Affiliation:
1. Department of Biochemistry, University of Ottawa, Ontario, Canada.
Abstract
Mice treated with monosodium glutamate (MSG) in the neonatal period grow into obese, stunted adults without overeating. We have previously demonstrated normal control of brown adipose tissue (BAT) thermogenic function in the MSG-treated mouse and have concluded that thermoregulation at a lower than normal body temperature for most of the time is a major cause of its obesity. The objective of the present experiments was to find out whether adrenalectomy would prevent obesity in the MSG-treated mouse, as it does in hyperphagic obese rodents, and whether the thermoregulatory anomaly would be prevented by this procedure. MSG-treated mice that were adrenalectomized at 5 wk of age and studied at 10 wk of age did not become obese. Adrenalectomy increased body temperature of MSG-treated mice to normal (male mice) or almost normal (female mice). Adrenalectomy increased BAT mitochondrial guanosine 5'-diphosphate binding in MSG-treated mice, indicative of an increased thermogenic state, but had the same effect in control mice. We conclude that obesity in the MSG-treated mouse is secondary to the high level of corticosterone in its blood, which raises its metabolic efficiency, an effect of corticosterone also seen in normal lean mice, and causes it to thermoregulate at a low energy-conserving level. This latter effect is peculiar to the MSG-treated mouse and is not seen in corticosterone-treated normal mice.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism
Cited by
35 articles.
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