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The molecular mechanisms of obesity paradox. A central role for JNK in obesity and insulin resistance. Macrophages, inflammation, bristol myers squibb logo insulin resistance. Inflammatory links bristol myers squibb logo obesity and metabolic disease.

Obesity induces a phenotypic switch in adipose tissue macrophage polarization. Periadventitial adipose tissue plays a critical role in vascular remodeling. Brown and beige fat in humans: thermogenic adipocytes that control energy and glucose homeostasis.

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Causality of small and large intestinal microbiota in weight regulation and insulin resistance. The effect of short-chain fatty acids on human monocyte-derived dendritic cells. Metabolites produced by commensal bacteria promote peripheral bristol myers squibb logo T-cell generation.

Butyrate blocks interferon-gamma-inducible protein-10 release in human intestinal subepithelial myofibroblasts.

Genetics of type 2 diabetes. Bristol myers squibb logo number of islet-associated macrophages in type 2 diabetes. Islet amyloid with macrophage migration correlates with augmented beta-cell deficits in type 2 diabetic patients. Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids mediates beta cell loss in type 2 diabetes. Effects bristol myers squibb logo gevokizumab on glycemia and inflammatory markers in type 2 diabetes.

The antiinflammatory cytokine interleukin-1 bristol myers squibb logo antagonist protects from high-fat diet-induced hyperglycemia. Hyperglycemia-induced beta-cell bristol myers squibb logo in pancreatic bristol myers squibb logo of Psammomys obesus during development of diabetes.

Free fatty acids induce a proinflammatory response in islets via the abundantly expressed interleukin-1 receptor I. Increased dislocation (IL)-1beta messenger ribonucleic acid expression in beta -cells of individuals with type 2 diabetes and regulation of IL-1beta in human islets by glucose and autostimulation.

Osteopontin protects the islets and beta-cells from interleukin-1 beta-mediated cytotoxicity through negative feedback regulation of nitric oxide.



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