Diabetes & Metabolism Journal

Original Articles

Effects of High Fat Diet on Lipolysis in Skeletal Muscle and Adipose Tissue in Rats.: Chul Hee Kim, Yun Ey Chung, Seong Jin Lee, Joong Yeol Park, Sung Kwan Hong, Hong Kyu Kim, Kyo Il Suh, Ki Up Lee; Korean Diabetes J. 2000;24(6):641-651. Published online January 1, 2001

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Abstract PDF: BACKGROUND
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.

The Effect of Increased Beta Cell Mass on Glucose Tolerance in Rat.: Eun Sook Oh, Kun Ho Yoon, Sun Hee Seo, Sook Young Lee, Seung Hyun Ko, Won Young Lee, Sung Rae Kim, Moo Il Kang, Bong Yon Cha, Kwang Woo Lee, Ho Young Son, Sung Goo Kang; Korean Diabetes J. 2000;24(6):629-640. Published online January 1, 2001

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Abstract PDF: BACKGROUND
The aim of the present study is to evaluate the effect of increased beta cell mass by continuous 96-hour 50% glucose infusion on glucose tolerance in insulin resistance state induced by high fat diet in normal Sprague-Dawley rats. METHODS: The adult Sprague-Dawley rats weighing 200-250 gm were infused with 50% glucose or 0.45% saline via external jugular vein catheter for 96 hours. The both groups of rats were then randomly stratified into the two subgroups, and fed either high fat diet (54% of energy from fat) or normal rat chow (8.6% of energy from fat) for 4 weeks. On day 28, blood was collected for measuring the serum concentration of insulin, and oral glucose tolerance test (2 gm/kg body weight) was performed after overnight fasting. The beta cell mass was counted with the morphometric point-counting technique of Weibel. RESULTS: After the 96 hour infusion, the percentage of beta cell mass was significantly increased in glucose-infused rats when compared to the saline-infused group (p=0.03) and maintained up to day 28. Body weight gains were significantly greater in glucose infused rats than those of saline infused group (Increased value of weight : 142.9+/-15.2 g in glucose infused rats vs 125.3+/-21.1 g in saline infused rats, p=0.01). In the saline infusion-high fat diet group, the number of rats with impaired glucose tolerance was higher than those of other group (p<0.005). The glucose values at 90 minute and 120 minute were higher in saline infusion-high fat diet group than in glucose infusion-high fat diet group (p< 0.05). CONCLUSION: Our findings suggest that the increased beta cell mass has a favorable effect on glucose tolerance in insulin resistance state which were evoked by high fat diet.

Effect of Exercise Training on Insulin Sensitivity and Intracellular Glucose Metabolism in Skeletal Muscle of High Fat-fed Rats.: Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Kyong Soo Park, Hong Kyu Lee, Ki Up Lee; Korean Diabetes J. 1998;22(2):231-242. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Insulin resistance is a major characteristic of non-insulin-dependent diabetes mellitus and obesity. Many studies have indicated that increased intake of fat are associated with obesity and insulin resistance. On the other hand, chronic exercise is known to improve insulin sensitivity. However, the mechanisms by which high fat diet induces insulin resistance and exercise trainmg improves insulin sensitivity are not established. This study was undertaken to examine the mechanisms by which high fat diet and exercise training affect the insulin sensitivity in the whole body and in skeletal muscles. METHODS: Male Sprague-Dawley rats were divided into three groups: high fat sedentary group, high fat exercise group, and control(low fat sedentary) group. High fat diet consists of 66.5% fat and 12.5% carbohydrate, and control(low fat) diet consists of 12 5% fat and 66.5% carbohydrate. Exercise training was performed by swimming three hours per day. After 3 weeks, animals underwent hyperinsulinemic euglycemic clamp study to measure whole body glucose metabolic fluxes. Glycogen synthase activity and glucose-6-phosphate (G-6-P) levels were measured in skeletal muscle at the end of the clamp study. RESULTS: In the high fat diet group, whole body glycolysis and glycogen synthesis were decreased. Exercise training reversed the insulin resistance induced by high fat diet by increasing both glycolysis and glycogen synthesis. Glycogen synthase activity in skeletal muscle was reduced in high fat diet group, and it was partially reversed by exercise training. G-6-P level in skeletal muscle was increased in high fat diet group, and it was further increased by exercise training. CONCLUSION: These results suggested that the insulin resistance in high fat diet-fed rats is due to the impairment in glucose metabolism at sites distal to G-6-P, i.e. glycolysis and glycogen synthesis. In contrast, the improvement in insulin sensitivity by exercise training in high fat-fed rats is primarily due to the increased glucose metabolic flux proximal to G-6-P, i.e. glucose transport and phosphorylation.

Mechanism of Insulin Resistance : Time Dependence of the Development of Insulin Resistance in High Fat Fed Rats.: Kyong Soo Park, Ki Up Lee, Sung Woo Park, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1997;21(2):168-175. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Increased FFA availability is known to induce insulin resistance by decrease in peripheral glucose utilization and increase in hepatic glucose procluction. However, there are conflicting results about the time dependence of the developrnent of insulin resistance with increased availability of FFA. METHODS: To elucidate the time dependence of the development of insulin resistance associated with increased availability of FFA, peripheral glucose utilization rate and hepatic glucose production rate were measured by euglycemic hyperinsulinemic clamp with 3-3H glucose infusion in rats fed high fat diet (1 week or 3 weeks) or control diet(ordinary chow diet). RESULTS: Basal plasrna FFA levels and steady state plasma insulin levels increased after high fat diet. After 1 week of high fat diet, suppressibility of hepatic glucose production rate by insulin was impaired(p<0.05 vs control). Insulin sensitivity index(glucose utilization rates/steady state plasma insulin concentrmtions X100) was decreased only after 3 weeks of high fat diet(p<0.05 vs control) which was accompanied by decreased glycogen synthase activity. CONCLUSION: High fat diet induces hepatic insulin resistance before peripheral insulin resistance and decreased glycogen synthase activity may contribute to the development of peripheral insulin resistance in rats fed high fat diet.

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