- Type II Diabetes and Uncoupling Protein.
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Woong Hwan Choi
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Korean Diabetes J. 2001;25(4):258-261. Published online August 1, 2001
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- Serum Plasema Leptin Levels, Abdominal Obesity, and Insulin Resistance in Type 2 Diabetic Patients.
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Dae Won Jun, Sung Hun Kim, Jae Hyung Lee, Woong Hwan Choi, Yong Soo Park, Tae Hwa Kim
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Korean Diabetes J. 2000;24(2):216-224. Published online January 1, 2001
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- BACKGROUND
There is growing evidence for a adipoinsular axis, between adipose tissue and pancreatic beta cells via the hormones leptin and insulin, in mice models, Insulin is adipogenic and increases the production of leptin by adipose tissue, Leptin feeds back to reduce both insulin secretion and insulin gene expression. But human obesity is a complex disorder, with many factors playing a parts; the pathophysiology of leptin is not as simple as it seems to be in mice models of obesity. We therefore explored the dysregulation between leptin and insulin concentration in human model. METHOD: Using radioimmunoassay, we measured serum leptin concentrations in Type 2 diabetic patients (male 26, male 52). Using body composition, we measured total and regional adiposity. The data were analyzed using t-tast to test difference in serum leptin concentration, and other factors were evaluated by partial correlation analysis. RESULT: Serum leptin concentrations in both sex was strongly and positively correlated with total adiposity (r=0.588, p<0.001), Serum leptin concentration was correlated with serum insulin concentration (r=0.41, p=0.002) even after adjusting for adiposity in both sex (r=0.32, p=0.021). Serum leptin concentration was more highly correlated with abdominal adiposity than peripheral adiposity(r=0.693 vs r=0,628). Leptin concentration were higher in women than men, even at the same adiposity, However, no independent association was seen between leptin and hypertension as well as total cholesterol. CONCLUSION: Serum leptin concentration was correlated with serum insulin concentration even after adjusting for adiposity in both sex, In human, such a putative loss of leptin reception by beta cell could result in dysregulation of the adipoinsular axls and a corresponding failure to suppress insulin secretion, resulting in chronic hyperinsutinemia.
- The Effect of Cyclosporine on Insulin Sensitivity in Streptozotocin Induced Diabetic Rats.
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Ju Seop Kang, Dong Sun Kim, Chang Beom Lee, Yong Soo Park, Woong Hwan Choi, Tae Wha Kim, Mok Hyun Kim
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Korean Diabetes J. 1999;23(2):142-146. Published online January 1, 2001
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- BACKGROUND
Cyclosporine (CsA), being used as a immunosuppressant is known to have deleterious effects on the liver and kidney, but the harmful effect on glucose tolerance has not been clearly elucidated. This study was undertaken to determine whether the CsA affected peripheral insulin sensitivity in streptozotocin (STZ)-induced diabetic Sprague-Dawley rats. METHODS: After the daily treatment of CsA (10mg/kg, i.p.) for 2 weeks, glucose tolerance tests were carried out by the intraperitoneal administration of glucose alone or in conjunction with insulin (5 U/kg, s.c.). The glucose tolerance and peripheral insulin sensitivity were determined by measuring the deremental area under the time-lasma glucose concentration curve (AUC; mg-min/mL) according to the trapezoidal rule. The plasma glucose levels (mg/dL) were measured by a glucose analyzer at 0, 10, 30, 60, 90 and 120min after glucose load (2 g/kg). The STZ-diabetic rats were divided into thre groups (GLU- as control, INS+GLU- and CsA+INS+GLU-treated group, n 7 in each groups). RESULTS: In STZ-diabetic rats, the AUC 0-120 of the CsA+INS+GLU-treated group was significantly (p<0.01) lower than those of the control group (48.6% of control), but significantly (p<0.03) higher thain those of the INS+GLUtreated group (28.1% of control). CONCLUSIONS: These results suggest that intraperitoneal injection of CsA gives rise to a deterioration of glucose etabolism which is probably due to a decrease of insulin sensitivity of peripheral tissue in STZ-diabetic rats.
- Prevalence of ICA and anti-GAD, HLA DRB1 / DQA1 / DQB1 Polymorphism in Korean IDDM Patients.
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Yong Soo Park, Jin Ho Shin, Jin Bae Kim, Woong Hwan Choi, You Hern Ahn, Tae Wha Kim, Mok Hyun Kim, Sei Won Yang, Seung Duck Hwang, Hee Bal Rhee
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Korean Diabetes J. 1997;21(3):289-299. Published online January 1, 2001
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- BACKGROUND
Although the HLA class II genes are cleaily associated with insulin-dependent diabetes mellitus(IDDM) in all ethnic. Groups, considerable variation in the associated genotypes is observed among the different ethnic groups. Mathods: In order to estimate what degree genetic and environmental determinants influence the true incidence of IDDM, ICA by imrnunohistochemistry, anti-GAD prevalence by radioimmunoprecipitation and HLA-DRB1, DQAl, and DQB1 polymorphisms after PCR amplification of genomic DNA were analyzed in 131 cases of IDDM, whose age at diagnosis were less than 15. RESULTS: 56% of them(73/131) were anti-GAD positive. 43% IDDM(56/131) were ICA positive. HLA DR3 and DR9 were susceptibility markers, whereas DR2 and DR5 were protective markers. DR3/4,, DR3/9, and DR3/X(X: other than 3, 4) were susceptible genotypes. HLA DQA1*0301 allele was increased, and DQB1*0301 and DQB1*0602 were decreased in IDDM. Not only HLA DQA1 Arg, but also DQBl non-Asp were found to be independent marker for IDDM, but their strength of association was weak. The highest prevalence of anti-GAD was observed in thosc homozygous for DR4(87.5%), exceeding that(47.8%) in those without this allele, and those with one DR4(63.5), whereas the highest prevealence of ICA was found in those homozygous for DR3(10G%), exceeding that in those with one DR3(64.3%) or in those without this allele(36.7%). There was a significant difference in numbers of HLA DQ susceptibility heterodimers in anti-GAD positive or negative patients. Conelusion: The prevalence of islet-specific auto-antibodies were present at comparable sensitivity and specificity in Korean IDDM patients. We could also assess that the immunoenetic markers for IDDM among Caucasians likewise confer disease susceptibility among Koreans. However, different HLA susceptibility alleles and a lower strength of association with known susceptibility markers, presumably because of differences in the genetic make-up of the population or in linkage disequilibrium patterns compared with other racial groups.
- Secretion of plasminogen activator by cultured bovine retinal endothelial cell:modulation by insulin-like growth factor-i.
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Dong Sun Kim, Eung Jin Kim, Woong Hwan Choi, Tae Wha Kim, Mok Hyun Kim
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Korean Diabetes J. 1993;17(4):359-366. Published online January 1, 2001
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- Characterization of glucose transporter group 4 in NIDDN patients.
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Woong Hwan Choi, Tae Wha Kim, Mok Hyun Kim
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Korean Diabetes J. 1993;17(2):161-167. Published online January 1, 2001
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- Autophosphorylation and tyrosine kinase activity of purified insulin receptors.
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Woong Hwan Choi, You Hern Ahn, Tae Wha Kim, Mokhyun Kim
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Korean Diabetes J. 1991;15(2):173-182. Published online January 1, 2001
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