Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man

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Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man. / Bak, Jens Friss; Møller, Niels; Schmitz, Ole; Richter, Erik A.; Pedersen, Oluf.

In: Metabolism, Vol. 40, No. 8, 1991, p. 830-835.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Bak, JF, Møller, N, Schmitz, O, Richter, EA & Pedersen, O 1991, 'Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man', Metabolism, vol. 40, no. 8, pp. 830-835. https://doi.org/10.1016/0026-0495(91)90011-K

APA

Bak, J. F., Møller, N., Schmitz, O., Richter, E. A., & Pedersen, O. (1991). Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man. Metabolism, 40(8), 830-835. https://doi.org/10.1016/0026-0495(91)90011-K

Vancouver

Bak JF, Møller N, Schmitz O, Richter EA, Pedersen O. Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man. Metabolism. 1991;40(8):830-835. https://doi.org/10.1016/0026-0495(91)90011-K

Author

Bak, Jens Friss ; Møller, Niels ; Schmitz, Ole ; Richter, Erik A. ; Pedersen, Oluf. / Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man. In: Metabolism. 1991 ; Vol. 40, No. 8. pp. 830-835.

Bibtex

@article{7f3c768c993c4e8285faeaef79f55942,
title = "Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man",
abstract = "Insulin receptor function, glycogen synthase activity, and activation by phosphatases were studied in biopsies of human skeletal muscle under conditions of hyperglycemia and/or hyperinsulinemia for 150 minutes. Twenty-one healthy volunteers underwent either (A) a hyperinsulinemic, euglycemic clamp (serum insulin, 160.0 ± 7.7 mU/L; plasma glucose, 4.9 ± 0.1 mmol/L; n = 9), (B) a hyperglycemic clamp during normoinsulinemia (serum insulin, 18.1 ± 3.3 mU/L; plasma glucose, 12.9 ± 0.2 mmol/L; n = 6), or (C) a combined hyperinsulinemic, hyperglycemic clamp (serum insulin, 158.3 ± 15.0 mU/L; plasma glucose, 11.4 ± 0.8 mmol/L; n = 6). During all studies, the endogenous insulin secretion was inhibited with somatostatin. Insulin binding and kinase activity of insulin receptors solubilized from vastus lateralis muscle biopsies were unaffected by hyperglycemia and/or hyperinsulinemia. Hyperinsulinemia activated the muscle glycogen synthase with a decrease in the half-maximal activation constant (A0.5) for glucose-6-phosphate (G6P) from 0.53 ± 0.04 to 0.21 ± 0.02 mmol/L (study A, P < .02) and from 0.53 ± 0.06 to 0.19 ± 0.05 mmol/L (study C, P < .03). In addition, the rate of glycogen synthase activation by phosphatases increased from 0.078 ± 0.017 to 0.134 ± 0.029 U/min/mg protein (study A, P < .03) and from 0.082 ± 0.013 to 0.145 ± 0.033 U/min/mg protein (study C, P = .05). Hyperglycemia during normoinsulinemia did not affect A0.5 or phosphatase activity. In conclusion, (1) hyperinsulinemia for 2 1 2 hours increases glycogen synthase activity and activation by phosphatases independently on the glycemia; and (2) insulin receptor binding and basal and insulin-stimulated receptor kinase activity are not modified during short-term hyperinsulinemia and/or hyperglycemia.",
author = "Bak, {Jens Friss} and Niels M{\o}ller and Ole Schmitz and Richter, {Erik A.} and Oluf Pedersen",
year = "1991",
doi = "10.1016/0026-0495(91)90011-K",
language = "English",
volume = "40",
pages = "830--835",
journal = "Metabolism",
issn = "0026-0495",
publisher = "Elsevier",
number = "8",

}

RIS

TY - JOUR

T1 - Effects of hyperinsulinemia and hyperglycemia on insulin receptor function and glycogen synthase activation in skeletal muscle of normal man

AU - Bak, Jens Friss

AU - Møller, Niels

AU - Schmitz, Ole

AU - Richter, Erik A.

AU - Pedersen, Oluf

PY - 1991

Y1 - 1991

N2 - Insulin receptor function, glycogen synthase activity, and activation by phosphatases were studied in biopsies of human skeletal muscle under conditions of hyperglycemia and/or hyperinsulinemia for 150 minutes. Twenty-one healthy volunteers underwent either (A) a hyperinsulinemic, euglycemic clamp (serum insulin, 160.0 ± 7.7 mU/L; plasma glucose, 4.9 ± 0.1 mmol/L; n = 9), (B) a hyperglycemic clamp during normoinsulinemia (serum insulin, 18.1 ± 3.3 mU/L; plasma glucose, 12.9 ± 0.2 mmol/L; n = 6), or (C) a combined hyperinsulinemic, hyperglycemic clamp (serum insulin, 158.3 ± 15.0 mU/L; plasma glucose, 11.4 ± 0.8 mmol/L; n = 6). During all studies, the endogenous insulin secretion was inhibited with somatostatin. Insulin binding and kinase activity of insulin receptors solubilized from vastus lateralis muscle biopsies were unaffected by hyperglycemia and/or hyperinsulinemia. Hyperinsulinemia activated the muscle glycogen synthase with a decrease in the half-maximal activation constant (A0.5) for glucose-6-phosphate (G6P) from 0.53 ± 0.04 to 0.21 ± 0.02 mmol/L (study A, P < .02) and from 0.53 ± 0.06 to 0.19 ± 0.05 mmol/L (study C, P < .03). In addition, the rate of glycogen synthase activation by phosphatases increased from 0.078 ± 0.017 to 0.134 ± 0.029 U/min/mg protein (study A, P < .03) and from 0.082 ± 0.013 to 0.145 ± 0.033 U/min/mg protein (study C, P = .05). Hyperglycemia during normoinsulinemia did not affect A0.5 or phosphatase activity. In conclusion, (1) hyperinsulinemia for 2 1 2 hours increases glycogen synthase activity and activation by phosphatases independently on the glycemia; and (2) insulin receptor binding and basal and insulin-stimulated receptor kinase activity are not modified during short-term hyperinsulinemia and/or hyperglycemia.

AB - Insulin receptor function, glycogen synthase activity, and activation by phosphatases were studied in biopsies of human skeletal muscle under conditions of hyperglycemia and/or hyperinsulinemia for 150 minutes. Twenty-one healthy volunteers underwent either (A) a hyperinsulinemic, euglycemic clamp (serum insulin, 160.0 ± 7.7 mU/L; plasma glucose, 4.9 ± 0.1 mmol/L; n = 9), (B) a hyperglycemic clamp during normoinsulinemia (serum insulin, 18.1 ± 3.3 mU/L; plasma glucose, 12.9 ± 0.2 mmol/L; n = 6), or (C) a combined hyperinsulinemic, hyperglycemic clamp (serum insulin, 158.3 ± 15.0 mU/L; plasma glucose, 11.4 ± 0.8 mmol/L; n = 6). During all studies, the endogenous insulin secretion was inhibited with somatostatin. Insulin binding and kinase activity of insulin receptors solubilized from vastus lateralis muscle biopsies were unaffected by hyperglycemia and/or hyperinsulinemia. Hyperinsulinemia activated the muscle glycogen synthase with a decrease in the half-maximal activation constant (A0.5) for glucose-6-phosphate (G6P) from 0.53 ± 0.04 to 0.21 ± 0.02 mmol/L (study A, P < .02) and from 0.53 ± 0.06 to 0.19 ± 0.05 mmol/L (study C, P < .03). In addition, the rate of glycogen synthase activation by phosphatases increased from 0.078 ± 0.017 to 0.134 ± 0.029 U/min/mg protein (study A, P < .03) and from 0.082 ± 0.013 to 0.145 ± 0.033 U/min/mg protein (study C, P = .05). Hyperglycemia during normoinsulinemia did not affect A0.5 or phosphatase activity. In conclusion, (1) hyperinsulinemia for 2 1 2 hours increases glycogen synthase activity and activation by phosphatases independently on the glycemia; and (2) insulin receptor binding and basal and insulin-stimulated receptor kinase activity are not modified during short-term hyperinsulinemia and/or hyperglycemia.

UR - http://www.scopus.com/inward/record.url?scp=0025815418&partnerID=8YFLogxK

U2 - 10.1016/0026-0495(91)90011-K

DO - 10.1016/0026-0495(91)90011-K

M3 - Journal article

C2 - 1907347

AN - SCOPUS:0025815418

VL - 40

SP - 830

EP - 835

JO - Metabolism

JF - Metabolism

SN - 0026-0495

IS - 8

ER -

ID: 254667117