
IndraLab
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"The overproduction of TNF could decrease the phosphorylation of insulin receptor substrates 1 and 2, inhibit phosphoinositol 3-kinase and protein kinase B, block the phosphorylation of glucose transporter 4, prevent the cell uptake of glucose [29], and increase plasma glucose levels."
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"Increased TNFalpha causes an adipocyte specific decrease in insulin receptor phosphorylation; decreased insulin receptor function; resistance to the antilipolytic effects of insulin; de-repression of adipocyte hormone sensitive lipase; increased, continuous lipolysis of the enlarged adipocyte TG mass; and a further increase in plasma LCFA."
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"Additionally, ADP can prevent the proliferation of monocyte precursor cells and have a negative regulatory effect on the expression of TNF-α, thereby reducing the degree of inflammatory response.19Imanparst F et al.20 have shown that TNF-α can inhibit insulin receptor self-phosphorylation, block insulin-stimulated glucose uptake, and downregulate the number of insulin receptors, thereby inducing hyperinsulinemia and exacerbating insulin resistance."