Endocrinology and Metabolism

Review Article

Diabetes, obesity and metabolism
SGLT2 Inhibitors as Systemic Metabolic Modulators: Linking Glucose Excretion to Liver Function Restoration: Seung Wan Noh, Han Sol Ryu, Yong-Ho Kim, Byung-Chul Oh; Endocrinol Metab. 2025;40(6):851-865. Published online December 24, 2025; DOI: https://doi.org/10.3803/EnM.2025.2786

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Sodium-glucose cotransporter 2 (SGLT2) inhibitors have emerged as paradigm-shifting therapeutics that extend beyond glycemic regulation, to conferring profound hepatometabolic benefits. This review delineates the multifaceted mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD), with an emphasis on systemic metabolic remodeling, mitochondrial protection, and intracellular calcium restoration. By promoting glucosuria-induced energy depletion, SGLT2 inhibition alleviates insulin resistance, suppresses hepatic lipogenesis, and activates adenosine monophosphate-activated protein kinase (AMPK)–sirtuin 1 (SIRT1)–peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α pathways that reprogram hepatocellular metabolism toward achieving lipid oxidation and autophagy. Mechanistically, SGLT2 inhibitors restore intracellular Ca²⁺ homeostasis via sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) activation, mitigating endoplasmic reticulum (ER) stress and normalizing Ca²⁺–phosphoinositide (PIP)–protein kinase B (AKT) signaling, collectively reinforcing insulin responsiveness and ER-mitochondrial crosstalk. Clinically, these effects translate into consistently reducing hepatic fat, aminotransferases, and fibrosis markers in both diabetic and nondiabetic patients with MASLD. Furthermore, SGLT2 inhibitors uniquely integrate renal energy regulation with hepatic resilience through the Ca²⁺–PIP–SERCA axis, positioning them as prototype systemic modulators of metabolic homeostasis. Future translational efforts should refine patient stratification using metabolomic and Ca²⁺-imaging biomarkers to delineate therapeutic responders and advance next-generation SGLT2 analogs targeting Ca²⁺-dependent metabolic signaling. Collectively, SGLT2 inhibitors represent a new metabolic therapeutic class that unify glucose, lipid, and Ca²⁺ regulation to restore hepatocellular functions in metabolic liver diseases.

Citations

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Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation
Senping Xu, Zhaoshan Zhang, Zhongquan Zhou, Jiawei Guo
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Protective effect of dapagliflozin against hepatic ischemia-reperfusion injury in rats
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Molecular Biology Reports.2026;[Epub] CrossRef
Ipragliflozin exerts anti-fibrotic effects via a novel multi-pathway mechanism: Targeting TLR4/NF-κB /TGF-β1 cascade
Mahdi H. Alsugoor, Naif ALSuhaymi, Passant E. Moustafa, Mevidette Elmadani, Nehal A. Afifi, Ahmed Derzawy, Noha E. Ibrahim, Hany M. Fayed, Sally A. El Awdan
The International Journal of Biochemistry & Cell Biology.2026; 197-198: 106964. CrossRef
Effects of SGLT-2 inhibitors and GLP-1 receptor agonists on liver function in patients with non-alcoholic fatty liver disease and type 2 diabetes
Wancheng Guo, Wenhe Li, Xianlin Li, Wen Shi, Yan Yan, Ting Yan, Jie Zhou, Yujie Huang
Frontiers in Endocrinology.2026;[Epub] CrossRef
Mitochondrial remodeling in obesity: mechanistic links to impaired energy metabolism and therapeutic perspectives
Welington Henrique Justo Neto, Camila de Oliveira Ramos, Claudio Teodoro De Souza
Physiology & Behavior.2026; 315: 115427. CrossRef
Calcium imbalance drives organelle network collapse and immune remodeling: novel pathogenic mechanisms in MASLD progression
Senping Xu, Ziyang Jiang, Qing Zhang, Jiawei Guo
Frontiers in Immunology.2026;[Epub] CrossRef

Original Article

Thyroid
Developmental Hypothyroidism Influences the Development of the Entorhinal-Dentate Gyrus Pathway of Rat Offspring: Ting Jin, Ranran Wang, Shiqiao Peng, Xin Liu, Hanyi Zhang, Xue He, Weiping Teng, Xiaochun Teng; Endocrinol Metab. 2022;37(2):290-302. Published online April 8, 2022; DOI: https://doi.org/10.3803/EnM.2021.1343

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Background
Developmental hypothyroidism impairs learning and memory in offspring, which depend on extensive neuronal circuits in the entorhinal cortex, together with the hippocampus and neocortex. The entorhinal-dentate gyrus pathway is the main entrance of memory circuits. We investigated whether developmental hypothyroidism impaired the morphological development of the entorhinal-dentate gyrus pathway.
Methods
We examined the structure and function of the entorhinal-dentate gyrus pathway in response to developmental hypothyroidism induced using 2-mercapto-1-methylimidazole.
Results
1,1´-Dioctadecyl-3,3,3´,3´-tetramethylindocarbocyanine perchlorate tract tracing indicated that entorhinal axons showed delayed growth in reaching the outer molecular layer of the dentate gyrus at postnatal days 2 and 4 in hypothyroid conditions. The proportion of fibers in the outer molecular layer was significantly smaller in the hypothyroid group than in the euthyroid group at postnatal day 4. At postnatal day 10, the pathway showed a layer-specific distribution in the outer molecular layer, similar to the euthyroid group. However, the projected area of entorhinal axons was smaller in the hypothyroid group than in the euthyroid group. An electrophysiological examination showed that hypothyroidism impaired the long-term potentiation of the perforant and the cornu ammonis 3–cornu ammonis 1 pathways. Many repulsive axon guidance molecules were involved in the formation of the entorhinaldentate gyrus pathway. The hypothyroid group had higher levels of erythropoietin-producing hepatocyte ligand A3 and semaphorin 3A than the euthyroid group.
Conclusion
We demonstrated that developmental hypothyroidism might influence the development of the entorhinal-dentate gyrus pathway, contributing to impaired long-term potentiation. These findings improve our understanding of neural mechanisms for memory function.

Citations

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Association of hippocampus, entorhinal cortex, and amygdala with thyroid function: a bilateral volumetric analysis
Asma Hallab
Thyroid Research.2026;[Epub] CrossRef
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Mengyan Wu, Xingdong Zeng, Yongle Cai, Haonan Chen, Hao Yang
Biomedicines.2025; 13(6): 1436. CrossRef
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Review Articles

Diabetes, Obesity and Metabolism
Receptor-Mediated Muscle Homeostasis as a Target for Sarcopenia Therapeutics: Jong Hyeon Yoon, Ki-Sun Kwon; Endocrinol Metab. 2021;36(3):478-490. Published online June 28, 2021; DOI: https://doi.org/10.3803/EnM.2021.1081

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Sarcopenia is a disease characterized by age-related decline of skeletal muscle mass and function. The molecular mechanisms of the pathophysiology of sarcopenia form a complex network due to the involvement of multiple interconnected signaling pathways. Therefore, signaling receptors are major targets in pharmacological strategies in general. To provide a rationale for pharmacological interventions for sarcopenia, we herein describe several druggable signaling receptors based on their role in skeletal muscle homeostasis and changes in their activity with aging. A brief overview is presented of the efficacy of corresponding drug candidates under clinical trials. Strategies targeting the androgen receptor, vitamin D receptor, Insulin-like growth factor-1 receptor, and ghrelin receptor primarily focus on promoting anabolic action using natural ligands or mimetics. Strategies involving activin receptors and angiotensin receptors focus on inhibiting catabolic action. This review may help to select specific targets or combinations of targets in the future.

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Diabetes, Obesity and Metabolism
An Update on Contraception in Polycystic Ovary Syndrome: Seda Hanife Oguz, Bulent Okan Yildiz; Endocrinol Metab. 2021;36(2):296-311. Published online April 15, 2021; DOI: https://doi.org/10.3803/EnM.2021.958

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Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women, characterized by hyperandrogenism, oligo/anovulation, and polycystic ovarian morphology. Combined oral contraceptives (COCs), along with lifestyle modifications, represent the first-line medical treatment for the long-term management of PCOS. Containing low doses of estrogen and different types of progestin, COCs restore menstrual cyclicity, improve hyperandrogenism, and provide additional benefits such as reducing the risk of endometrial cancer. However, potential cardiometabolic risk associated with these agents has been a concern. COCs increase the risk of venous thromboembolism (VTE), related both to the dose of estrogen and the type of progestin involved. Arterial thrombotic events related to COC use occur much less frequently, and usually not a concern for young patients. All patients diagnosed with PCOS should be carefully evaluated for cardiometabolic risk factors at baseline, before initiating a COC. Age, smoking, obesity, glucose intolerance or diabetes, hypertension, dyslipidemia, thrombophilia, and family history of VTE should be recorded. Patients should be re-assessed at consecutive visits, more closely if any baseline cardiometabolic risk factor is present. Individual risk assessment is the key in order to avoid unfavorable outcomes related to COC use in women with PCOS.

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Diabetes, Obesity and Metabolism
In Vivo and In Vitro Quantification of Glucose Kinetics: From Bedside to Bench: Il-Young Kim, Sanghee Park, Yeongmin Kim, Yewon Chang, Cheol Soo Choi, Sang-Hoon Suh, Robert R. Wolfe; Endocrinol Metab. 2020;35(4):733-749. Published online December 23, 2020; DOI: https://doi.org/10.3803/EnM.2020.406

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Like other substrates, plasma glucose is in a dynamic state of constant turnover (i.e., rates of glucose appearance [R_a glucose] into and disappearance [R_d glucose] from the plasma) while staying within a narrow range of normal concentrations, a physiological priority. Persistent imbalance of glucose turnover leads to elevations (i.e., hyperglycemia, R_a>R_d) or falls (i.e., hypoglycemia, R_a<R_d) in the pool size, leading to clinical conditions such as diabetes. Endogenous Ra glucose is divided into hepatic glucose production via glycogenolysis and gluconeogenesis (GNG) and renal GNG. On the other hand, R_d glucose, the summed rate of glucose uptake by tissues/organs, involves various intracellular metabolic pathways including glycolysis, the tricarboxylic acid (TCA) cycle, and oxidation at varying rates depending on the metabolic status. Despite the dynamic nature of glucose metabolism, metabolic studies typically rely on measurements of static, snapshot information such as the abundance of mRNAs and proteins and (in)activation of implicated signaling networks without determining actual flux rates. In this review, we will discuss the importance of obtaining kinetic information, basic principles of stable isotope tracer methodology, calculations of in vivo glucose kinetics, and assessments of metabolic flux in experimental models in vivo and in vitro.

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Special Article

Miscellaneous
Diagnosis and Treatment of Growth Hormone Deficiency: A Position Statement from Korean Endocrine Society and Korean Society of Pediatric Endocrinology: Jung Hee Kim, Hyun Wook Chae, Sang Ouk Chin, Cheol Ryong Ku, Kyeong Hye Park, Dong Jun Lim, Kwang Joon Kim, Jung Soo Lim, Gyuri Kim, Yun Mi Choi, Seong Hee Ahn, Min Ji Jeon, Yul Hwangbo, Ju Hee Lee, Bu Kyung Kim, Yong Jun Choi, Kyung Ae Lee, Seong-Su Moon, Hwa Young Ahn, Hoon Sung Choi, Sang Mo Hong, Dong Yeob Shin, Ji A Seo, Se Hwa Kim, Seungjoon Oh, Sung Hoon Yu, Byung Joon Kim, Choong Ho Shin, Sung-Woon Kim, Chong Hwa Kim, Eun Jig Lee; Endocrinol Metab. 2020;35(2):272-287. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.272

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Growth hormone (GH) deficiency is caused by congenital or acquired causes and occurs in childhood or adulthood. GH replacement therapy brings benefits to body composition, exercise capacity, skeletal health, cardiovascular outcomes, and quality of life. Before initiating GH replacement, GH deficiency should be confirmed through proper stimulation tests, and in cases with proven genetic causes or structural lesions, repeated GH stimulation testing is not necessary. The dosing regimen of GH replacement therapy should be individualized, with the goal of minimizing side effects and maximizing clinical improvements. The Korean Endocrine Society and the Korean Society of Pediatric Endocrinology have developed a position statement on the diagnosis and treatment of GH deficiency. This position statement is based on a systematic review of evidence and expert opinions.

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Original Articles

Changes in Serum Lipids and Apolipoproteins Levels According to the Thyroxine Treatment in The Patients with Subclinical Hypothyroidism.: Hye Young Park, Bo Youn Cho, Won Bae Kim, Hong Gyu Lee, Chang Soon Koh, Geon Sang Park, Hyung Kyu Park, Sook Kyung Kim, Chan Soo Shin, Seong Yeon Kim; J Korean Endocr Soc. 1996;11(1):41-51. Published online November 7, 2019

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Abstract PDF: Background
Subclinical hypothyroidism(SCH) is a common biochemical abnormality which can be found in routine screening tests of thyroid function. We are increasingly faced with the question of whether its an indication for thyroxine replacement therapy. The effect of thyroxine replacement on lipid profile in SCH has aroused a great interest because of an association of overt hypothyroidism(OVH) with hyperlipidemia and increased risk of coronary artery disease. Method: We prospectively evaluated the changes in lipids and apoproteins before and after thyroxine replacement therapy in 23 patients with SCH and in 37 patients with OVH. We measured serum total cholesterol and triglyceride using autoanalyzer, high density lipoprotein(HDL) chole-sterol by dextran sulfate method, Apo A1 and Apo B by immunonephelometric assay. Results: Thyroxine replacement therapy significantly decreased total cholesterol, low density lipoprotein(LDL) cholesterol and apo B levels, but did not affect the level of triglyceride, HDL cholesterol or apo AI in patients with OVH. In SCH, thyroxine replacement therapy with the doses to normalize serum TSH concentrations also decreased significantly the level of cholesterol and LDL cholesterol albeit apo B levels did not change. Moreover, in most of patients with OVH (11 of 12) and in all of patients with SCH(5 of 5) who had had hyperchlesterolemia before treatment, thyroxine replament normalized their cholesterol and LDL cholesterol levels. Conclusion: In regard to the beneficial changes in blood lipid levels, patients with SCH should be treated, especially in cases who have other risk factors for the development of atherosclerosis. If thyroxine replacement only will reduce the incidence of coronary artery disease in SCH remains to be elucidated by long-term prospective studies.

Plasma Angiotensin - Converting Enzyme Activity, NAG, Renin and Atrial Natriuretic Peptide in Korean Male Subjects.: Jin Hong Lee, Suhn Hee Kim, Ho Shin Song, Sang Hun Han, Kyung Woo Cho, Gou Young Koh; J Korean Endocr Soc. 1994;9(1):18-24. Published online November 6, 2019

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Abstract PDF: The purpose of the present study was to define the normal range of plasma concentration of angiotensin I-converting enzyme(ACE), N-acetyl-b-D-glucosaminidase(NAG), inactive and active renin, and atrial natriuretic peptide(ANP) in normal Korean adult male in terms of aging. Both plasma ACE activity and NAG concentration were measured by spectrofluorometry, and the plasma renin activity and ANP concentration were measured using radioimmunoassay. The ACE was 67.7+-3.6 nM His-Leu/min/ml and did not change in terms of age. The plasma NAG activity tended to decrease. Both plasma active and inactive renin activities were 2.1+-0.2 and 3.0+-0.3 ngAI/ml/h and tended to decrease in terms of aging. The percentage of inactive renin to total renin was 57.2+-2.9% at age 21-30 and also tended to decrease in terms of aging. Plasma ANP concentration at age 22 was 59.6+-2.9 pg/ml.

Letter

Adrenal gland
An Ectopic Cortisol-Producing Adrenocortical Adenoma Masquerading as a Liposarcoma in the Pararenal Space: Sunyoung Kang, Seung Shin Park, Jae Hyun Bae, Kyu Eun Lee, Jung Hee Kim, Chan Soo Shin; Endocrinol Metab. 2018;33(3):423-424. Published online August 14, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.3.423

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Review Article

Epigenetic Modifications: Novel Therapeutic Approach for Thyroid Cancer: Xuguang Zhu, Sheue-yann Cheng; Endocrinol Metab. 2017;32(3):326-331. Published online September 18, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.3.326

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The incidence of thyroid cancer is growing the fastest among all cancers in the United States, especially in women. The number of patients with thyroid neoplasm is part of an even larger number of patients who often need to undergo an operation to exclude a cancer diagnosis. While differentiated thyroid cancer (papillary thyroid cancer and follicular thyroid cancer) accounts for most cases of thyroid cancer and has a relatively good prognosis, effective treatments for patients with de-differentiated and anaplastic thyroid cancer are still gravely needed. Despite progress in the identification of genetic changes in thyroid cancer, the impact of aberrant epigenetic alterations on thyroid cancer remains to be fully elucidated. Understanding of the roles of epigenetic changes in thyroid cancer could open new opportunities for the identification of innovative molecular targets for novel treatment modalities, especially for anaplastic thyroid cancer for which treatment is very limited. This article briefly reviews the studies that exemplify the potential for and promise of using epigenetic regulators in the treatment of thyroid cancer.

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Original Articles

The Effect of Hormone Replacement Therapy on Carotid Intima-Media Thickness in Healthy Postmenopausal Women.: Jang Yel Shin, Bong Soo Cha, Choon Hee Chung, Won Heum Shim, Hyun Chul Lee; J Korean Endocr Soc. 2006;21(1):14-21. Published online February 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.1.14

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Abstract PDF: BACKGROUND
Cardiovascular disease is the leading cause of death in postmenopausal women. The use of hormone replacement therapy (HRT) preventing for cardiovascular disease in postmenopausal women remains controversial. We investigated the effect of HRT on carotid intima-media thickness (IMT) according to the HRT duration in healthy postmenopausal women. METHODS: One hundred and twenty postmenopausal women (mean age: 55.4 +/- 3.3 years) were classified into never users, short-term, and long-term users according to the HRT duration. Carotid IMT was measured, and the clinical and biochemical cardiovascular risk factors were examined. RESULTS: The mean IMT was significantly thinner in the long-term users than that in the never users (0.62 +/- 0.11 vs. 0.71 +/- 0.14 mm, P < 0.01). Also, the maximal IMT was significantly thinner in the short-term and the long-term users. However, there is no significant difference in the mean and maximal IMTs between the estrogen alone and estrogen plus progestins used group. The period exposed to menopause was significantly shorter in the long-term users than that in the never users (1.8 +/- 2.3 vs. 4.3 +/- 3.3 years, P < 0.001). CONCLUSION: Our findings suggest that if HRT is initiated during early postmenopausal period before the onset of atherosclerosis, HRT may have a beneficial effect on the prevention of carotid atherosclerosis.

The Effects on Visceral Fat and Cardiovascular Risk Factors of Testosterone Replacement in Secondary Hypogonadal Men.: Eui Sil Hong, Sung Yeon Kim, Young Ju Choi, Sang Wan Kim, Chan Soo Shin, Kyong Soo Park, Hak Chul Jang, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee; J Korean Endocr Soc. 2005;20(3):252-260. Published online June 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.3.252

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Abstract PDF

BACKGROUND
Increased body fat, abdominal obesity and insulin resistance are important clinical features in hypogonadal men. Several studies have demonstrated that a low testosterone concentration in men is associated with coronary heart disease, visceral obesity and insulin resistance. In this study, the effects of testosterone replacement therapy on the abdominal visceral fat and cardiovascular risk factors in hypogonadal men were investigated. METHODS: We selected 26 men with secondary hypogonadism (mean serum testosterone+/-SD 0.39+/- 0.57ng/mL), who were then treated with testosterone for 12 months. We measured the body composition, including the abdominal visceral fat area by abdominal CT at the L4 level, both before and 12 months after treatment, and the lipid profile, fasting plasma insulin, HOMA-IR and the serum homocysteine, CRP and IL-6 before and 6, 12 months after treatment. RESULTS: With respect to the body composition, the lean body mass had significantly increased 12 months after treatment(P= 0.002), but there were no significant changes in the body fat mass and abdominal visceral fat area. There was a trend toward a decreased fasting plasma insulin and HOMA-IR, but this did not reach statistical significance. The total cholesterol had decreased significantly at 12 months(P=0.04) and the HDL cholesterol decreased significantly over the course of study(P=0.02). There were no significant changes in the serum homocysteine, CRP and IL-6 after treatment. CONCLUSIONS: After 12 months testosterone replacement therapy in the 26 men with hypogonadism, the lean body mass had increased significantly, but there was no significant change on the abdominal visceral fat during the treatment period. Testosterone replacement had deleterious effect on HDL cholesterol, but not significant effects on insulin resistance and the serum homocysteine, CRP and IL-6. These results suggest that testosterone replacement therapy may have a few adverse effects on cardiovascular diseases in hypogonadal men. However, it will be necessary to examine the long-term effects of testosterone replacement on the incidence of cardiovascular events as well as the cardiovascular risk factors in men with hypogonadism

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Androgen Receptor Gene CAG Repeat Polymorphism and Effect of Testosterone Therapy in Hypogonadal Men in Korea
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Effects of Androgen on the Cardiovascular System in the Aging Male
Jin Wook Kim, Je Jong Kim, Du Geon Moon
Korean Journal of Andrology.2011; 29(1): 10. CrossRef

Determination of Glucocorticoid Replacement Therapy and Adequate Maintenance Dose in Patients with Secondary Adrenal Insufficiency.: Sang Wan Kim, Hye Seung Jung, Seong Hee Kwon, Do Joon Park, Chan Soo Shin, Kyung Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee; J Korean Endocr Soc. 2003;18(5):456-464. Published online October 1, 2003

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Abstract PDF: BACKGROUND
Determination of the adequate dose of glucocorticoid replacement therapy, in patients with secondary adrenal insufficiency, is of great importance to avoid the consequences of under or over treatment. The aims of this study were: 1) to assess the value of adrenal cortical function tests in determining whether glucocorticoid replacement should be given, and 2) to investigate the adequate maintenance dose of glucocorticoid in patients with secondary adrenal insufficiency. METHODS: Forty patients, with secondary adrenal insufficiency, confirmed by the insulin-induced hypoglycemia test (IHT), were studied. All subjects underwent basal serum cortisol measurement, IHT and 250 g rapid ACTH stimulation tests (AST). The clinical usefulness of these tests, for the determination of glucocorticoid replacement therapy, was evaluated in patients with secondary adrenal insufficiency. 26 of the 40 patients had received prednisolone (Pd) (5 mg per day) replacement due to symptoms from adrenal insufficiency. The dose of Pd was serially changed from 5 to 3.75, and then to 6.25 mg per day, every 3 month. The measured lipid parameters, serum osteocalcin and urinary N-telopeptide were measured and the quality of life evaluated by the administration of an Addisonian questionnaire, both before and after the dose changes. RESULTS: 1) For all tests, cut-offs were selected that would provide adequate specificity and sensitivity. When the cut-offs were set to provide 95% specificity, the corresponding sensitivitycut-off values, obtained with basal serum cortisol, peak serum cortisol in IHT and AST were: 88.4% <5 microgram/dL, 80.7% <11 microgram/dL and 76.9% <16 microgram/dL. 2) The urinary type I collagen N-telopeptide, total cholesterol, HDL- and LDL-cholesterol levels were significantly increased, and the serum osteocalcin levels significantly decreased when the daily dose of Pd was increased to 6.25 from 3.75 or 5 mg. The LDL-cholesterol levels especially, were significantly increased, even though the change in the Pd from 3.75 to 5 mg per day was subtle. CONCLUSION: The basal cortisol levels, HPA axis tests and the symptoms of patients may be helpful to determine whether prednisolone replacement therapy should be given. It is suggest that an adequate dose of glucocorticoid replacement therapy should be not exceed Pd 5mg per day, so as not to have adverse effects on the bone and lipid metabolisms.

Case Report

A Case of Pancytopenia Caused by Sheehan's Syndorme Improved with Hormone Replacement Therapy.: Sung Ki Kim, Yoon Ju Oh, Park Young Joo, Young Whan Kim, Seong Bin Hong, Mi Rim Kim, Moon Suk Nam, Yong Seong Kim; J Korean Endocr Soc. 2000;15(4-5):595-599. Published online January 1, 2001

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Abstract PDF: Postpartum ischemic necrosis of the pituitary gland, known as Sheehan's syndrome, is well- established clinical entity. In anterior pituitary insufficiency, there is very often a normochromic or hypochromic anemia but pancytopenia secondary to the hypopituitarism is less common. We report a case of pancytopenia due to complete aplasia of the bone marrow associated with Sheehan's syndrome, in which hormone replacement therapy alone produced full hematological recovery.

Original Articles

Changes of Biochemical Bone Markers and Bone Mineral Density after Hormone Replacement Therapy in Korean Women.: Kyong Soo Park, Do Joon Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Jae Hyeon Kim, Jeong Goo Kim; J Korean Endocr Soc. 2000;15(2):226-236. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Biochemical bone markers have been suggested to reflect postmenopausal high bone turnover. These markers could be useful in following response to hormone replacement therapy (HRT). But we have few studies about the sequential changes of biochemical bone markers and bone mass after HRT in Korean women, and it is unclear whether women with early menopause have different response to HRT from women with normal menopause. The aims of the present study were to see the sequential changes of biochemical bone markers and bone mass after HRT in Korean women, to examine whether a single baseline biochemical bone marker or a change in biochemical bone marker could predict subsequent bone mass, and to determine the difference of response to HRT between women with early menopause and women with normal menopause. METHODS: Postmenopausal women (n=21) were divided with into three groups according to their age at menopause (AAM): the first group with AAM < or = 43 years (early menopause group, n=7), the second group with 43 years < or = AAM < or = 50 years (n=4), and the third group with AAM > or = 50 years (normal menopause group, n=10). For the HRT, conjugated estrogen (0.625mg per day) and continuous or cyclic medroxyprogesterone (2.5-10mg per day) were administered. Bone mineral density (BMD) was measured at baseline and 12 months and biochemical bone markers were measured at baseline and 3, 6, and 12 months during HRT. RESULTS: Deoxypyridinoline, type 1 collagen N-telopeptide, bone alkaline phosphatase, and osteocalcin were significantly decreased at 3 months, and mean percent changes from baseline of bone resorption markers were larger than those of bone formation markers. At 12 months, BMD was significantly increased at lumbar spine and Ward's triangle. But BMD was not significantly increased at femur neck and femur trochanter. Two baseline bone markers (bone alkaline phosphatase and type 1 collagen N-telopeptide) correlated with changes of BMD but any changes of bone markers at 3, 6 months didn't correlate with changes of BMD. In early menopause group, changes of bone markers and BMD were larger than those in normal menopause group, but the difference between the two groups was not significant. CONCLUSION: All four bone markers showed significant reduction at 3 months, but bone resorption markers were decreased more markedly and rapidly, and some baseline bone markers can predict the change of BMD after HRT. The difference of response to HRT between early menopause group and normal menopause group was not significant.

Association of Estrogen Receptor Genotypes with Serum Lipids and Responsiveness of Serum Lipids to Hormonal Replacement Therapy in Korean Postmenopausal Women.: So Ra Park, Jae Eun Park, Chung Kyu Hwang, Phil Ho Jung, Chang Hoon Yim, Ho Yeon Chung, Ki Ok Han, Hyun Ku Yoon, Hak Chul Jang, In Kwon Han; J Korean Endocr Soc. 1999;14(3):553-561. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Several biologically plausible mechanisms have been proposed for estrogen-mediated caridoprotection, including estrogen-assocaited changes in lipid metabolism and endothelial function of vessel walls. These effects are thought to be mediated via estrogen receptor (ER). Relationships between ER polymorphisms and serum lipid levels were not investigated enoughly. METHODS: Three restriction fragment length polymorphisms (RFLPs) at the ER gene locus, represented as B-variant, PvuII and XbaI, and their relationship to serum lipid levels were examined in 318 postmenopausal women. Their mean age was 54.5+/-6.5 years (mean+SD). An association between ER genotypes and changes in lipid levels after 1 year of estrogen replacement therapy was also investigated in follow-up 251 women. RESULTS: The B-variant was not found in Korean women. The distribution of the PvuII and XbaI polymorphisms was as follows: PP 109 (34%), Pp 166 (52%), pp 43 (14%), and XX 204 (64%), Xx 95 (30%), xx 19 (6%). Significant relationship was found between genotypes and changes in serum total cholesterol levels after lyr estrogen replacement therapy. There was no significant relationship between ER genotypes and changes in HDL cholesterol, LDL cholesterol and triglyceride levels after estrogen therapy. CONCLUSION: These data indicate that these polymorphisms are possible predictor on lipid response to estrogen replacement therapy.

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