The occurrence and severity of obesity-and insulin resistance-related disorders vary according to the diet. The aim of the present longitudinal study was to examine the effects of a high-fat or a high-fructose diet on body weight (BW), body fat mass, insulin sensitivity (IS) and lipid profiles in a rat model of dietary-induced obesity and low IS. A total of eighteen, 12-week-old male Wistar rats were divided into three groups, and were fed with a control, a high-fat (65 % lipid energy) or a high-fructose diet (65 % fructose energy) for 10 weeks. BW, body fat mass ( 2 H 2 O dilution method), IS (euglycaemic -hyperinsulinaemic clamp technique), plasma glucose, insulin, NEFA, TAG and total cholesterol were assessed before and at the end of 10-week period. Cholesterol was measured in plasma lipoproteins separated from pooled samples of each group and each time period by using fast-protein liquid chromatography. All rats had similar BW at the end of the 10-week period. Body fat mass was higher in the high-fat group compared to the control group. There was no change in basal glycaemia and insulinaemia. The IS was lower in the high-fat group and was unchanged in the high-fructose group, compared to the control group. Plasma TAG concentration and cholesterol distribution in lipoproteins did not change over time in any group. Plasma NEFA concentration decreased, whereas plasma TAG concentration increased over time, regardless of the diet in both cases. The 10-week high-fat diet led to obesity and low IS, whereas rats fed with the high-fructose diet exhibited no change in IS and lipidaemia. The high-fat diet had more deleterious response than high-fructose diet to induce obesity and low IS in rats.Key words: insulin resistance: obesity: dyslipidemia: high-fat diet: high-fructose diet: rat There is a growing prevalence of obesity and low insulin sensitivity (IS), often called insulin resistance, in human subjects. Thus, there is a need for an animal model to study the time course of these metabolic disturbances as well as their unhealthy consequences. Different animal models have been used to study obesity and IS, notably the rat, in which obesity can be caused by genetic mutations or induced by nutritional interventions. As human obesity is mainly due to nutritional habits, animal models of obesity and low IS induced by specific diets may be preferable to genetic models.Various nutritional interventions have been used to induce obesity, low IS and dyslipidaemia in rats. High-fat diets have been shown to cause these metabolic disorders in previous studies, but there has been a large variability in the intensity of the metabolic changes (1 -5) . High-fructose diets have also been shown to lower IS and promote mild-to-severe dyslipidaemia (6 -9) . The differences in nutritional interventions, such as diet composition and interventional duration, have complicated the comparisons of these studies. Therefore, it is difficult to define the best nutritional intervention to induce obesity in an animal model that closely ...
The study of the expression of genes involved in obesity‐related disorders has been promising for a better understanding of the links between components of the metabolic syndrome.Our aim was to measure the effects of a high‐fructose diet on metabolic status and on the mRNA expression of several genes involved in insulin‐signaling pathway, and glucido‐lipid metabolism in rats, and to assess the effects of EPA supplementation.Rats were given for 10 wk either a control or a high‐fructose diet (65% fructose cal), supplemented or not with EPA (120 mg/d). At the end of the 10‐wk period, body composition and IS were assessed, lipid plasma were assayed, and mRNA expression of insulin receptor, IRS1, perilipin, leptin, ACC, FAS, HSL, LPL, GLUT, TNFα, SREBP‐1c, PPARγ was semi‐quantified from adipose tissue biopsies.In high‐fructose rats, IS tended to be lower, plasma triglyceride level tended to be higher, and Glut4 expression was lower than in control rats. In rats fed with high‐fructose diet plus EPA, plasma NEFA concentration was lower, and PPARγ and FAS mRNA levels were higher than in rats fed with unsupplemented high fructose diet.Our results show change in Glut4 expression in rats fed highfructose diet that could reflect an alteration of glucose uptake, and impair systemic IS. They also show that EPA could stimulate transcription of PPARγ and its target gene FAS that could account for its beneficial effect on lipidemia.
The study of expression of genes involved in obesity‐related disorders provides a tool to elucidate the links between obesity, loss of insulin sensitivity (IS), and dyslipidemia. Our aim was to measure the effects of a high‐fructose diet and EPA supplementation on metabolic status and mRNA expression of genes involved in insulin‐signaling pathway, and glucido‐lipid metabolism in rats.Rats were given for 10 wk either control diet or high‐fat high‐fructose diet (40% fructose, 40% lipid cal), supplemented or not with EPA (120 mg/d). At the end of the 10‐wk period, body composition and IS were assessed, lipid plasma were assayed, and mRNA expression of insulin receptor, IRS1, perilipin, leptin, ACC, FAS, HSL, LPL, GLUT, TNFα, SREBP‐1c, PPARγ was semi‐quantified from adipose tissue biopsies.In rats fed with high‐fat high‐fructose diet, plasma cholesterol level was higher than in control rats, as well as ACC and FAS mRNA levels. In rats fed with the same diet plus EPA, plasma cholesterol level was lower and PPARγ mRNA level higher compared with the rats fed with high‐fat high‐fructose diet.Our results show changes in expression of lipogenic genes in rats fed high‐fat high‐fructose diet, that could reflect the obesogenic effect of such a diet. They also show that EPA could stimulate the transcription of PPARγ that could account for its beneficial effect on lipidemia.
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