Send to:

Choose Destination
See comment in PubMed Commons below
Physiol Behav. 1993 May;53(5):995-1000.

Sympathoadrenal responses to glucoprivation and lipoprivation in rats.

Author information

  • 1Department of Animal Physiology, University of Groningen, Haren, The Netherlands.


The effects of glucoprivation and lipoprivation on sympathoadrenal outflow were investigated in rats with permanent intra-atrial catheters. Glucoprivation was induced by infusion of a hypoglycemic dose of insulin (3 U/kg) or by infusion of the glucose antimetabolite, 2-deoxy-D-glucose (2-DG, 200 mg/kg). Lipoprivation was induced by infusion of sodium mercaptoacetate (MA, 600 mumol/kg), which blocks beta oxidation of fatty acids. Stress-free blood samples for measurement of blood glucose, plasma nonesterified fatty acids (NEFA), and epinephrine (E) and norepinephrine (NE) concentrations were collected remotely before and after drug injection. Glucoprivation and lipoprivation differed significantly in their effects on the sympathoadrenal system. Both 2-DG- and insulin-induced glucoprivation appeared to increase adrenomedullary secretion selectively, leading to dramatically increased plasma E levels. Although plasma NE levels also rose during glucoprivation, other evidence suggests that this effect may be secondary to the rise in E. In contrast, MA-induced lipoprivation increased the outflow of NE from the sympathetic nerve endings without a significant effect on plasma E concentrations. Plasma E levels rose only late in the test, as blood glucose levels began to fall. Results indicate that glucoprivation and lipoprivation are distinct metabolic signals, each capable of selectively activating one branch of the sympathoadrenomedullary system and thereby facilitating the mobilization of metabolic fuels appropriate for the specific metabolic challenge.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk