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Growth hormone regulates the distribution of L-type calcium channels in rat adipocyte membranes

1  Department of Physiology, University of Massachusetts Medical School, Worcester 01655; and 2  Department of Biology, College of the Holy Cross, Worcester, Massachusetts 01610 Earlier studies demonstrated that deprivation of growth hormone (GH) for 3 h decreased basal and maximally stimulated cyto...

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Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology 1998-08, Vol.275 (2), p.C505-C514
Main Authors: Gaur, Shikha, Morton, Mary E, Frick, G. Peter, Goodman, H. Maurice
Format: Article
Language:English
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Summary:1  Department of Physiology, University of Massachusetts Medical School, Worcester 01655; and 2  Department of Biology, College of the Holy Cross, Worcester, Massachusetts 01610 Earlier studies demonstrated that deprivation of growth hormone (GH) for 3 h decreased basal and maximally stimulated cytosolic Ca 2+ in rat adipocytes and suggested that membrane Ca 2+ channels might be decreased. Measurement of L-type Ca 2+ channels in purified plasma membranes by immunoassay or dihydropyridine binding indicated a two- to fourfold decrease after 3 h of incubation without GH. No such decrease was seen in unfractionated adipocyte membrane preparations. The decrease in plasma membrane channel content was largely accounted for by redistribution of channels to a light microsomal membrane fraction. Immunoassay of 1 -, 2 / -, and -channel subunits in membrane fractions indicated that the channels redistributed as intact complexes. Addition of GH during the 1st h of incubation prevented channel redistribution, and addition of GH after 3 h restored channel distribution to the GH-replete state of freshly isolated adipocytes. The studies suggest that GH may regulate the abundance of Ca 2+ channels in the adipocyte plasma membrane and thereby modulate sensitivity to signals, the expression of which is Ca 2+ dependent. immunoassay; tritiated PN-200-110; cell fractionation; intracellular calcium concentration
ISSN:0363-6143
1522-1563
DOI:10.1152/ajpcell.1998.275.2.C505