The insulin resistance in skeletal muscle is a characteristic in diabetics people. Although its mechanism is not totaly known, there is correlation between insulin resistance and intracellular lipid content. However, there is consensus that there is a strong correlation between insulin resistance, physical inactivity and high intracellular lipid content. Our proposal is to evaluate the effect of gene expression of HIF1± in mitochondrial biogenesis in uptake and metabolism of glucose, fatty acid, reactive species production and proteolysis. In order to have a positive control, the effect of its inhibition on the variables mentioned in cells resistant to insulin will also be assess . Our hypothesis is that HIF1± may protect against insulin resistance in the muscle improving mitochondrial function. Confirming our hypothesis, the HIF1±, or even pharmacological compounds that are capable of inhibiting expression of this gene may constitute itself important therapeutic targets against of development insulin resistance in muscle tissue.
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