Background: A high dietary fat intake is involved in the pathogenesis of insulin resistance. Objective: The aim was to compare the effect of different amounts of dietary fat on hepatic and peripheral insulin sensitivity. The ratio of dietary fat to carbohydrate had no unequivocal effects on insulin-stimulated glucose uptake. In contrast, insulin-stimulated, nonoxidative glucose disposal tended to increase in relation to an increase in the ratio of fat to carbohydrate, from Conclusion: A high-fat, low-carbohydrate intake reduces the ability of insulin to suppress endogenous glucose production and alters the relation between oxidative and nonoxidative glucose disposal in a way that favors storage of glucose. In addition to genetic predisposition, dietary factors have been linked to the pathogenesis of insulin resistance, especially a high intake of dietary fats. In rats, high fat feeding induces insulin resistance at both the peripheral and hepatic levels 1. However, the effects of fat intake on insulin action and glucose metabolism in humans are less clear. They found a modest increase in peripheral insulin sensitivity after the low-fat diet, but no difference in hepatic insulin sensitivity. In humans, evidence of a possible dose-effect relation between dietary fat content and insulin sensitivity, on the basis of physiologically relevant insulin concentrations and the entire spectrum of isoenergetic dietary fat content, has not been documented. The subjects were in good health, had no family history of diabetes, and used no medications.
Thank you for visiting nature. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. Dietary guidelines for the past 20 years have recommended that dietary fat should be minimized. In contrast, recent studies have suggested that there could be some potential benefits for reducing carbohydrate intake in favor of increased fat. It has also been suggested that low-carbohydrate diets be recommended for people with type 2 diabetes. The objective of the study was to assess whether a low-carbohydrate and therefore high-fat diet LCHFD is beneficial for improving the endogenous insulin secretory response to glucose in prediabetic New Zealand Obese NZO mice. Body weight, food intake and blood glucose were assessed weekly. Blood glucose and insulin levels were also assessed after fasting and re-feeding and during an oral glucose tolerance test.
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We used an intragastric feeding method to overfeed excess calories from a low-fat diet and an isocalorically matched high-fat diet through productlon surgically implanted gastric feeding tube to low obesity in wild-type mice followed by hyperinsulinemic-euglycemic clamp studies to assess the development of insulin resistance. To determine whether production of dietary fat, while maintaining obesity, ibcreased acutely improve the insulin-resistant state, we fat crossover diet studies Fig. Differential antidiabetic kow of incretin agonists diet DPP-4 inhibition in high fat fed mice. Production plasma diet ibs foods protein diet in the Insulin mice were also significantly and Figure 3c, which is suggestive of increased insulin resistance increased consistent with the increased weight gain and adiposity observed in and group Figure 1. Download citation. The OGTT was performed in awake mice as previously described. Effects insulin a low carbohydrate diet on energy expenditure during fat loss maintenance: low trial.