Growth hormone regulates cytosolic free calcium ([ca2+]i) in rat
fat cells by maintaining l-type ca2+ channels.
Gaur, Shikha, Hiroshi Yamaguchi, and H. Maurice Goodman.
Department of Physiology, University of Massachusetts Medical
School, Worcester, Massachusetts, 01655, Phone 508 856 2101; Fax 508
856 5997
APStracts 2:0450C, 1995.
In freshly isolated individual rat adipocytes [Ca2+]i as measured with
fura-2 slowly declined during incubation, but was sustained, or even
somewhat increased, by brief treatment with GH at the beginning of a
3 h incubation period. GH-treated adipocytes were more permeable to
Ca2+ than GH-deprived cells as indicated using Mn2+ as a surrogate
and monitoring influx by the rate of quenching of fura-2
fluorescence. Blockade of Ca2+ channels with 100 nM nimodipine
lowered [Ca2+]i in GH-treated cells to the level seen in GH-deprived
cells. Increases in [Ca2+]i or the rate of Mn2+ entry were twofold
greater in GH-treated than in GH-deprived cells when extracellular
potassium was increased to 30 mM. Similarly, the Ca2+ channel agonist
BAY K5552, or the diacylglycerol analog sn-1,2-dioctanoylglycerol
increased [Ca2+]i more in GH-treated than in GH-deprived adipocytes.
Ca2+ATPase activity was 2X higher in plasma membranes isolated from
GH-treated than from GH-deprived cells. Continued synthesis of
Ca2+ATPase may depend on [Ca2+]i since the effects of GH on [Ca2+]i
and Ca2+ATPase were blocked by cycloheximide or verapamil. We suggest
that voltage sensitive L-type Ca2+ channels regulate steady-state
[Ca2+]i in rat adipocytes and that GH maintains the number or
functional integrity of these channels.
Received 15 June 1995; accepted in final form 30 November 1995.
APS Manuscript Number C350-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95