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Quantification of the Pancreatic -cell Mass in Normal and Type 2 Diabetic Subjects in Korea.
Kun Ho Yoon, Seung Hyun Ko, Jung Min Lee, Sung Rae Kim, Sun Hee Seo, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Yong Gui Kim, In Sung Moon, Myung Deuk Lee, Dong Ku Kim, Kyo Young Lee, Chan Suk Kang, Byung Ki Kim
Korean Diabetes J. 2000;24(5):524-532.   Published online January 1, 2001
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AbstractAbstract
BACKGROUND
There have been several reports about insulin secretory impairment in non-obese type 2 diabetic patients and even in impaired glucose tolerant subjects in Korea. Insulin secretory impairment might be induced by insufficient beta-cell mass, functional defects of beta-cells or both. To clarify the cause of impaired insulin secretion in type 2 non-obese diabetic patients in Korea, beta- cell masses were quantified in normal and type 2 diabetic subjects. METHOD: Normal pancreases were procured by 6 heart-beating non-diabetic donors under informed consent from relatives and approval of the university ethical committee. To quantify the beta cell mass and insulin content in various part of the pancreas, first we divided it into 3 parts: head, body and tail, and then each three parts were weighed and subdivided again into 8 segments equally. For diabetic patients, tissue sections were obtained from 15 partial or total pancreatectomized type 2 diabetic patients of any causes. After being fixed, tissues were immunostained using the Streptavidin-biotin-peroxidase method with anti-insulin antibody. Beta cells were counted by point count method. RESULTS: The mean value of total pancreas weight of normal subjects (n=6) was 77.1+/-14.6 g, that of mean relative volume of beta cells in the pancreas was 2.1+/- 0.9%, ranging from 1.4% to 3.1% (head 2.3+/-0.6%, body 1.8+/-0.2%, tail 2.2+/-0.4%). Mean value of total beta cell mass which was calculated from relative volume of beta-cells and weight of each portions was 1.3+/-0.3 g, ranging from 1.2 g to 1.9 g (head 0.6+/-0.3 g, body 0.4+/-0.2 g, tail 0.4+/-0.2 g). Mean insulin content per pancreas was 63.6+/-46.6 g, ranging from 27.8 to 137.2 g/pancreas (head 25.1+/- 19.1 g, body 20.8+/-15.5 g, tail 17.7+/-14.9 g). In diabetic patients, relative volume of beta cells in tissues were variable from 0.4% to 2.8% and there was good correlation between beta-cell mass and body mass index of the diabetic patients. However we can't find the correlation among relative volume of beta-cell, (r2=0.55, p<0.05) duration of diabetes and age. Remarkable heterogeneity for loss of beta-cells in the islets of diabetic patients was observed even in the same lobe of pancreas. There were no evidence of lymphocytic infiltration in the islets. CONCLUSION: Insufficient beta cell mass seems to be a main cause for insulin secretory impairment in non-obese type 2 diabetic patients in Korea.
Pathogenetic Heterogeneity of Type 2 Diabetes Mellitus in Korea.
Seok Won Park, Yong Seok Yun, Young Duk Song, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 1999;23(1):62-69.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Insulin resistance and insulin sec- retory dysfunction are considered as pathogenetic meehanisms leading to type 2 diabetes mellitus. In Korea, clinical features of type 2 diabetes are quite different from those of western countries. There are many non-obese patients and some even experienced considerable weight 1oss around the onset of diabetes mellitus. We investigated the insulin secretory function and in vivo insulin sensitivity in Korean patients with type 2 diabetes. METHODS: 38 patients with type 2 diabetes mellitus (age; 47.3+/-9.1 yrs) and 30 control subjects (age; 25.72.7 yrs) were included in this study. Type 2 diabetic subjects were further divided into obese (BMI >25, n=13) and non-obese (BMI<25, n=25) groups. Insulin secretory responses to the 75g aal gluxse loading and euglycemic hyperinsulinemic clamp test were performed on all subjects. RESULTS: Type 2 diabetic subjects had significantly lower serum insulin levels at 30 min of OGTT, regardless of their obesity, compared to the control subjects. Mean glucose disposal rates (M-values) were decreased by 36% in non-obese type 2 diabetic subjects and 58% in obese type 2 diahetic subjects compared to the control subjects. But, about half (12/25) of non-obese type 2 diabetic subjects and 30% (4/13) of obese type 2 diabetic subjects had normal insulin sensitivity, defined by 95% confidence interval of control subjects. Insulin sensitivity index (M-value) was correlated with BMI, WHR, fasting insulin, and HDL-cholesterol concentrations in type 2 diabetic subjects. CONCLUSION: In Korean type 2 diabetic subjects, impairment of early-phase insulin secretion may be an universal finding, but insulin resistance is observed in about 60% of subjects. This result suggest that there is pathogenetic heterogeneity of type 2 diabetes rnellitus in Korea.

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