)D tended to increase, but without significance. In the Fosamax Plus(R) group (n = 27), the serum 25(OH)D significantly increased by 77% from baseline at 3 months (microd = 9.87; +/- 2.32 SE; P < 0.05) and it remained significantly higher than baseline at 6 months (microd = 3.49; +/- 0.86 SE; P < 0.05) and 12 months (microd = 10.47; +/- 0.71 SE; P < 0.001). However, the serum PTH showed no significant decrease. In the Maxmarvil(R) group, the serum osteocalcin significantly decreased by 26% from baseline at 12 months (microd = -5.15; +/- 0.35 SE; P < 0.05), and in the Fosamax Plus(R) group, the serum osteocalcin significantly decreased by 19% from baseline at 6months (microd = -2.64; +/- 0.73 SE; P < 0.05) and it remained suppressed to 12 months (microd = -2.99; +/- 0.37 SE; P = 0.32) without significance. CONCLUSION: Maxmarvil(R) and Fosamax Plus(R) both improved the bone metabolism in Korean osteoporosis patients. Maxmarvil(R) significantly lowered the serum PTH levels, whereas Fosamax Plus(R) significantly elevated the serum 25(OH)D levels.

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Efficacy and Safety of Weekly Alendronate Plus Vitamin D35600 IU versus Weekly Alendronate Alone in Korean Osteoporotic Women: 16-Week Randomized Trial
Kwang Joon Kim, Yong-Ki Min, Jung-Min Koh, Yoon-Sok Chung, Kyoung Min Kim, Dong-Won Byun, In Joo Kim, Mikyung Kim, Sung-Soo Kim, Kyung Wan Min, Ki Ok Han, Hyoung Moo Park, Chan Soo Shin, Sung Hee Choi, Jong Suk Park, Dong Jin Chung, Ji Oh Mok, Hong Sun Ba
Yonsei Medical Journal.2014; 55(3): 715. CrossRef

Relationship between Serum Osteoprotegerin-Receptor Activator of NF-kappaB Ligand Levels and Bone Mineral Metabolism in Men.: Ki Won Oh, Eun Joo Yun, Eun Jung Rhee, Won Young Lee, Ki Hyun Baek, Moo Il Kang, Cheol Young Park, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park; J Korean Endocr Soc. 2004;19(4):332-345. Published online August 1, 2004

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Abstract PDF: BACKGROUND
Osteoporosis is a growing health problem, not only in women, but in men also. Sex hormones and insulin-like growth factor-I (IGF-I) have been shown to be the major determinant in male bone metabolism. Osteoprotegerin (OPG) is a recently identified cytokine, which acts as a decoy receptor for the receptor activator of the NF- B ligand (RANKL). OPG and RANKL have been shown to be important regulators of osteoclastogenesis in animal models. The relationship between the OPG-RANKL system and male bone status in human populations is unclear. The aim of this study was to investigate the relationship between circulating the OPG-RANKL system and bone mineral metabolism in 80 Korean men. METHODS: The subjects of this study were 80 men aged between 42 and 70 (mean age, 54.5 yr). The serum concentrations of OPG and RANKL were measured by ELISA. The serum concentrations of estradiol, total testosterone, IGF-I and biochemical markers of bone turnover were measured by standard methods. The bone mineral densites (BMD) at the lumbar spine and femoral neck were measured by dual energy x-ray absorptiometry. RESULTS: A significant correlation was observed between the serum OPG/RANKL ratios and osteocalcin levels (r=-0.229, p<0.05). The serum OPG levels were significantly correlated to the femoral neck BMD (r=-0.227, p<0.05). The mean value of the serum OPG was found to be greater in patients with osteoporosis at the femoral neck (mean SD, 4.72.1 pmol/L) than in subjects with a normal BMD (3.30.9 pmol/L, p<0.05). The serum RANKL/OPG ratios were significantly positively correlated to the serum estradiol level (r=0.401, p<0.001). Also, there was a significant negative correlation between the serum OPG and estradiol levels (r=-0.288, p<0.05). In a multiple regression analysis, the BMI, serum OPG and RANKL levels, and the serum IGF-I level were identified as significant predictors of the femoral neck BMD. In another multiple regression analysis, only the serum estradiol level was identified as a significant predictor of the serum OPG level. CONCLUSION: In conclusion, our data show that the serum OPG and RANKL levels are partly associated with bone mineral metabolism, and are related to the endogenous estrogen levels in human male populations. Therefore, the possibility exists that the OPG-RANKL system may be a mediator of the estradiol in male bone metabolism. However, there have been few study published on the relation between the serum OPG and estradiol levels in men. Further studies are needed to clarify this relationship

Adverse Effects of Antiepileptic Drugs on Bone Mineral Density in Women with Epilepsy.: Yong Won Cho, In Kyu Lee, Seung Ho Hur; J Korean Endocr Soc. 2002;17(2):218-225. Published online April 1, 2002

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Abstract PDF: BACKGROUND
Osteoporosis or osteopenia has been reported in patients taking antiepileptic drugs, but the precise pathophysiological mechanisms of these abnormalities are unclear. The aim of this study was to assess the relationship of antiepileptic drugs on bone mass by analyzing bone mineral density (BMD). METHODS: We compared 62 epileptic women on long-term antiepileptic therapy the same number of age and weight matched healthy control subjects. We measured the serum calcium, phosphorus, protein, alkaline phosphatase and osteocalcin for analyzing factors, that have an influence on bone metabolism and BMD. BMD was measured on the lumbar spine by dual-energy X-ray absorptiometry. RESULTS: The serum level of calcium and osteocalcin were not different between the groups. The serum level of phosphorus and protein were significantly lower in the patient group compared to their controls. The serum level of alkaline phosphatase was significantly higher in the patient group than in their controls. The BMD was significantly lower in the patient group than in their controls. There was a significant correlation between the BMD and the duration of therapy in the patient group. CONCLUSION: The long-term use of antiepileptic drugs leads to a decreased BMD, and the degree of bone mineral density was related to the duration of the therapeutic use of antiepileptics.

The Effects of Type 1 diabetes on the Metabolism and Density of Bone in Children.: Sang Jun Lee, Dong Wook Lee, Hyun Dae Yoon, Kyu Chang Won, Hyoung Woo Lee, Yoon Jung Cho, Heung Sik Kim, Seung Beom Han, In Kyu Lee, Hee Ja Lee; J Korean Endocr Soc. 2000;15(4-5):582-590. Published online January 1, 2001

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Abstract PDF: BACKGROUND
The effects of type 1 diabetes mellitus on the metabolism and density of bone in children are still controversial. The aim of this study was to evaluate the effects of type 1 diabetes on markers of bone metaboism and BMD in children by analyzing BMI, HbA1c, biochemical markers, sex hormones, bone metabolism and BMD related factors. MRTHODS: We compared 36 patients (15 males, 21 females) with type 1 diabetes mellitus to 167 healthy children (84 males, 83 females) who lived in Taegu. We measured FBS, serum calcium, phosphorus, HbA1c, osteocalcin, testosterone and estradiol for analyzing the factors which influence on bone metabolism and BMD. BMD was measured at lumbar spine, femur and total body by DEXA. RESULTS: The BMI and serum level of osteocalcin were not different in both groups. Serum calcium level was significantly lower in the diabetic group than that of control group. BMD had no difference in both groups. There was no correlation between BMD and glycemic control (HbA1c) or duration of diabetes. There was good correlation (r=0.78, p<0.01) between serum testosterone level and BMD in male patient group. There was negative correlation (r=-0.4) between serum osteocalcin level and BMD. There was significant correlation (male: r=0.76, female: r=0.66) between lean body mass and BMD in both group. CONCLUSION: The BMD was not decreased significantly and bone turn-over was normal in children with noncomplicated type 1 diabetes mellitus, and BMD was not influenced by the duration or degree of metabolic control of diabetes. But, we need further study including other risk factors that have influences on BMD and bone metabolism in type 1 diabetes mellitu.

The Effects of Growth Hormone Tretment on Body Composition and Glucose Metabolism in Adult Hypophysectomized Rats.: Kwan Woo Lee, Hyun Chul Lee, Kap Bum Huh, Yoon Sok Chung, Deok Bae Park, Yup Kang, Hyeon Man Kim, Seoung Oh Yang; J Korean Endocr Soc. 1997;12(1):53-60. Published online January 1, 2001

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Abstract PDF: BACKGROUND
It is well known that growth hormone (GH) stimulates animal growth, but studies on metabolic effects of growth hormone have recently been increasing. The purpose of this study was to clarify the effects of growth hormone treatment on body composition and glucose metabolism in hypophysectomized growth hormone-deficient rats. METHODS: The 20-week-old rnale Sprague-Dawley rats were hypophysectomized and replaced with cortisol and thyroxine for 8 weeks, then administered with recombinant human growth hormone for 2 weeks. Group 1 consisted of intact controls (n 15), while group 2 consisted of hypophysectomized controls (n 12), and group three consisted of those with GH treatment (n 13). The body weights, body composition, blood glucose levels, plasma insulin-like growth factor-I (IGF-I) levels, euglycemic hyperinsulinemic clamp test, and glycogen synthase activities in gastrocnemius muscle were measured before and after growth hormone treatment. RESULTS: Plasma IGF-I levels in GH-treated group increased to intact control group levels after 2 weeks of GH treatment. There were significant changes in body composition after the treatment (fat mass significantly decreased and lean body mass significantly increased). There were no changes in glucose metabolism in peripheral tissue after 2 weeks of GH treatment. CONCLUSION: Human GH treatment (4 IU/kg/day) in adult hypophysectomized GH-deficient rats changed the body composition, but did not alter the glucose metabolism in peripheral tissue.

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