检索条件"作者=Hong-qi FAN~ Nan GU~ Feng LIU~2.Li EEI~2.Xiao-qin PAN~2.Mei GUO~2.Rong-hua CHEN~ Xi-rong GUO~2.Department of Pediatrics,nanjing Maternal and Child Health Hospital of nanjing Medical University,nanjing 2.0004,china"
Aim:To assess the effects and mechanisms of the action of resistin on basal andinsulin-stimulated glucose uptake in rat skeletal muscle ***:Rat myo-blasts(L6)were cultured and differentiated into myotubes followed b...
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Aim:To assess the effects and mechanisms of the action of resistin on basal andinsulin-stimulated glucose uptake in rat skeletal muscle ***:Rat myo-blasts(L6)were cultured and differentiated into myotubes followed by stimula-tion with single commercial resistin(130 ng/mL,0-24 h)or cultured supernatantfrom 293-T cells transfected with resistin-expressing vectors(130 ng/mL,0-24 h).liquid scintillation counting was used to quantitate[3H]2-deoxyglucose *** translocation of insulin-sensitive glucose transporters GLUT4 and GLUT1,synaptosomal-associated protein 23(SNAP23)and GLUT protein content,as wellas the tyrosine phosphorylation status and protein content of insulin receptorsubstrate(IRS)-1,were assessed by Western ***:Treatment of L6myotubes with single resistin or cultured supernatant containing recombinantresistin reduced basal and insulin-stimulated 2-deoxyglucose uptake and impairedinsulin-stimulated GLUT4 *** SNAP23 protein content wasdecreased,no effects were noted in GLUT4 or GLUT1 protein *** diminished insulin-stimulated IRS-1 tyrosine phosphorylation levels withoutaffecting its protein *** effects of recombinant resistin from 293-T cellstransfected with resistin-expressing vectors were greater than that of single ***:Resistin regulated IRS-1 function and decreased GLUT4translocation and glucose uptake in response to *** downregulatedexpression of SNAP23 may have been partly attributed to the decrease of glucoseuptake by resistin *** observations highlight the potential role ofresistin in the pathophysiology of type 2 diabetes related to obesity.
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