Endocrinology and Metabolism

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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The Current Landscape of Pharmacotherapies for Sarcopenia
Gulistan Bahat, Serdar Ozkok
Drugs & Aging.2024; 41(2): 83. CrossRef
Associations of micronutrient dietary patterns with sarcopenia among US adults: a population-based study
Yining Liu, Xiangliang Liu, Linnan Duan, Yixin Zhao, Yuwei He, Wei Li, Jiuwei Cui
Frontiers in Nutrition.2024;[Epub] CrossRef
Impact of Vitamin D Level on Sarcopenia in Elderly People: A Critical Review
Saniya Khan, Sunil Kumar, Sourya Acharya, Anil Wanjari
Journal of Health and Allied Sciences NU.2023; 13(04): 453. CrossRef
Novel Potential Targets for Function-Promoting Therapies: Orphan Nuclear Receptors, Anti-inflammatory Drugs, Troponin Activators, Mas Receptor Agonists, and Urolithin A
Waly Dioh, Vihang Narkar, Anurag Singh, Fady Malik, Luigi Ferrucci, Cendrine Tourette, Jean Mariani, Rob van Maanen, Roger A Fielding, Lewis A Lipsitz
The Journals of Gerontology: Series A.2023; 78(Supplement): 44. CrossRef
Alverine citrate promotes myogenic differentiation and ameliorates muscle atrophy
Jong Hyeon Yoon, Seung-Min Lee, Younglang Lee, Min Ju Kim, Jae Won Yang, Jeong Yi Choi, Ju Yeon Kwak, Kwang-Pyo Lee, Yong Ryoul Yang, Ki-Sun Kwon
Biochemical and Biophysical Research Communications.2022; 586: 157. CrossRef
Adeno-associated virus-mediated expression of an inactive CaMKIIβ mutant enhances muscle mass and strength in mice
Takahiro Eguchi, Yuji Yamanashi
Biochemical and Biophysical Research Communications.2022; 589: 192. CrossRef
Gastric Mobility and Gastrointestinal Hormones in Older Patients with Sarcopenia
Hsien-Hao Huang, Tse-Yao Wang, Shan-Fan Yao, Pei-Ying Lin, Julia Chia-Yu Chang, Li-Ning Peng, Liang-Kung Chen, David Hung-Tsang Yen
Nutrients.2022; 14(9): 1897. CrossRef
Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia
Marcela Kanova, Pavel Kohout
International Journal of Molecular Sciences.2022; 23(15): 8396. CrossRef

Diabetes, Obesity and Metabolism
Recent Advances in Understanding Peripheral Taste Decoding I: 2010 to 2020: Jea Hwa Jang, Obin Kwon, Seok Jun Moon, Yong Taek Jeong; Endocrinol Metab. 2021;36(3):469-477. Published online June 18, 2021; DOI: https://doi.org/10.3803/EnM.2021.302

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Abstract PDF PubReader ePub

Taste sensation is the gatekeeper for direct decisions on feeding behavior and evaluating the quality of food. Nutritious and beneficial substances such as sugars and amino acids are represented by sweet and umami tastes, respectively, whereas noxious substances and toxins by bitter or sour tastes. Essential electrolytes including Na⁺ and other ions are recognized by the salty taste. Gustatory information is initially generated by taste buds in the oral cavity, projected into the central nervous system, and finally processed to provide input signals for food recognition, regulation of metabolism and physiology, and higher-order brain functions such as learning and memory, emotion, and reward. Therefore, understanding the peripheral taste system is fundamental for the development of technologies to regulate the endocrine system and improve whole-body metabolism. In this review article, we introduce previous widely-accepted views on the physiology and genetics of peripheral taste cells and primary gustatory neurons, and discuss key findings from the past decade that have raised novel questions or solved previously raised questions.

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Multidimensional exploration of the bitterness amelioration effect of roasting on Wuyi Rock tea
Weiying Su, Li Ni, Yizhe Chen, Daoliang Wang, Chih-Cheng Lin, Yuan Liu, Zhibin Liu
Food Chemistry.2024; 437: 137954. CrossRef
Physiology of the tongue with emphasis on taste transduction
Máire E. Doyle, Hasitha U. Premathilake, Qin Yao, Caio H. Mazucanti, Josephine M. Egan
Physiological Reviews.2023; 103(2): 1193. CrossRef
Polycystic kidney disease 2-like 1 channel contributes to the bitter aftertaste perception of quinine
Takahiro Shimizu, Takuto Fujii, Keisuke Hanita, Ryo Shinozaki, Yusaku Takamura, Yoshiro Suzuki, Teppei Kageyama, Mizuki Kato, Hisao Nishijo, Makoto Tominaga, Hideki Sakai
Scientific Reports.2023;[Epub] CrossRef
Sweet Taste Preference: Relationships with Other Tastes, Liking for Sugary Foods and Exploratory Genome-Wide Association Analysis in Subjects with Metabolic Syndrome
Rebeca Fernández-Carrión, Jose V. Sorlí, Oscar Coltell, Eva C. Pascual, Carolina Ortega-Azorín, Rocío Barragán, Ignacio M. Giménez-Alba, Andrea Alvarez-Sala, Montserrat Fitó, Jose M. Ordovas, Dolores Corella
Biomedicines.2021; 10(1): 79. CrossRef

Original Article

Studies on the Specific Estradiol Binding Site on Rat Uterine Membranes.: Mi Chung Yoon, Kyung Za Ryu; J Korean Endocr Soc. 1996;11(4):510-516. Published online November 7, 2019

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Abstract PDF: Backgroand: In our previous study, it was demonstrated that estradiol-dependent prostaglandin synthesis may be mediated by cAMP elevation during the process of iplantation in rats. The present study was undertaken to investigate if estradio1, a hydrophobic molecule could interact with uterine plasma membrane, thereby influencing adenylate cyclase and cAMP. Methods: The specific binding of [3H]estradiol to plasma membrane prepared from rat uterus has been identified and characterized. Results: The association of [3H]estradiol to plasma membrane preparations reached equilibrium at 24 hrs. [3H]estradiol binding was directly proportional to the concentration of plasma membrane preparations and its binding was temperature-sensitive. This binding was saturable, reversible and binding site was one type with high affinity(Kd=0.16+0.03 nM) and high binding capacity(Bmax= 2.03 + 0.38pmol/mg protein). The dissociation constant was estimated as 1.6*10(-10)M. In a competition assay, binding was specific for estrogenic compounds. When 100% specific binding was detennined in the presence of 3*10(-6) M diethylstilbestrol, 17B-estradiol and tamoxifen displaced specific binding by 115% and 23%, respectively. Neither progesterone nor cortisol at 500-fold excess displaced the specific binding. Conclusion: These data suggest the presence of specific binding sites on the plasma membrane for estradiol in the rat uterus.

Review Articles

Reproduction and Metabolism: Insights from Polycystic Ovary Syndrome.: Prathima Jasti, Andrea Dunaif; Endocrinol Metab. 2012;27(3):180-190. Published online September 19, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.3.180

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Until the 1980s, polycystic ovary syndrome (PCOS) was considered to be a poorly defined reproductive disorder. During that decade, it was recognized that PCOS was associated with profound insulin resistance and a substantially increased risk for type 2 diabetes mellitus in young women. Accordingly, the mechanisms linking the reproductive and metabolic features of the syndrome became the subject of intense investigation. Insulin is now recognized as a reproductive as well as a metabolic hormone and insulin signaling in the central nervous system participates in normal reproductive function. These insights have been directly translated into a novel therapy for PCOS with insulin sensitizing drugs. Androgens also have reversible metabolic actions to decrease insulin sensitivity and increase visceral fat. Prenatal androgen administration to non-human primates, sheep and rodents produces reproductive and metabolic features of PCOS suggesting that the disorder also has developmental origins. PCOS is highly heritable and male as well as female relatives have reproductive and metabolic phenotypes. A number of confirmed genetic susceptibility loci have now been mapped for PCOS and genes in well-known as well as novel biologic pathways have been implicated in disease pathogenesis.

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The Role of Foxo3 in Leydig Cells
Young Suk Choi, Joo Eun Song, Byung Soo Kong, Jae Won Hong, Silvia Novelli, Eun Jig Lee
Yonsei Medical Journal.2015; 56(6): 1590. CrossRef
FoxO1 Is a Negative Regulator of FSHβ Gene Expression in Basal and GnRH-Stimulated Conditions in Female
Young-Suk Choi, Hyeon Jeong Lee, Cheol Ryong Ku, Yoon Hee Cho, Mi Ran Seo, Yoo Jeoung Lee, Eun Jig Lee
Endocrinology.2014; 155(6): 2277. CrossRef

RET: A Multi-Faceted Gene in Human Cancer.: Massimo Santoro, Francesca Carlomagno, Rosa Marina Melillo; Endocrinol Metab. 2012;27(3):173-179. Published online September 19, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.3.173

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Abstract PDF: REarranged during Transfection (RET) gene encodes a receptor tyrosine kinase and it was initially discovered as an in vitro transforming gene. For many years, RET has been involved in papillary thyroid carcinoma and medullary thyroid carcinoma. More recently, lung adenocarcinoma and chronic myelomonocytic leukemia samples have been found to display RET gene rearrangements. This knowledge is stimulating the search for protein kinase inhibitors to combat RET-driven malignancies.

Original Articles

Crosstalk Between cAMP and Phosphoinositide System in Signal Transduction Pathways Through TSH Receptor.: Byung Sool Moon, Young Joo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Do Joon Park; J Korean Endocr Soc. 2003;18(4):404-413. Published online August 1, 2003

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Abstract PDF: BACKGROUND
TSH stimulates both the adenyl cyclase and phospholipase C (PLC) pathways by binding to a single cell surface receptor that is coupled to G protein, and we examined crosstalk between these two signaling pathways. METHODS: FRTL-5 rat thyroid cells were grown in 6H medium, then incubated with 5H medium before the stimulation. Then cells were incubated for 24 hours with 5H mix containing 1 mCi/L myo-(2-N-3H) inositol. After pretreatment of 100 microM Rp-cAMP, 100 microM forskolin, 50 nM staurosporine, or 100 nM PMA (phorbol-12-myristate-13-acetate), TSH were added in different experiments. After 30 min at 37 degrees C, cells were disrupted and IP formation was determined. RESULTS: Stimulation with 100 microU/mL TSH resulted in a 1.65 fold increase in IP generation. In pursuing the possibility that the two post-receptor events might be linked in some way, we examined the effect of exogenously administrated Rp-cAMP, protein kinase A antagonist, and forskolin, a direct stimulant of protein kinase A, on IP generation achieved at a dose of 100 microU/mL TSH. The pretreatment of 100 M Rp-cAMP at a concentration sufficient to inhibit protein kinase A enhanced TSH-induced IP production. This effect of Rp-cAMP was dose-dependent. Forskolin attenuatedTSH-stimulated increases in phosphatidylinositide turnover. PMA, a protein kinase C (PKC) activator and staurosporine, a PKC inhibitor did not affect TSH-induced IP generation. CONCLUSION: These data suggested that activation of adenylate cyclase/cAMP post-receptor signalling casacde, which results in the protien kinase A activation, has an inhibitory effect on IP turnover activated by TSH.

Impaired Metabolic Signal Transduction Networks in Isolated Skeletal Muscle in Korean type 2 Diabetic Patients.: Joon Hyuck Choi, Kwan Woo Lee, Hyo Jeong Kim, Dong Hun Lee, Jong Woo Lee, Jung Eun Kim, Hyun Chae Yim, Kyung Mi Kim, Sung Yi Choi, Yoon Sok Chung, Hyeon Man Kim; J Korean Endocr Soc. 2002;17(5):685-697. Published online October 1, 2002

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Abstract PDF: BACKGROUND
The glucose uptake rate is the limiting step in glucose utilization and storage. The failure of insulin to stimulate glucose uptake in muscle appears to be a primary defect of insulin resistance. This study was undertaken to examine the effect of physiological hyperinsulinemia on the phosphorylation of the insulin receptor (IR-beta), insulin receptor substrate (IRS), Akt kinase and GSK-3 in isolated skeletal muscle, in people with type 2 diabetes (n=9) and control subjects (n=11). METHODS: 75g OGTT and euglycemic hyperinsulinemic clamp test were done. And vastus lateralis muscle was obtained before and 30 min into the euglycemic clamp. Western blots were performed for tyrosine phosphorylation of insulin receptor substrate (IRS) and phosphorylation of the insulin receptor(IR-beta), Akt and GSK-3. RESULT: There were no statistical differences in the mean age, BMI and body fat between the control subjects and diabetic patients. The fasting blood sugar and HbA1c in controls and diabetic patients were 98.+/-1.3 and 208.1+/-16.5 ng/dl, and 5.4+/-0.5 and 9.2+/-0.6%, and 1.4+/-0.2 in the control subjects, and 72.2+/-52.3% (p<0.01) and 10.2+/-6.3 (p<0.01) in the diabetic patients, respectively. The insulin resistance from the euglycemic hyperinsulinemic clamp tests were 8.2+/-0.6 mg/kg/min and 3.7+/-1.1 ng/kg/min in the control subjects and in the diabetic patients, respectively (p<0.01). Compared with the normal controls, insulin-stimulated IR phosphorylation was no different to that in the diabetic patients. However, insulin-stimulated IRS phosphorylation, insulin-stimulated Akt phosphorylation and insulin-stimulated GSK-3 phosphorylation were reduced in the diabetic patients compared with the normal controls by 24, 43 and 25%, respectively (p<0.05). CONCLUSION: In korean type 2 diabetic patients, the insulin resistance may be due to the impairment of the upstream insulin signal molecular network. Further studies will focus on determining whether these signaling defects are the cause of the development of insulin resistance, or secondary to the altered metabolic state, associated with type 2 diabetes mellitus

Expression of Phospholipase C-B3 using Recombinant Baculovirus Expression System.: Do Joon Park; J Korean Endocr Soc. 1997;12(2):283-294. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Although phospholipase C (PLC)-B3 is thought to be a very important enzyme in intracellular signal transduction, the sophisticated and complicated purification steps make it difficult to obtain sufficient amount of protein to study regulation of its activity by G proteins or other proteins. In order to get large amount of PLC-B3 protein, I employed baculovirus expression system which is known to express large amount of functionally active proteins. METHODS: In order to make recombinant baculovirus which expresses PLC-B3 gene, partial cDNA of PLC-B3 which lacked 51 nucleotides was used to make full length PLC-B3 cDNA. By PCR, 5-end sequence of PLC-B3 was ligated into partial rat PLC-B3 cDNA and later cloned into pVL1393 transfer vector to make recombinant baculovirus. This recombinant baculovirus containing PLC-B3 sequence was used to infect Sf9 insect cells. RESULTS: Infection of Sf9 cells with recombinant baculovirus rendered expression of 152 kDa-PLC-B3 protein, which was confirmed by immunoblot assay and PLC activity assay. CONCLUSION: The whole length PLC-B3 cDNA was expressed in Sf9 cells using baculovirus expression system. By using it, homogeneous enzyme is expected to be purified to study precise activation and regulation mechanisms of PLC-B3.

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