Affiliation:
1. Departments of 1Pharmaceutical Sciences and
2. Research Service, Stratton Veterans Affairs Medical Center, Albany, New York
3. Arts and Sciences, Albany College of Pharmacy and Health Sciences, Albany;
Abstract
We tested the hypothesis that food deprivation alters body temperature (Tb) responses to bacterial LPS by enhancing inflammatory signaling that decreases Tb (cryogenic signaling) rather than by suppressing inflammatory signaling that increases Tb (febrigenic signaling). Free-feeding or food-deprived (24 h) rats received LPS at doses (500 and 2,500 μg/kg iv) that are high enough to activate both febrigenic and cryogenic signaling. At these doses, LPS caused fever in rats at an ambient temperature of 30°C, but produced hypothermia at an ambient temperature of 22°C. Whereas food deprivation had little effect on LPS fever, it enhanced LPS hypothermia, an effect that was particularly pronounced in rats injected with the higher LPS dose. Enhancement of hypothermia was not due to thermogenic incapacity, since food-deprived rats were fully capable of raising Tb in response to the thermogenic drug CL316,243 (1 mg/kg iv). Neither was enhancement of hypothermia associated with altered plasma levels of cytokines (TNF-α, IL-1β, and IL-6) or with reduced levels of an anti-inflammatory hormone (corticosterone). The levels of PGD2 and PGE2 during LPS hypothermia were augmented by food deprivation, although the ratio between them remained unchanged. Food deprivation, however, selectively enhanced the responsiveness of rats to the cryogenic action of PGD2 (100 ng icv) without altering the responsiveness to febrigenic PGE2 (100 ng icv). These findings support our hypothesis and indicate that cryogenic signaling via PGD2 underlies enhancement of LPS hypothermia by food deprivation.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
33 articles.
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