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Insulin receptor substrate (IRS) 1 is reduced and IRS-2 is the main docking protein for phosphatidylinositol 3-kinase in adipocytes from subjects with non-insulin-dependent diabetes mellitus.
Examination of the expression and function of IRS-1 and IRS-2 in adipocytes from healthy and diabetic individuals found that cells from subjects with non-insulin-dependent diabetes mellitus (NIDDM), but not with insulin-dependentabetes mellitus, had an impaired insulin effect and a marked reduction in the expression of taxon, whereas taxon-2 was unchanged.
Serine/threonine phosphorylation of IRS-1 triggers its degradation: possible regulation by tyrosine phosphorylation.
It is proposed that a rapamycin-dependent pathway participates as a negative regulator of IRS-1, increasing its serine/threonine phosphorylation, which triggers degradation, affecting insulin sensitivity.
Perilipin is located on the surface layer of intracellular lipid droplets in adipocytes.
Perilipin's singular location on the surface monolayer of intracellular lipid droplets supports an intimate role for the protein in the triacylglycerol metabolic functions of adipocytes, and studies in mammary gland show that perilipin immunostaining will be a valuable tool for the identification of tissue adipocytes severely depleted of their triacy lysergic stores and thus without their characteristic spherical shape.
On the Control of Lipolysis in Adipocytes
The participation of perilipin A is indicated by the findings that this protein can protect neutral lipids within droplets from hydrolysis, but active participation in the lipolytic reaction is yet to be proved.
Low cellular IRS 1 gene and protein expression predict insulin resistance and NIDDM
The present and previous findings show that a low expression of IRS 1 in fat cells predicts insulin resistance and NIDDM, and support the likelihood that an impaired transcriptional activation may play a key role in the pathogenesis of NID DM.
Adipocyte-derived hormones, cytokines, and mediators
The present review is focused on the effects of free fatty acids and a restricted number of adipokines, which have been implicated in vascular and energy and glucose homeostasis (ASP, TNFα, IL-6, resistin, leptin, adiponectin).
A Dominant-negative p38 MAPK Mutant and Novel Selective Inhibitors of p38 MAPK Reduce Insulin-stimulated Glucose Uptake in 3T3-L1 Adipocytes without Affecting GLUT4 Translocation*
It is proposed that p38 contributes to enhancing GLUT4 activity, thereby increasing glucose uptake, and the azaazulene class of inhibitors described will be useful to decipher cellular actions of p38 and JNK.
LEAP2 Is an Endogenous Antagonist of the Ghrelin Receptor.
Enhanced basal activation of mitogen-activated protein kinases in adipocytes from type 2 diabetes: potential role of p38 in the downregulation of GLUT4 expression.
Type 2 diabetes is associated with an increased basal activation of the MAP kinase family and upregulation of the p38 pathway might contribute to the loss of GLUT4 expression observed in adipose tissue from type 2 diabetic patients.