AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 2 403-R407, Copyright © 1989 by American Physiological Society
Energy expenditure during stress ulcer formation in vulnerable rats
D. Greenberg and S. H. Ackerman
Department of Psychiatry, Cornell University Medical College, White Plains, New York.
Rat pups separated early from their mothers at day 15 become vulnerable to
hypothermia and gastric erosion formation when food deprived and physically
restrained on postnatal day 30 (S.H. Ackerman, M. A. Hofer, and H. Weiner,
Science Wash. DC. 201: 373-376, 1978, and Gastroenterology 75: 649-654,
1978). We tested the hypothesis that this hypothermia is associated with a
decrease in oxidative metabolism. We measured O2 consumption of 30-day-old
rat pups that had been previously separated at either day 15 (15w) or day
21 (21w). When food was available, 15w rats used as much O2 as 21w rats.
When rats were food deprived or food deprived and restrained, 15w rats used
significantly less O2 than 21w rats, implying less heat production. We
hypothesized that this decrease in heat production during food deprivation
and/or restraint was due to impaired thermogenesis resulting from
inadequate release of endogenous norepinephrine (NE), which is a stimulant
of brown adipose tissue- (BAT) mediated thermogenesis. To test this
hypothesis we administered exogenous NE to 15w to 21w rats. Exogenous NE
failed to increase O2 consumption in 21w or 15w rats when injected during
either food deprivation or restraint. We concluded that 30-day-old 15w rats
have decreased oxidative metabolism during food deprivation and restraint
and therefore become hypothermic. This decreased oxidative metabolism does
not appear to be attributable to insufficient endogenous NE, since it is
not reversed by the addition of exogenous NE. We suggest that a decrease in
oxidative metabolism may explain susceptibility to stress ulcers in a
number of previously reported experimental models.
