Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation. Export

@article{citeulike:282315, abstract = {We examined the effect of physiological hyperinsulinemia on insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation and phosphatidylinositol (PI) 3-kinase activity in skeletal muscle from six lean-to-moderately obese NIDDM patients and six healthy subjects. A rise in serum insulin levels from approximately 60 to approximately 650 pmol/l increased IRS-1 tyrosine phosphorylation sixfold over basal levels in control muscle (P < 0.01), whereas no significant increase was noted in NIDDM muscle. The reduced IRS-1 phosphorylation in the NIDDM muscle was not related to changes in IRS-1 protein content, since IRS-1 protein expression was similar between control and NIDDM subjects (16.0 +/- 1.7 vs. 22.9 +/- 4.0 arbitrary units/mg protein for control and NIDDM, respectively; NS). Physiological hyperinsulinemia increased PI 3-kinase activity in control muscle twofold (P < 0.01), whereas no increase in insulin-stimulated PI 3-kinase activity was noted in the NIDDM muscle. Furthermore, in vitro insulin-stimulated (600 pmol/l) 3-O-methylglucose transport was 40\% lower in isolated muscle from NIDDM subjects (P < 0.05). The present findings couple both reduced insulin-stimulated IRS-1 tyrosine phosphorylation and PI 3-kinase activity to the impaired insulin-stimulated glucose transport in skeletal muscle from lean-to-moderately obese NIDDM subjects.}, address = {Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.}, author = {Bj\"{o}rnholm, M. and Kawano, Y. and Lehtihet, M. and Zierath, J. R.}, citeulike-article-id = {282315}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/9032113}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=9032113}, issn = {0012-1797}, journal = {Diabetes}, keywords = {insulin, insulinresistance, insulinsignalling, pi3k, t2dm}, month = {March}, number = {3}, pages = {524--527}, posted-at = {2005-08-15 15:10:58}, priority = {2}, title = {Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/9032113}, volume = {46}, year = {1997} }

TY - JOUR ID - citeulike:282315 L3 - citeulike-article-id:282315 N2 - We examined the effect of physiological hyperinsulinemia on insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation and phosphatidylinositol (PI) 3-kinase activity in skeletal muscle from six lean-to-moderately obese NIDDM patients and six healthy subjects. A rise in serum insulin levels from approximately 60 to approximately 650 pmol/l increased IRS-1 tyrosine phosphorylation sixfold over basal levels in control muscle (P < 0.01), whereas no significant increase was noted in NIDDM muscle. The reduced IRS-1 phosphorylation in the NIDDM muscle was not related to changes in IRS-1 protein content, since IRS-1 protein expression was similar between control and NIDDM subjects (16.0 +/- 1.7 vs. 22.9 +/- 4.0 arbitrary units/mg protein for control and NIDDM, respectively; NS). Physiological hyperinsulinemia increased PI 3-kinase activity in control muscle twofold (P < 0.01), whereas no increase in insulin-stimulated PI 3-kinase activity was noted in the NIDDM muscle. Furthermore, in vitro insulin-stimulated (600 pmol/l) 3-O-methylglucose transport was 40% lower in isolated muscle from NIDDM subjects (P < 0.05). The present findings couple both reduced insulin-stimulated IRS-1 tyrosine phosphorylation and PI 3-kinase activity to the impaired insulin-stimulated glucose transport in skeletal muscle from lean-to-moderately obese NIDDM subjects. IS - 3 JF - Diabetes SN - 0012-1797 AD - Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden. EP - 527 TI - Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation. VL - 46 SP - 524 KW - insulin KW - insulinresistance KW - insulinsignalling KW - pi3k KW - t2dm AU - Björnholm, M AU - Kawano, Y AU - Lehtihet, M AU - Zierath, JR PY - 1997/03// UR - http://view.ncbi.nlm.nih.gov/pubmed/9032113 ER -