Differential Effects of High-carbohydrate and High-fat Diet Composition on Muscle Insulin Resistance in Rats

Abstract

This study was conducted to evaluate whether the composition of carbohydrate or fat diet affects insulin resistance by measuring the muscle glucose transport rate. Both high-sucrose and high-starch diet with or without high-fat decreased insulin-stimulated glucose transport, but there were no significant differences among groups. Calorie intake in both high-sucrose and high-starch diet groups was higher than in chow group. The high-fat high-sucrose diet induced decrease in insulin-stimulated glucose transport was partially improved by supplement with fish oil. Calorie intake in high-fat high-sucrose and fish oil supplemented groups was higher than in chow group. The decreased insulin-stimulated glucose transport was accompanied by the increase in visceral fat mass, plasma triglyceride and insulin levels. These changes were improved by the supplement with fish oil. These results demonstrate that the composition of fat in diet is clearly instrumental in the induction of muscle insulin resistance. However, in high carbohydrate diet, it is likely that the amount of calorie intake may be a more important factor in causing insulin resistance than the composition of carbohydrate. Thus, the compositions of carbohydrate and fat in diet differentially affect on muscle insulin resistance.

Early postnatal overnutrition increases adipose tissue accrual in response to a sucrose-enriched diet

“…The effect of a diet rich in carbohydrates on weight gain is not clear from the literature since it has been reported to increase (38,46), decrease (9,22,28,36), or have no effect (2,13,21,39,49,50,52,62) on BW. These contrasting outcomes could be due to differences in species, sex, type of carbohydrate, the age that the diet was introduced, or the length of exposure to the diet.…”

Pathophysiological Changes in Liver Tissues of Hypercalorie Diet-Induced Obese Rats

“…Dysregulation of hepatic lipids, pro-inflammatory cytokines, and oxidative stress interact each other synergistically to promote hepatic fat accumulation over time [12]. Different dietary combinations and amounts have been used in various NAFLD induction studies [13][14][15][16][17]. Peroxisome proliferator-activated receptor γ (PPARγ) is a major transcription regulator particularly for liver lipogenesis [18].…”

Changes in glucose tolerance and leptin responsiveness of rats offered a choice of lard, sucrose, and chow

“…A recent review by Panchal and Brown (46) concludes that rats fed high-fat, high-carbohydrate diets provide the best rodent model of human metabolic syndrome due to the development of obesity, hyperinsulinemia, hyperlipidemia, hepatic steatosis, and cardiovascular abnormalities. Hepatic and skeletal muscle insulin resistance is evident within 4 wk (12,63), but it may take months for additional aspects of the metabolic syndrome to develop in mice (42,47) and rats (48). We and others have demonstrated that rats offered lard and sucrose solution in addition to chow (choice) overeat and rapidly gain body fat (3,36).…”