Subcellular distribution and phosphorylation state of insulin receptors from insulin- and isoproterenol- treated rat adipose cells

Teresa M. Weber, Hans G. Joost, Masao Kuroda, Samuel W. Cushman, Ian Simpson

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Rat adipose cells treated with insulin followed by isoproterenol exhibit a change in glucose transporter intrinsic activity (lowered maximal activity) and a decrease in insulin sensitivity (rightward shift of the concentration-response curve) when assayed for 3-O-methylglucose transport. To investigate the latter phenomenon, the distribution and phosphorylation state of insulin receptors was examined. Isoproterenol augmented the effect of insulin cell surface receptors by 20-30%. These receptors were recovered in microsomal fractions. Isoproterenol also markedly reduced insulin-stimulated [32P]phosphate incorporation into the plasma membrane receptor β-subunit. These effects may account for the effect of isoproterenol to decrease the sensitivity of the glucose transport response to insulin.

Original languageEnglish (US)
Pages (from-to)51-58
Number of pages8
JournalCellular Signalling
Volume3
Issue number1
DOIs
StatePublished - Jan 1 1991

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Insulin Receptor
Isoproterenol
Phosphorylation
Insulin
3-O-Methylglucose
Facilitative Glucose Transport Proteins
Cell Surface Receptors
Insulin Resistance
Phosphates
Cell Membrane
Glucose

All Science Journal Classification (ASJC) codes

  • Cell Biology

Cite this

Weber, Teresa M. ; Joost, Hans G. ; Kuroda, Masao ; Cushman, Samuel W. ; Simpson, Ian. / Subcellular distribution and phosphorylation state of insulin receptors from insulin- and isoproterenol- treated rat adipose cells. In: Cellular Signalling. 1991 ; Vol. 3, No. 1. pp. 51-58.
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Subcellular distribution and phosphorylation state of insulin receptors from insulin- and isoproterenol- treated rat adipose cells. / Weber, Teresa M.; Joost, Hans G.; Kuroda, Masao; Cushman, Samuel W.; Simpson, Ian.

In: Cellular Signalling, Vol. 3, No. 1, 01.01.1991, p. 51-58.

Research output: Contribution to journalArticle

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