- The percent change of body weight in patients with type 2 diabetes using rosiglitazone for 1 year.
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Seong Bin Hong, Hwi Ra Park, Eun A Kim, Kyung wook Lee, Moonsuk Nam, Yong Seong Kim
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Korean Diabetes J. 2006;30(1):47-53. Published online January 1, 2006
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DOI: https://doi.org/10.4093/jkda.2006.30.1.47
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 Abstract
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- BACKGROUND
Rosiglitazone(RSG) is known as a potent agonist for the PPARgamma. It improves glycemic control by improving insulin sensitivity in peripheral tissues. And it is associated with body weight gain. The Pro12Ala polymorphism of the gene encoding the peroxisome proliferator-activated receptor(PPAR)gamma2 has recently been shown to be associated with insulin sensitivity. This study was performed to evaluate the body weight change during the long term rosiglitazone treatment and the role of PPARgamma2 polymorphism, Pro12Ala as an indicator to predict the clinical response of RSG in type 2 diabetes patients. METHOD: The study subjects were 214 type 2 diabetic patients(117 male, 97 female) who were received a daily 1 year course of 4 mg RSG combined with sulfonylurea or metformin. The Pro12Ala polymorphism of the PPARgamma2 was determined by the restriction fragment length polymorphism(RFLP) method. Body weight, height, waist circumference, fasting glucose, insulin, c-peptide and lipid profile were measured. RESULTS: After RSG treatment, body weight change was 2.4 +/- 3.8%, 4.5 +/- 9.8% of baseline body weight at 12, 24 weeks respectively. Body weight gains were increased to 5.6 +/- 10.1% at the end of 1 year. The HbA1C, serum insulin level and HOMA index were decreased following the rosiglitazone therapy. The allele frequency of the Ala12Pro polymorphism of the PPARgamma2 was 0.016. The number of Ala12Pro variant of the PPARgamma2 was too low to predict clinical response of RSG. Body weight gain was correlated with basal fasting plasma glucose, post-prandial 2 hour glucose and HbA1c level(p<0.05). There was no correlation between baseline body weight and change. CONCLUSION: This results showed that Pro12Ala polymorphism was not acceptable for the predictor of RSG induced weight gain and clinical response. However, body weight gain was increased in who had high glucose level, and correlated positively with glucose decrease. 1st 3 month weight gain was best predictor of weight change during 1 year.
- High Carbohydrate Diet Effects on the Development of Diabetes Mellitus and Modification of Pancreatic Islets in OLETF Rats.
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Sung Ki Kim, Seong Bin Hong, Hwi Ra Park, Eun A Kim, Kyung Wook Lee, Moon Suk Nam, Yong Seong Kim
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Korean Diabetes J. 2004;28(3):187-198. Published online June 1, 2004
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Abstract
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- BACKGROUND
Diet has long been believed to be an important risk factor for type 2 diabetes. The composition of carbohydrates in the diet was higher in the past, where as now it is considerably reduced in the diet of Korean peoples, which is probably associated with the risk of developing type 2 diabetes. The aim of the present study was to investigate the long-term effect of high carbohydrate/low protein diets on the glucose and lipid metabolism and the pancreatic islet in OLETF(Otsuka Long-Evans Tokushima Fatty) rats, the animal model of type 2 diabetes. METHODS: Seven week old male OLETF rat were fed a high carbohydrate/low protein diet(carbohydrate 71.0%, fat 14.5%, protein 14.5%) as the experimental group, with an ordinary chow diet(carbohydrate 63.5%, fat 14.5%, protein 22%) fed to the controls. The plasma insulin, lipid profiles, free fatty acid and oral glucose tolerance were analyzed at 16 and 32 weeks. After the glucose tolerance test, the pancreas was excised, and immunohistochemical staining was conducted for the islet morphology and insulin mRNA to quantify the insulin secretory capacity. RESULTS: The basal glucose levels tended to be higher in the control group, but with no significant statistical difference. There were no differences in the serum insulin, total cholesterol, triglyceride, HDL-cholesterol and plasma free fatty acid levels between the two groups. The pancreatic islets of the control group showed multilobulation, with fibrotic changes; where as those of the experimental group were maintained normal profiles. A higher expression of insulin mRNA was observed in the experimental than in the control group. CONCLUSION: A high carbohydrate diet induced lower body weight increases, and protected against beta cell injury and decreased the development of abnormal glucose tolerance in OLETF rats. This may explain the growing incidence of diabetes with respect to the change in carbohydrate composition in the diet of Korean peoples. However, whether the protective effect of a high carbohydrate diet, against the development of diabetes in OLETF rats, can be attributed to small weight increases or if the change in food composition itself, or both needs to be determined.
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KDA
