Tissue-specific regulation of lipoprotein lipase by isoproterenol
in normal weight humans.
Eckel, Robert H., Dalan R. Jensen, Isabel R. Schlaepfer, Trudy J.
Yost.
Division of Endocrinology, Metabolism and Diabetes, Department of
Medicine, University of Colorado Health Sciences Center, 4200 East
Ninth Avenue, Denver, CO 80262
APStracts 3:0184R, 1996.
Lipoprotein lipase (LPL) is a hydrolytic enzyme, involved in
lipoprotein metabolism and nutrient partitioning, that is subject to
tissue-specific regulation. Evidence for divergent regulation of the
lipase by insulin has been demonstrated, but alterations in the
tissue specific response of LPL to catecholamines has not been
studied in humans. The regulation of LPL in gluteal adipose tissue
and vastus lateralis muscle by isoproterenol (epinephrine isopropyl
homolog) in humans was examined over 2h in subjects infused with 0
(saline), 8 or 24 ng/kg/min of isoproterenol. The infusion of normal
saline into control subjects failed to alter adipose tissue or
skeletal muscle LPL activity. However, in the saline-infused subjects
there was a positive correlation between the percent change in plasma
norepinephrine concentrations and the percent change in muscle LPL
activity (r=0.826, p<0.05). Isoproterenol infusion did not
change LPL in either adipose tissue or muscle compared to saline
infused controls, but plasma insulin levels in addition to plasma
glucose, free fatty acids and glycerol were increased. To prevent the
isoproterenol-induced hyperinsulinemia, a pancreatic clamp technique
was utilized. An increase in muscle LPL was demonstrated (p=0.037)
with no change in adipose tissue LPL. The change in muscle LPL
activity after the 2h infusion correlated with the change in muscle
mRNA (p=0.021). Overall, these studies indicate that in humans, the
response of LPL to catecholamines is tissue-specific with no effect
in adipose tissue, but a stimulation in skeletal muscle. Endogenous
regulation of LPL in muscle by catecholamines could be important in
muscle fuel metabolism, and could relate to effects of cyclic AMP
and/or fatty acids at the level of the LPL gene.
Received 4 December 1995; accepted in final form 1 May 1996.
APS Manuscript Number R762-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96