Diabetes & Metabolism Journal

Original Articles

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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Abstract 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.

Effects of PPAR-alpha and-gamma Agonists on Fatty Acid Metabolism of Muscle Cells in Hyperlipidemic and Hyperglycemic Conditions.: Yong jik Lee, Zheng Shan Zhao, Soo Kyung Kim, Hae Jin Kim, Wan Sub Shim, Chul Woo Ahn, Hyun Chul Lee, Bong Soo Cha; Korean Diabetes J. 2006;30(5):324-335. Published online September 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.5.324

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BACKGROUND
Studies for the regulation of fatty acid metabolism are deficient relatively in skeletal muscle and heart. The investigations in pathological conditions for malonyl-CoA decarboxylase (MCD) and for the relation of MCD and PPAR-alpha.-gamma agonists are insufficient in particular. METHODS: In the current study, fully differentiated H9c2 muscle cells were exposed to pathological conditions such as hyperlipidemic (0.1 mM Palmitate) and hyperglycemic (16.5 mM Glucose) condition with 5 uM PPAR-gamma agonist (rosiglitazone) and 10 uM PPAR-alpha agonist (WY14,643) and then experiments such as MCD activity assay, MCD real-time RT-PCR, MCD reporter gene assay, MCD Western blotting, PPAR-alpha Western blotting, and palmitate oxidation test were carried out. RESULTS: Only PPAR-alpha agonist increased MCD activity. In the result of real-time RT-PCR, both PPAR-alpha and PPAR-gamma agonists elevated MCD mRNA expression in hyperlipidemic condition. MCD protein expression was decreased in hyperlipidemic condition, however, increased in rosiglitazone, or WY14,643 treated conditions. Rosiglitazone, and WY14,643 treated groups showed incresed MCD protein expression in hyperglycemic condition. Hyperlipidemic control group and PPAR-alpha.-gamma agonists treated groups presented about 3.8 times more increased palmitate oxidation level than normolipidemic control group in hyperlipidemic condition. PPAR-alpha agonist treated group showed 49% more increased palmitate oxidation rate than hyperlipidemic control group in primary cultured rat skeletal muscle cells. The amount of palmitate oxidation from differentiated H9c2 muscle cells that had overexpressed PPAR-alpha structural genes was more increased than control group. CONCLUSION: This study suggests that PPAR-alpha agonist ameliorates the defects induced by hyperlipidemic condition through the regulation of MCD. In summary, a closely reciprocal relation among PPAR-alpha agonist, MCD, and fatty acid oxidation existed distinctly in hyperlipidemic condition, but not in hyperglycemic condition.

Citations

Citations to this article as recorded by

Beneficial effect of Combination with Korean Red Ginseng and Morus alba in metabolic syndrome
Yun Jung Lee, Hye Yoom Kim, Jung Joo Yoon, So Min Lee, You Mee Ahn, Joung Hyun Kho, Min Chul Kho, Ho Sub Lee, Kyung Min Choi, Dae Gill Kang
The Korea Journal of Herbology.2012; 27(6): 99. CrossRef
Effects of Mixed Extract from Lycium chinense, Cordyceps militaris, and Acanthopanax senticosus on Glucose-Regulating Enzymes of HepG2 in Hyperglycemic Conditions
Dae-Jung Kim, Jeong-Mi Kim, Tae-Hyuk Kim, Jong-Mi Baek, Hyun-Sook Kim, Myeon Choe
Journal of the Korean Society of Food Science and Nutrition.2010; 39(9): 1257. CrossRef

Case Reports

A Case of Hyperglycemic Hyperosmolar Syndrome Induced by Steroid Treatment for Idiopathic Thrombocytopenic Purpura.: Soo Yeon Park, Se Yune Kim, Dong IL Kim, Hye Suk Kim, Sae Jeong Yang, Ju Ri Park, Dong Jin Kim, Hye Jin Yoo, Soon Beom Kwon, Sei Hyun Baik; Korean Diabetes J. 2005;29(6):571-573. Published online November 1, 2005

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Abstract PDF: Steroid induced diabetes mellitus, a complication due to corticosteroids, is commonly regarded as a form of type 2 diabetes mellitus. Hyperglycemic hyperosmolar syndrome, which requires relative insulin deficiency and concomitant elevation of counterregulatory hormones, such as glucagon, catecholamine, cortisol, and growth hormone, is acute a complication of type 2 diabetes mellitus. Here we report a case of hyperglycemic hyperosmolar syndrome induced by short-term steroid treatment in idiopathic thromobocytopenic purpura.

A Case of Diabetic Ketoacidosis in a GAD Antibody-positive Diabetes Patients who Recently Experienced Hyperglycemic Hyperosmolar State.: Jang Won Son, Seok Hong Lee, Jung Ahn Lee, Jaetaek Kim, Yeon Sahng Oh, Soon Hyun Shinn; Korean Diabetes J. 2005;29(3):267-270. Published online May 1, 2005

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Abstract PDF: The term latent autoimmune diabetes in adults(LADA) was introduced to define adult diabetic patients who initially do not require insulin, but they have the immune markers of type 1 diabetes and in a number of cases, these patients progress to insulin dependency. LADA patients have several features of classic type 1 diabetes in addition to islet cell antibody positivity, including high rates of HLA-DR3 and DR4. We describe here a case of a patient with a diagnosis of LADA who, having been diagnosed with type 2 diabetes, was affected with diabetic ketoacidosis. In April 2000, a 65-year-old man was admitted to Chung-Ang University Hospital due to his decreased cognitive ability. The patient was diagnosed with type 2 diabetes 30-years ago and he was diagnosed 6-month ago as being in a hyperglycemic hyperosmolar state. He was positive for antibodies against GAD(anti-GAD, 31U/mL). His weight was 70kg, height 167cm, BMI 25 kg/m2 and the blood pressure was 86/52mmHg. No abnormalities on the physical examination were found. His acid-base balance was pH 6.937, serum bicarbonate 2.2mmol/L and the anion gap 38; he also had a strong positive reaction for ketones in his urine and serum. During half a year, the fasting C-peptide level decreased from 0.65nmol/L to 0.13nmol/L, which means the rapid progression of beta-cell destruction. Intensive treatment of LADA with insulin may improve this type of patients' quality of life, and so potentially save the beta-cell function and perhaps lessening the risk of a hyperglycemic crisis

Original Article

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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Abstract 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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