High-glycemic index carbohydrates abrogate the antiobesity effect of fish oil in mice

Abstract

index carbohydrates abrogate the antiobesity effect of fish oil in mice. Am J Physiol Endocrinol Metab 302: E1097-E1112, 2012. First published February 14, 2012 doi:10.1152/ajpendo.00524.2011Fish oil rich in n-3 polyunsaturated fatty acids is known to attenuate diet-induced obesity and adipose tissue inflammation in rodents. Here we aimed to investigate whether different carbohydrate sources modulated the antiobesity effects of fish oil. By feeding C57BL/6J mice isocaloric high-fat diets enriched with fish oil for 6 wk, we show that increasing amounts of sucrose in the diets dose-dependently increased energy efficiency and white adipose tissue (WAT) mass. Mice receiving fructose had about 50% less WAT mass than mice fed a high fish oil diet supplemented with either glucose or sucrose, indicating that the glucose moiety of sucrose was responsible for the obesity-promoting effect of sucrose. To investigate whether the obesogenic effect of sucrose and glucose was related to stimulation of insulin secretion, we combined fish oil with high and low glycemic index (GI) starches. Mice receiving the fish oil diet containing the low-GI starch had significantly less WAT than mice fed high-GI starch. Moreover, inhibition of insulin secretion by administration of nifedipine significantly reduced WAT mass in mice fed a high-fish oil diet in combination with sucrose. Our data show that the macronutrient composition of the diet modulates the effects of fish oil. Fish oil combined with sucrose, glucose, or high-GI starch promotes obesity, and the reported anti-inflammatory actions of fish oil are abrogated. In conclusion, our data indicate that glycemic control of insulin secretion modulates metabolic effects of fish oil by demonstrating that high-GI carbohydrates attenuate the antiobesity effects of fish oil. energy efficiency; glucose tolerance; insulin secretion; n-3 polyunsaturated fatty acids

Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

“…In agreement with previous studies in male mice (14,30,32), intake of a diet with high protein/sucrose ratio did not protect the mice against high-fat diet-induced impairment of glucose tolerance at 3 mo (Fig. 2B).…”

“…However, these models cannot be used to distinguish whether the observed metabolic dysfunctions result from the obese state or from the high-fat feeding. Rodent studies have shown that obesity is prevented if the increase in dietary fat is accompanied by a high protein-to-sucrose ratio (12,14,30,32,33,36). This may reflect higher satiety and diet-induced thermogenesis when the protein content in the diet is increased (31).…”

Indomethacin Treatment Prevents High Fat Diet-induced Obesity and Insulin Resistance but Not Glucose Intolerance in C57BL/6J Mice

“…These differences impinge on the important question as to whether hyperinsulinemia is a compensatory action to counteract obesity-elicited inflammation and peripheral insulin resistance or whether increased plasma insulin precedes obesity development, inflammation, and insulin resistance. Whereas the canonical view favors the first possibility (1, 40), we and others have recently argued that a high level of insulin is a prerequisite for HF diet-induced obesity (41)(42)(43). In keeping with this view, adipose-specific insulin receptor knock-out mice are protected against diet-induced obesity (44).…”

Transcriptome profiling of brown adipose tissue during cold exposure reveals extensive regulation of glucose metabolism

“…Mice were killed by cervical dislocation. iBAT, iWAT, and eWAT were dissected as previously described (15). All mouse experiments were approved by the Norwegian or Danish Animal Research Authority.…”