Is the increase in circulating resistin levels partly responsible for the development of insulin resistance ?
To address this question, we sought to reverse the diet-induced increase in circulating resistin levels to assess its impact on insulin action and glucose fluxes. To this end, we used a sequence-specific ASO that targets the resistin gene. Indeed, treatment with resistin ASO lowered the plasma resistin levels in HF-fed mice to the levels observed in SC-fed mice. Because food intake and body weight were similar in all HF-fed mice, this experimental approach allowed us to isolate the contribution of hyper-resistinemia to the metabolic alteration induced by high-fat feeding. Indeed, normalization of the circulating resistin concentration per se markedly improved hepatic insulin action in HF-fed mice. This effect was sufficient to completely reverse the increase in GP induced by high-fat feeding. On the other hand, the decrease in the plasma resistin levels failed to modify the rate of glucose uptake. Thus, the elevation in circulating resistin levels induced by high-fat feeding plays an i
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