Fever and the acute elevation in whole-body thermogenesis induced by lateral hypothalamic lesions

Terry A. Lennie; Matt D. Hirvonen; Donna O. McCarthy; Richard E. Keesey

doi:10.1016/0031-9384(95)00045-K

Fever and the acute elevation in whole-body thermogenesis induced by lateral hypothalamic lesions

Terry A. Lennie
, Matt D. Hirvonen
, Donna O. McCarthy
, Richard E. Keesey

College of Nursing

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Three studies investigated the role of fever in the acute elevation of heat production induced by lateral hypothalamic (LH) lesions and the mechanisms by which this thermogenic response can be attenuated by reductions in body weight. In Study 1, reducing the weights of rats prior to lesioning the LH attenuated both the usual postlesion fever and elevation in thermogenesis. In Study 2, blocking prostaglandin synthesis with indomethacin likewise blunted both the lesion-induced fever and thermogenesis. In Study 3, treating already weight-reduced rats with indomethacin attenuated, but still failed to eliminate, the lesion-induced fever. Together, these results suggest that both the fever and increased thermogenesis induced by LH lesions are mediated, at least in part, by prostaglandin mechanisms which themselves are influenced by body energy status.

Original language	English
Pages (from-to)	237-243
Number of pages	7
Journal	Physiology and Behavior
Volume	58
Issue number	2
DOIs	https://doi.org/10.1016/0031-9384(95)00045-K
State	Published - Aug 1995

Bibliographical note

Funding Information:
ACKNOWLEDGEMENT Support for this research was provided by NRSA Predoctoral Fellowship 5 F31 NR06420 from the NCNR, and NIH grant DK 19944.

Funding

ACKNOWLEDGEMENT Support for this research was provided by NRSA Predoctoral Fellowship 5 F31 NR06420 from the NCNR, and NIH grant DK 19944.

Funders	Funder number
National Institutes of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases	R01DK019944
NIST Center for Neutron Research
Israel National Road Safety Authority	5 F31 NR06420

Keywords

Body weight
Core temperature
Fever
Heat production
Lateral hypothalamic lesions
Oxygen consumption Indomethacin
Rat

ASJC Scopus subject areas

Experimental and Cognitive Psychology
Behavioral Neuroscience

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10.1016/0031-9384(95)00045-K

Cite this

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title = "Fever and the acute elevation in whole-body thermogenesis induced by lateral hypothalamic lesions",

abstract = "Three studies investigated the role of fever in the acute elevation of heat production induced by lateral hypothalamic (LH) lesions and the mechanisms by which this thermogenic response can be attenuated by reductions in body weight. In Study 1, reducing the weights of rats prior to lesioning the LH attenuated both the usual postlesion fever and elevation in thermogenesis. In Study 2, blocking prostaglandin synthesis with indomethacin likewise blunted both the lesion-induced fever and thermogenesis. In Study 3, treating already weight-reduced rats with indomethacin attenuated, but still failed to eliminate, the lesion-induced fever. Together, these results suggest that both the fever and increased thermogenesis induced by LH lesions are mediated, at least in part, by prostaglandin mechanisms which themselves are influenced by body energy status.",

keywords = "Body weight, Core temperature, Fever, Heat production, Lateral hypothalamic lesions, Oxygen consumption Indomethacin, Rat",

author = "Lennie, \{Terry A.\} and Hirvonen, \{Matt D.\} and McCarthy, \{Donna O.\} and Keesey, \{Richard E.\}",

note = "Funding Information: ACKNOWLEDGEMENT Support for this research was provided by NRSA Predoctoral Fellowship 5 F31 NR06420 from the NCNR, and NIH grant DK 19944.",

year = "1995",

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doi = "10.1016/0031-9384(95)00045-K",

language = "English",

volume = "58",

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AU - Lennie, Terry A.

AU - Hirvonen, Matt D.

AU - McCarthy, Donna O.

AU - Keesey, Richard E.

N1 - Funding Information: ACKNOWLEDGEMENT Support for this research was provided by NRSA Predoctoral Fellowship 5 F31 NR06420 from the NCNR, and NIH grant DK 19944.

PY - 1995/8

Y1 - 1995/8

N2 - Three studies investigated the role of fever in the acute elevation of heat production induced by lateral hypothalamic (LH) lesions and the mechanisms by which this thermogenic response can be attenuated by reductions in body weight. In Study 1, reducing the weights of rats prior to lesioning the LH attenuated both the usual postlesion fever and elevation in thermogenesis. In Study 2, blocking prostaglandin synthesis with indomethacin likewise blunted both the lesion-induced fever and thermogenesis. In Study 3, treating already weight-reduced rats with indomethacin attenuated, but still failed to eliminate, the lesion-induced fever. Together, these results suggest that both the fever and increased thermogenesis induced by LH lesions are mediated, at least in part, by prostaglandin mechanisms which themselves are influenced by body energy status.

AB - Three studies investigated the role of fever in the acute elevation of heat production induced by lateral hypothalamic (LH) lesions and the mechanisms by which this thermogenic response can be attenuated by reductions in body weight. In Study 1, reducing the weights of rats prior to lesioning the LH attenuated both the usual postlesion fever and elevation in thermogenesis. In Study 2, blocking prostaglandin synthesis with indomethacin likewise blunted both the lesion-induced fever and thermogenesis. In Study 3, treating already weight-reduced rats with indomethacin attenuated, but still failed to eliminate, the lesion-induced fever. Together, these results suggest that both the fever and increased thermogenesis induced by LH lesions are mediated, at least in part, by prostaglandin mechanisms which themselves are influenced by body energy status.

KW - Body weight

KW - Core temperature

KW - Fever

KW - Heat production

KW - Lateral hypothalamic lesions

KW - Oxygen consumption Indomethacin

KW - Rat

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ER -

Fever and the acute elevation in whole-body thermogenesis induced by lateral hypothalamic lesions

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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