Endocrinology and Metabolism

Youngsun Hong (Hong Y)

4 Articles

Calpain-10 Polymorphism in Korean Women with Polycystic Ovary Syndrome.: Hye jin Lee, Gun Woo Pyun, Eun Kyung Byun, Ji Young Oh, Jee Young Oh, Youngsun Hong, Yeon Ah Sung, Hye Won Chung; J Korean Endocr Soc. 2008;23(5):319-326. Published online October 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.5.319

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BACKGROUND
Polycystic ovary syndrome (PCOS) is characterized by chronic anovulation, hyperandrogenism and insulin resistance, and PCOS is known to be associated with an increased risk of type 2 diabetes mellitus (DM). PCOS has also been proposed to share a common genetic background with type 2 DM. The calpain 10 (CAPN10) gene is known to be associated with type 2 DM in several different population. We examined the association of CAPN10 gene polymorphisms and their influence on the metabolic abnormalities in Korean women who suffer with PCOS. METHODS: One hundred sixty four women with PCOS and 325 control women were studied. The CAPN10 gene polymorphisms were genotyped by amplifying the genomic DNA. Anthropometric measures, a 75g oral glucose tolerance test and measurement of insulin sensitivity by the euglycemic hyperinsulinemic clamp technique were performed. RESULTS: The frequencies of CAPN10 UCSNP-43, UCSNP-19, UCSNP-63 and the haplotype combinations were not different between the women with PCOS and the control subjects. In the women with PCOS and who had the UCSNP-43 GA genotype, the post-load 90 minute plasma glucose level was significantly greater and the HDL cholesterol and insulin mediated glucose uptake were significantly lower compared to the women with PCOS and who had the GG genotype. CONCLUSION: The CAPN10 UCSNP-43 genotype might be responsible for insulin resistance, yet further study is required to confirm the role of this genetic polymorphism in the development of PCOS and the presentation of its disease features.

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Comments on the latest meta-analysis of CAPN10 polymorphism associations with polycystic ovary syndrome
Sidra Raihan, Dawood Shariff, Sami Bizzari
Gene.2019; 717: 144006. CrossRef

Adiponectin and Ghrelin Polymorphism in Korean Women with Polycystic Ovary Syndrome.: Hyejin Lee, Eun Kyung Byun, Hwi Ra Park, Jee Young Oh, Youngsun Hong, Yeon Ah Sung, Hyewon Chung; J Korean Endocr Soc. 2006;21(5):394-401. Published online October 1, 2006; DOI: https://doi.org/10.3803/jkes.2008.21.5.394

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Abstract PDF: BACKGROUND
Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism and chronic anovulation, and this is a common disorder in premenopausal women. However, the pathogenesis is still uncertain. There has been no studies about PCOS-related genetic abnormalities in Korea. In this study, we examined the frequency of the adiponectin and ghrelin genotypes in Korean women with PCOS. METHODS: Fifty four women with PCOS and 174 regular cycling healthy women were recruited for the study, and their reproductive hormones and metabolic profiles were measured. The polymorphisms of the ghrelin and adiponectin genes were analyzed. RESULTS: The frequency of ghrelin gene polymorphism was not different between the women with PCOS and the controls. The frequency of the TG adiponectin genotype was higher and the frequency of the TT genotype was lower in the women with PCOS compared to the controls (P < 0.05). For the PCOS women with GG adiponectin genotype, their triglycerides levels were significantly higher compared to the PCOS women with the TT and TG genotypes even after adjusting for the BMI. CONCLUSION: Adiponectin gene polymorphism is associated with presence of PCOS and it is responsible for the dyslipidemia seen in PCOS. Yet further study is required to confirm the role of this genetic polymorphism in the susceptibility to PCOS and the associated metabolic features.

Associations of Polymorphisms in Uncoupling Protein 2 and 3-Adrenergic Receptor with Obesity in Korean Adults.: Hyejin Lee, Hyeyoung Park, Youngsun Hong, Yeon Ah Sung; J Korean Endocr Soc. 2002;17(2):236-245. Published online April 1, 2002

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Abstract PDF: BACKGROUND
The genetic and environmental factors involved in the development of obesity and several candidate genes have been suggested to have an influence on energy and fuel metabolism. However, the specific genetic defects responsible for human obesity have not been identified yet. It is likely that a combination of polymorphisms in one or more candidate genes may affect energy metabolism and the development of obesity. We performed this study to determine the role of 45 bp insertion in the uncoupling protein (UCP)2 exon 8 and Trp64Arg polymorphism of beta3-adrenergic receptor ( 3-AR) gene in the regulation of body weight and the pattern of fat distribution. METHODS: In 114 subjects (male: 40, female: 74, mean body mass index: 24.1+/-2.7 kg/m2, 80 subjects with normal glucose tolerance, 34 subjects with impaired glucose tolerance), body fat distribution patterns were assessed by anthropometric measurement, bioelectric impedance analysis and computed tomogram. The genotypes of UCP genes were determined by polymerase chain reaction (PCR), and mutation in 3-AR gene by PCR followed by enzymatic digestion. RESULTS: In UCP2 genes, the frequency of deletion homozygote (DD) was 59.4%, heterozygote (DI) was 3.5% and insertion homozygote (II) was 3.1% Meanwhile, in 3-AR, the frequency of TrpTrp was 67.9%, TrpArg was 29.5% and ArgArg was 2.7%. In the lean group (subjects with a BMI less than 25 kg/m2), the frequencies of insertion allele and Arg64 allele were not significantly different than those among the overweight subjects (BMI > or = 25 kg/m2). There was not significant difference in clinical, biochemical or body fat distribution patterns between the groups according to UCP2 polymorphism. In the case of the polymorphism in 3-AR gene, the subjects with ArgArg homozygotes had lower HDL-cholesterol level (p<0.05). For the individuals over 40 years of age, BMI was greater among those with the deletion homozygotes and Arg64 allele, as compared to other groups according to the combination of UCP2 and 3-AR genotypes (p<0.05). CONCLUSION: These results suggest that genetic variations in UCP2 and 3-AR can synergistically affect metabolic rate and susceptibility to weight gain, thereby and contribute to the change in body weight in later life.

Relationship between Plasma Leptin Levels and Carotid Intima-Medial Thickness in Korean Adults.: Hyejin Lee, Eunsoon Hong, Youngsun Hong, Yeon Ah Sung; J Korean Endocr Soc. 2002;17(1):87-94. Published online February 1, 2002

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Abstract PDF: BACKGROUND
Many studies have recently shown that leptin can promote angiogenesis via endothelial leptin receptors and induce oxidative stress in endothelial cells; These findings suggest the relationship between cardiovascular risk and blood leptin concentration. In the present study, we investigated the relationship between leptin concentration and carotid intima-medial thickness (CIMT) as an indicator of early atherosclerosis in adults. METHEODS: The study subjects comprised 138 (45 men and 93 women; mean age 42.4+/-7.5 years; mean BMI 24.0+/-2.7 kg/m2) without history of diabetes, hypertension or cardiovascular disease. We measured CIMT by high resolution ultrasonography and plasma leptin levels by radioimmunoassay. RESULTS: 1) No significant differences in age, BMI or CIMT between male and female subjects were noted, but the leptin levels in female were significantly higher than those in males. (8.42+/-5.90 ng/mL vs. 3.08+/-1.00 ng/mL, p<0.001) 2) CIMT showed a significant positive correlation with age (r=0.31, p< 0.001), BMI (r=0.25, p<0.01) and level (r=0.42, p<0.05) in simple regression analysis. 3) When male and female subjects were each divided into 3 groups by leptin concentration, no significant difference in CIMT among female subjects was found. In male subjects, CIMT was significantly higher in the highest tertile of leptin level than in the other 2 groups (0.65+/-0.03 mm vs. 0.56+/-0.07 mm and 0.53+/-0.07 mm, p<0.01) after adjustment for BMI and age. However, this difference was not significant after adjustment for smoking. 4) CIMT (0.61+/-0.05 mm vs. 0.53+/-0.07 mm, p<0.01) and leptin concentrations (3.57+/-2.13 ng/mL vs. 2.20+/-1.39 ng/mL, p<0.05) were significantly higher in male smokers than in male non-smokers. CONCLUSION: Our results demonstrated significant correlation of CIMT to plasma leptin level before adjustment for smoking. A possible explanation is the permissive action of smoking on the atherogenic effect of leptin. However, further studies to elucidate the relationships and interactions among smoking, leptin level and the development of atherosclerosis will be needed.

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