Interactions among chronic cold, corticosterone and puberty on energy intake and deposition.
We have shown that chronic cold stress strongly interacts with corticosterone (B) to determine subsequent regulation of the hypothalamo-pituitary-adrenal (HPA) axis responses to novel stress. These studies, using the same 2 sets of rats, show that chronic cold also interacts with B and testosterone on signals of energy balance. The two groups of rats differed in weight by 20% and in age by 2 weeks (44-59 days of age). Adrenalectomized rats, replaced with varying doses of B, were exposed to cold or served as controls. Food intake and body weight during the experiments and hormones, metabolites and fat depots were measured on day 5. B, but not cold, affected food intake in the younger rats; by contrast, cold, but not B, affected food intake in the older rats. Testosterone was higher in older control rats and was markedly depressed by cold; younger rats had lower testosterone that was minimally affected by cold. Weight gain decreased in all rats at room temperature with increasing B, whereas they all lost weight in cold independently of B. Cold stimulated and B inhibited interscapular brown adipose tissue DNA content (reflecting sympathetic stimulation of thermogenesis). B stimulated insulin, whereas cold inhibited leptin and insulin; B also increased white adipose tissue weight gain in controls and inhibited its loss in cold. Leptin was unrelated to white adipose tissue depots in older control rats but was strongly related to these stores in younger rats and in all rats in cold. We conclude that: 1. By decreasing signals that act centrally to inhibit food intake (insulin, leptin and testosterone) cold allows B to stimulate food intake; 2. B inhibits weight gain although it causes accrual of fat; 3. Cold, probably through sympathetic stimulation of white adipose tissue, causes fat loss which is modulated by the inhibitory effect of B on sympathetic outflow; and, 4. The slope of the relationship between fat depot size and leptin becomes flatter in cold, possibly because of increased sympathetic outflow to these depots.
Akana
S F
SF
Department of Physiology, University of California San Francisco, San Francisco, CA 94143-0444, USA. akana@itsa.ucsf.edu
Strack
A M
AM
Hanson
E S
ES
Horsley
C J
CJ
Milligan
E D
ED
Bhatnagar
S
S
Dallman
M F
MF
D002001:Adipose Tissue, Brown / Q000187:drug effects / Q000378:metabolism*; D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D003080:Cold Temperature; D003345:Corticosterone / Q000097:blood* / Q000494:pharmacology; D004435:Eating; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005934:Glucagon / Q000032:analysis; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D010913:Pituitary-Adrenal System / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012741:Sexual Maturation / Q000502:physiology*; D013312:Stress, Physiological / Q000378:metabolism*; D013739:Testosterone / Q000097:blood; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D014280:Triglycerides; D013739:Testosterone; D005934:Glucagon; D003345:Corticosterone