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2 "Hyperglycemic clamp"
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Thiazolidinediones on Insulin Resistance and Insulin Secretion in Obese Diabetic OLETF Rats.
Jung hyun Noh, Seung hyun Hong, Kyoung hee Lee, Kyoung Min Min, Tae young Yang, Myung shik Lee, Kwang won Kim, Moon kyu Lee
Korean Diabetes J. 2007;31(1):33-43.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.33
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AbstractAbstract PDF
BACKGROUND
Thiazolidinediones are synthetic peroxisome proliferator-activated receptor-gamma agonists that decrease insulin resistance but, as in vitro and in vivo studies suggest, may have direct beneficial effects on pancreatic beta cells. Here, we investigated the effects of thiazolidinediones (TZDs) on the insulin resistance, beta-cell mass and insulin secretion in obese diabetic OLETF rats. METHODS: We studied insulin resistance (by hyperinsulinemic euglycemic clamp) and insulin secretion (by hyperglycemic clamp) in TZDs administered OLETF and LETO rats. Histologic alterations of the islets were observed and beta-cell mass was also measured by point counting method. RESULTS: Chronic administration of troglitazone (TGZ, 0.15%) or pioglitazone (PGZ, 0.02%) prevented the development of glucose intolerance in OLETF rats, as assessed by oral glucose tolerance test. There was significant difference in submaximal glucose infusion rate between TGZ-treated and untreated OLETF rats during euglycemic clamp studies at 24 weeks of age. At 16 and 24 weeks of ages, beta-cell mass significantly increased in TGZ-treated OLETF rats compared to untreated animals. At 19 weeks and 30 weeks of age, first-phase insulin secretion was not different in PGZ-treated OLETF rats from untreated OLETF rats during hyperglycemic clamp study. At 30 weeks of age, late-phase insulin secretion was decreased in PGZ-treated OLETF rats compared to untreated OLETF rats. The expression of alpha-smooth muscle actin, a marker of activated pancreatic stellate cells that are involved in the fibrosis of the pancreas, in the islets was suppressed by TGZ treatment at 24 weeks of age. CONCLUSION: The treatment of TGZ prevented the development of diabetes, and increased insulin sensitivity and pancreatic beta-cell mass in OLETF rats. These results might be related with the suppression of pancreatic stellate cells. Insulin secretion was not affected by PGZ treatment.
The Role of Insulin Secretion and Insulin Resistance in the Development of Korean Type 2 Diabetes Mellitus.
Bong Nam Chae, Seong Kyu Lee, Eun Gyoung Hong, Yoon Sok Chung, Kwan Woo Lee, Hyeon Man Kim
Korean Diabetes J. 1998;22(4):491-503.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Impaired insulin secretinn, peripheral insulin resistance, a disproportionately elevated rate of hepatic glucose production and influence of inherited or enviromental factors contribute to the pathogenesis of type 2 diabetes mellitus(DM). But, which defect is primary is still controversial To determine whether insulin resistance or insulin deficiency is primary in the pathogenesis of type 2 DM, we studied normal glucose tolerant offsprings of type 2 diabetic patients. METHODS: 22 offsprings of type 2 diabetic patients with normal glucose tolerance, ranging in age from 20 to 40 years, and 17 control subjects in same age range who had no family history of diabetes, and 21 diabetic subjects were included. We performed 75 g oral glucose tolerance test, euglycemic hyper-insulinemic clamp test and hyperglycemic clamp test. RESULTS: With euglycemic clamp test, the values of peripheral insulin sensitivity, M, were 8.59+0.94 mg/kg/min in control group, 6.98+0.65 mg/kg/min in offspring group, and 5.19+0.89 mg/kg/min in diabetes group (P<0.05). Considering that lower limit of the normal range were 3.78 mg/kg/min in M and 3.10 mg/kg/min in M/I, the frequency of insulin resistance was 14.3% in the offspring group and 33.3 % in diabetes group. First and second phase insulin secretion during hyperglycemic clamp test were blunted in diabetes group. In the offspring group, first and second phase insulin secretion during hyperglycemic clamp test were increased greater than control group, though statistically insignificant. The mean first phase insulin secretion were 38.55+6.81 pU/mL in control group, 55.09+9.40 pU/mL in the offspring group and 6.02+0.98 pU/mL in diabetes group (P<0.05). The mean second phase insulin secretion were 65.11+15.5 pU/mL in control group, 90.25 + 11.9 pU/mL in the offspring group and 17.6 +2.71 pUmL in diabetes group(P<0,05). Considering that lower limit of the normal range were 19.5 pU/mL in the first phase insulin secretion and 26.1 pU/mL in the second phase insulin secretion, the frequency of impaired insulin secretion was 14.3 % in the offspring group and 100 % in diabetes group. There was an inverse relation between insulin resistance and insulin secretion in control subjects. But in the offspring group, this relation was absent. CONCLUSION: Our results show that both insulin resistance and impaired insulin secretion contribute to the development of type 2. DM in Koreans. In addifion, diabetic subjects had more severe impairment in insulin secretory capacity than insulin resistance.

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