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Exerts an important anti-inflammatory effect in adipose cells by impairing the interleukin-6 signal at several levels. Exerts an important anti-inflammatory effect in adipose cells by impairing the interleukin-6 signal at several levels. IA-2beta, but not IA-2, is induced by ghrelin and inhibits glucose-stimulated insulin secretion. Ins1 is a 'defective gene' relative to Ins2, and mouse lines created provide a novel model of sex-dimorphic insulin-deficient diabetes. Ins1 locus is unlikely to be imprinted in common laboratory mice. Insulin B-chain peptides represent another example of a weak major histocompatibility complex-binding ligand that is highly immunogenic, giving rise to distinct populations of autoimmune T cells. Insulin inhibition of the expression of IGFBP-1, PEPCK, and G6Pase genes occurs through different regulatory pathways. Insulin up-regulates and leptin down-regulates adipocyte fatty acid uptake, leading to alterations in fatty acid partitioning that affect adiposity. JNK1 loss in liver up-regulates proliferator-activated receptor gamma coactivator 1 beta and increases plasma triglyceride despite reduced glucose and insulin levels in diet-induced obese mice. PGC-1alpha gene expression is down-regulated by Akt- mediated phosphorylation and nuclear exclusion of FoxO1 in insulin-stimulated skeletal muscle. Pdx-1 directly regulates insulin transcription through formation of a complex with transcriptional coactivators on the proximal insulin promoter. Pdx-1 occupies the endogenous insulin promoter in betaTC3 cells but not in mPAC cells, a finding that is independent of the intracellular Pdx-1 protein concentration. SHIP mediates inhibition of insulin- and platelet-derived growth factor-stimulated mitogen-activated protein kinase activity in 3T3-L1 adipocytes. STAT 5 proteins are not activated by physiological levels of insulin in adipose tissue. Treatment with celecoxib increased insulin release from INS-1E cultured cells in a dose-dependent manner in glucose concentrations ranging from 5 to 17 mM. Acidic granular pH is important for insulin secretion but the acute further acidification produced by glucose is not essential for the augmentation of secretion via the amplifying pathway. An insulin splice-variant overexpressed in diabetes, obesity, and insulin resistance results in increased insulin translation. Analysis of glucocorticoid receptor-dependent inhibition of insulin signaling. In skeletal myotubes, FAK regulates the insulin-mediated cytoskeletal rearrangement essential for normal glucose transport and glycogen synthesis. Increased hepatocyte CYP2E1 expression and the presence of steatohepatitis result in the down-regulation of insulin signaling. Insulin and epinephrine control lipin primarily by changing localization rather than intrinsic PAP activity. Insulin increases the level of M2-PK mRNA in adipocytes by acting at transcriptional and post-transcriptional levels through signaling pathways involving both PI3K and MAPK kinase. Insulin-specific Tregs producing IL-10, TGF-beta, and IL-4 are enhanced by suppression of CD3epsilon in a mouse model of autoimmune diabetes. Interleukin-6 has a role in insulin signal transduction via insulin receptor substrate-1 in skeletal muscle cells. Proinsulin/insulin molecules have a sequence that is a primary target of the autoimmunity that causes diabetes of the non-obese diabetic (NOD) mouse. Regulation of hepatic glucose production by leptin and adiponectin, but not insulin, requires hepatic AMPKalpha2 activity. The degradation of C-peptide in kidney and placenta follows similar patterns, dominated by endopeptidase cleavages N-terminal of Leu. The proximal insulin promoter is hyperacetylated at histone H3 and hypermethylated at H3-K4 in beta cells.
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