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Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice.
Experimental evidence thatHypoxia occurs in adipose tissue in obese mice and that adipose hypoxia may contribute to the endocrine alterations is provided and a potential role of hypoxIA in the induction of chronic inflammation and inhibition of adiponectin in the adipose tissues in obesity is suggested. Expand
Serine phosphorylation of insulin receptor substrate 1 by inhibitor kappa B kinase complex.
It is suggested that IRS- 1 is a novel direct substrate for IKK and that phosphorylation of IRS-1 at Ser(312) (and other sites) by IKK may contribute to the insulin resistance mediated by activation of inflammatory pathways. Expand
Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice
Dietary supplementation of butyrate can prevent and treat diet-induced insulin resistance in mouse and the mechanism ofbutyrate action is related to promotion of energy expenditure and induction of mitochondria function. Expand
Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids*
The results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility thatTLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and uns saturated fatty acids. Expand
Serine Phosphorylation of Insulin Receptor Substrate 1 by Inhibitor κB Kinase Complex* 210
Insulin resistance contributes importantly to the pathophysiology of type 2 diabetes mellitus. One mechanism mediating insulin resistance may involve the phosphorylation of serine residues in insulinExpand
A role of miR‐27 in the regulation of adipogenesis
It is demonstrated that the miR‐27 gene family is downregulated during adipogenic differentiation, and represents a new class of adipogenic inhibitors and may play a role in the pathological development of obesity. Expand
Aspirin Inhibits Serine Phosphorylation of Insulin Receptor Substrate 1 in Tumor Necrosis Factor-treated Cells through Targeting Multiple Serine Kinases*
Aspirin may enhance insulin sensitivity by protecting IRS proteins from serine phosphorylation catalyzed by multiple kinases, as assessed by phospho-specific antibodies. Expand
Inhibition of insulin sensitivity by free fatty acids requires activation of multiple serine kinases in 3T3-L1 adipocytes.
The FFA-signaling pathway that contributes to serine phosphorylation and degradation of IRS-1 in adipocytes and in dietary obese mice is explored and this molecular mechanism may be responsible for insulin resistance associated with hyperlipidemia. Expand
Role of hypoxia in obesity-induced disorders of glucose and lipid metabolism in adipose tissue.
The data suggest that ATH may promote FFA release and inhibit glucose uptake in adipocytes by inhibition of the insulin-signaling pathway and induction of cell death in ob/ob mice. Expand
S6K Directly Phosphorylates IRS-1 on Ser-270 to Promote Insulin Resistance in Response to TNF-α Signaling through IKK2*
A new mechanism for TNF-α to induce insulin resistance that involves activation of S 6K by an IKK2-dependent pathway is presented and S6K directly phosphorylates IRS-1 on multiple serine residues to inhibit insulin signaling. Expand