[The molecular mechanism of high glucose-induced insulin resistance in 3T3-L1 adipocytes].
We investigated the cellular effect of high glucose using 3T3-L1 adipocytes on glucose transport activity, the expression of insulin signaling proteins and IRS1 tyrosine phosphorylation. Results showed that adipocytes treated with different high glucose (10, 15 and 25 mmol.L-1) for 24 hours showed to impair the basal and insulin-induced increase in glucose uptake in a dose-dependent manner and decreased significantly IRS1 tyrosine phosphorylation. High concentration of glucose produced opposite effects on IRS1 and IRS2: down-regulated IRS1 protein expression level and tightly up-regulated IRS2 contents. p85 and PKB were unaffected. Chronic exposure to high glucose can inhibit glucose uptake and induce insulin resistance. The mechanism may be involved in affecting the expression of insulin signaling peptides and tyrosine phosphorylation.
Liu
H X
HX
Department of Internal Medicine, Xiangya Hospital, Central Sooth University, Changsha 410008, China.
D016475:3T3 Cells / Q000187:drug effects*; D017667:Adipocytes / Q000187:drug effects*; D000818:Animals; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007333:Insulin Resistance; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects; D021382:Protein Sorting Signals / Q000187:drug effects; D014443:Tyrosine / Q000378:metabolism
D021382:Protein Sorting Signals; D014443:Tyrosine; D005947:Glucose