- Effects of Rosiglitazone on Body Fat Mass and Distribution in Type 2 Diabetic Patients.
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Hong Kyu Kim, Hyo Joong Yoon, Seung Min You, Ki Young Lee, Hye Young Park, Moon Ho Kang
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Korean Diabetes J. 2003;27(3):272-279. Published online June 1, 2003
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Rosiglitazone, an insulin-sensitizing drug of the thiazolidinediones class, has a high affinity for the ligands of the peroxisome proliferator activated receptor-gamma(PPAR-gamma), is highly expressed in adipose tissue, and plays an important role in the differentiation of adipocyte. The influence of rosiglitazone was investigated on the total fat mass and regional adiposity in type 2 diabetic patients. METHODS: Rosiglitazone (4 mg/day) was administered for 6 months to type 2 diabetic patients (n=20) whose glycemic control was unacceptable with the use of other treatments. Measurements of the total, trunk and leg region body fats (by dual energy X-ray absorptiometry) and abdominal fat distributions (by computed tomography) were compared before and after treatment. RESULTS: Nine patients received rosiglitazone monotherapy and 11 a combined therapy of sulfonylurea and/or metformin. The HbA1C, serum insulin level and homeostasis model assessment insulin resistance index were decreased following the rosiglitazone therapy, but the body weight and BMI were increased. As for the body fat changes, the total (19,382+/-4,786 vs. 22,940+/- 7,300 g, p<0.01), trunk (11,399+/- 2,678 vs. 13,960+/-4,698 g, p<0.01) and leg (4,734+/-1,319 vs. 6,203+/-2,231g, p<0.05) region fat masses were significantly increased. The percentage increase in the total, trunk and leg region fat masses were 20+/-25, 25+/-35 and 58+/-130%, respectively. As for abdominal fat distribution after the treatment, the visceral fat area (225+/-84 vs. 187+/-87 cm2, p<0.05) was significantly decreased, while the subcutaneous fat area tended to increase (178+/-83 vs. 201+/-80 cm2, NS), although these were not statistically significant. The visceral/subcutaneous fat ratio (V/S ratio) was significantly decreased (1.45+/- 0.64 vs. 0.95+/-0.25, p<0.05). CONCLUSION: Although the total body fat mass was increased following the rosiglitazone therapy, a shift in the body fat distribution, from the visceral to the subcutaneous region, was observed, which may be associated with an improvement in insulin resistance. However, a long-term assessment of the consequences of an increasing total fat mass and change in the body fat distribution will be required.
- Dissociation of Microangiopathy and Macroangiopathy in Patients with Type 2 Diabetes.
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C J Seo, K Y Lee, K S Song, Y S Jung, Hong Kyu Kim, H Y Park, W G Lee, M H Kang
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Korean Diabetes J. 2001;25(2):133-141. Published online April 1, 2001
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Type 2 diabetes is a heterogeneous disease. As to its complications, microangiopathy predominantly develop in some patients while macroangiopathy is more predominant in others. Therefore, this study was performed to identify the factors associated with such dissociation. METHODS: Type 2 diabetic patients were classified into the macro and microangiopathy groups by carotid intima-medial thickness (IMT) and the presence of severe diabetic retinopathy. Patients with IMT
- Effects of High Fat Diet on Lipolysis in Skeletal Muscle and Adipose Tissue in Rats.
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Chul Hee Kim, Yun Ey Chung, Seong Jin Lee, Joong Yeol Park, Sung Kwan Hong, Hong Kyu Kim, Kyo Il Suh, Ki Up Lee
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Korean Diabetes J. 2000;24(6):641-651. Published online January 1, 2001
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It has been hypothesized that increased fat oxidation reduces glucose utilization in skeletal muscle, and is responsible for the insulin resistance associated with obesity or high-fat feeding. In contrast, there have been reports that fat oxidation capacity was decreased in skeletal muscles from insulin resistant subjects. This study was undertaken to examine whether insulin resistance in high- fat fed rats is associated with increased lipolysis in skeletal muscle and adipose tissue. METHODS: Two groups of Sprague-Dawley rats were fed either high-fat or low-fat diets for 4 weeks. Lipolysis in skeletal muscle and adipose tissue was determined by measurement of interstitial glycerol concentrations by a microdialysis method in basal and hyperinsulinemic-euglycemic clamp conditions. RESULTS: In basal state, plasma glycerol levels and interstitial glycerol concen trations of skeletal muscle, and adipose tissue were lower in high-fat fed than in low-fat fed rats. The degree of suppression of glycerol release by the hyperinsulinemia was smaller in the high-fat diet than in the low-fat diet group. However, plasma and interstitial glycerol concentrations during the hyperinsul inemic euglycemic clamps were also lower in the high-fat diet group. CONCLUSION: Lipolysis was decreased in skeletal muscle and adipose tissue of insulin resistant, high-fat fed rats. These results support the idea that limited fat oxidation capacity resulting in lipid accumulation in tissues, rather than increased fat oxida tion per se, is responsible for the insulin resistance associated with high-fat feeding.
- Effects of Free Fatty Acids on Glutathione Redox Status in Cultured Endothelial Cells.
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Joong Yeol Park, Chul Hee Kim, Yun Ey Chung, Hong Kyu Kim, Young Il Kim, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
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Korean Diabetes J. 1998;22(3):262-270. Published online January 1, 2001
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Although plasma free fatty acids (FFA) are frequently elevated in diabetes mellitus, its role in the pathogenesis of diabetic vascular complications has not been well investigated. Recent stuclies reported that FFA may cause endothelial dysfunction through an enhancement of oxidative damage by decreasing glutathione redox cycle, an important anti-oxidant defense system in endothelial cells. In this study, we examined the effects of increased availability of FFA on intracellular glutathione redox cycle. METHODS: Bovine pulonary endothelial cells were exposed to 90 umol/L linoleic acid with or without 0.1 mM 2-bromopalmitate, an inhibitor of mitochondrial fatty acid oxidation, for 6hr. Components of the glutathione redox cycle such as total glutathione, reduced glutathione(GSH) and oxidized glutathione(GSSG) concentrations were measured by HPLC. RESULTS: Total glutathione concentration in cultured endothelial cells exposed to linoleic acid was significantly lower than that in control cells (10.8+ 0.5 vs 14.1+0.8 umol/g protein, P<0.05). Linoleic acid significantly decreased GSH concentrations (10.5+0.4 vs. 13.8+0.5 pmol/g protein, P<0.05) and the ratio of GSH/GSSG(26.3+1.3 vs. 47.0+2,1, P<0.05). Compared to cells exposed linoleic acid alone, total glutathione(13.5+0.5umol/g protein, P<0.05) and GSH concentration(13.2+0.4 pmol/g protein, P<0.05) significantly increased in cells treated with 2-bromopalmitate and linoleic acid. The ratio of GSH/GSSG in cells treated with 2-bromopalmitate and linoleic acid was higher th.an that in cells exposed to linoleic acid alone(44.1+1.3, P<0.05). CONCLUSION: Increased provision of FFA resulted in a derangement of glutathione redox cycle in cultured endothelial cells, which appears to be related to an increase in mitochondrial FFA oxidation. These results suggested that FFA can increase the risk of diabetic vascular complications.
- Changes in Serum True Insulin and C-peptide Levels during Oral Glucose Tolerance Test in Koreans with Glucose Intolerance.
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Young Il Kim, Chul Soo Choi, Sang Wook Kim, Hong Kyu Kim, Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
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Korean Diabetes J. 1998;22(2):192-198. Published online January 1, 2001
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Previous studies have shown that progression from normal glucose tolerance(NGT) to impaired glucose tolerance(IGT) is associated with the development of insulin resistance and hyper-insulinemia, while further progression from IGT to NIDDM results from an inability of the 8-cell to maintain high rate of insulin secretion. However, it is not established whether similar findings are also observed in Korean subjects with glucose intolerance. The aim of this study was to examine insulin secretory response after oral glucose stimulation in obese and non-obese Korean subjects according to varying degree of glucose intolerance. METHODS: Eighty eight Korean men underwent 75g oral glucose tolerance test. The subjects were classified into NGT(n=30), IGT(n=23), NIDDM(n= 35) according to National Diabetes Data Group criteria. Obesity was defined as body mass index (BMI) > 25 kg/m . Serum true insulin and C-peptide concentrations were measured by radioimmunoassay. RESULTS: Fasting serum true insulin and C-peptide levels were not different from each other among NGT, IGT and NIDDM groups, both in obese and non-obese subjects. Obese subjects with IGT had significantly higher serum true insulin and C-peptide levels at 120 min than those in NGT subjects, but the levels at 30 and 60 min were not different. On the other hand, non-obese subjects with IGT had lower serum true insulin level at 30 min and lower serum C-pepitde level at 60 min compared to those in NGT subjects. True insulin and C-pepitde levels at 30 and 60 min were significantly lower in patients with NIDDM than in those with NGT, both in obese and non-obese subjects. CONCLUSION: Hyperinsulinemia, especially at a later phase of oral glucose tolerance test, is apparent in obese subjects with IGT. On the other hand, early phase insulin secretory defect is prominent in non-obese subjects with IGT. These results suggest that impaired insulin secretion may play a primary role in the pathogenesis of non-obese NIDDM in Korea.
- Effects of Free Fatty Acid on Insulin Secretion in Cultured Rat Pancreatic Islets.
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Hong Kyu Kim, Young Il Kim, Chul Hee Kim, Joong Yoel Park, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
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Korean Diabetes J. 1997;21(4):381-387. Published online January 1, 2001
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It has been recently suggested that enhanced fat oxidation is responsible for the abnormal insulin secretory pattern in non-insulin-dependent diabetes mellitus. This study was undertaken to assess the effect of chronic exposure of pancreatic islets to free fatty acid on insulin secretion. METHODS: Rat pancreatic islets were cultured in various concentrations of glucose(5.5, 11, 27 mM) for 48 hrs with or without addition of free fatty acid(90 upM linoleic acid), and the basal and glucose-stimulated insulin secretion were measured. The effect of fatty acid oxidation inhibitor(2-bromopalmitate) was also tested. RESULTS: Islets cultured in high glucose concentrations showed a marked increase in basal insulin secretion. Free fatty acid stimulated the basal insulin secretion in islets cultured at 5.5 or 11 mM glucose, but no additional effect was seen in islets eultured at 27 mM glucose. In contrast, glucose-stimulated insulin secretion was decreased in islets cultured in high glucose media. Exposure to free fatty acid exerted an additive inhibitory effect on glucose-induced insulin secretion in islets cultured at 5.5 or 1 1 mM glucose, but not in islets cultured at 27M glucose, An inhibitor of fatty acid oxidation, 2-bromopalmitate, prevented the fatty acid-induced changes in both basal and glucosestimulated insulin secretion. CONCLUSION: These results showed that longterm exposure of pancreatic islets to free fatty acid altered the dynamics of insulin secretion, probably through a glucosefatty acid cycle.
- Plasminogen Activator Inhibitor ( PAI-1 ) Levels in Patients with non-insulin Dependent Diabetes Mellitus ( NIDDM ).
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Hong Kyu Kim, Chul Hee Kim, Eun Sug Shin, Hyo Jung Kim, Joong Yeol Park, Sung Kwan Hong, Hyun Sook Chi, Ki Up Lee
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Korean Diabetes J. 1997;21(1):29-38. Published online January 1, 2001
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Conventional cardiovascular risk factors cannot fully explain high risk of cardiovascular disease in patients with non-insulin dependent diabetes mellitus(NIDDM). This study was undertaken to know whether plasma PAI-1 levels are increased in NIDDM patients, and to identify factors intluencing Pal-1 levels. METHODS: Forty three microalbuminuric, 41 normoalbuminuric NIDDM patients and 39 normal controls matched with age, sex and body mass index (BMI) participated in this study. Clinical characteristies and laboratory findings such as lipid profile, fasting serum C-peptide and PAI-1 levels were evaluated, RESULTS: NIDDM patients showed significantly higher PAI-1 levels than normal controls(44.3+17.4 ng/mL vs. 26.3+12.6ng/mL, p<0.05). However, we failed to show the differences in PAI-1 levels between NIDDM patients with microalbuminuria and normoalbuminuria. PAI-1 levels were significantly correlated to BMI, fasting plasma glucose, HbA1, triglyceride and serum C-peptide levels. Multiple regression analysis showed that serum triglyceride and fasting serum C-peptied levels were independently related to PAI-1 levels. Conclusion; These findings suggested that elevated PAI-1 levels may contribute to increased risk of cardiovascular disease in patients with NIDDM.
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