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Low fish oil intake improves insulin sensitivity, lipid profile and muscle metabolism on insulin resistant MSG-obese rats
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Background: Obesity is commonly associated with diabetes, cardiovascular diseases and cancer. The purpose of
this study was to determinate the effect of a lower dose of fish oil supplementation on insulin sensitivity, lipid
profile, and muscle metabolism in obese rats.
Methods: Monosodium glutamate (MSG) (4 mg/g body weight) was injected in neonatal Wistar male rats. Threemonth-old rats were divided in normal-weight control group (C), coconut fat-treated normal weight group (CO),
fish oil-treated normal weight group (FO), obese control group (Ob), coconut fat-treated obese group (ObCO) and
fish oil-treated obese group (ObFO). Obese insulin-resistant rats were supplemented with fish oil or coconut fat (1
g/kg/day) for 4 weeks. Insulin sensitivity, fasting blood biochemicals parameters, and skeletal muscle glucose
metabolism were analyzed.
Results: Obese animals (Ob) presented higher Index Lee and 2.5 fold epididymal and retroperitoneal adipose
tissue than C. Insulin sensitivity test (Kitt) showed that fish oil supplementation was able to maintain insulin
sensitivity of obese rats (ObFO) similar to C. There were no changes in glucose and HDL-cholesterol levels amongst
groups. Yet, ObFO revealed lower levels of total cholesterol (TC; 30%) and triacylglycerol (TG; 33%) compared to
Ob. Finally, since exposed to insulin, ObFO skeletal muscle revealed an increase of 10% in lactate production, 38%
in glycogen synthesis and 39% in oxidation of glucose compared to Ob.
Conclusions: Low dose of fish oil supplementation (1 g/kg/day) was able to reduce TC and TG levels, in addition
to improved systemic and muscle insulin sensitivity. These results lend credence to the benefits of n-3 fatty acids
upon the deleterious effects of insulin resistance mechanisms.
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YAMAZAKI, R. K. et al. Low fish oil intake improves insulin sensitivity, lipid profile and muscle metabolism on insulin resistant MSG-obese rats. Lipids in Health and Disease, [S.l.], v. 10, 2011.
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Exceto quando indicado de outra forma, a licença deste item é descrita como Attribution 4.0 International

