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1 Department of Animal Physiology, University of Groningen, 9750 AA Haren, The Netherlands; 2 Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267; Departments of 3 Psychology, 5 Psychiatry and Behavioral Sciences, and 7 Medicine, University of Washington and Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108; 4 Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104; and 6 Department of Metabolic Diseases, Hoffmann-La Roche, Nutley, New Jersey 07110
To investigate whether brain leptin
involves neuropeptidergic pathways influencing ingestion, metabolism,
and gastrointestinal functioning, leptin (3.5 µg) was infused daily
into the third cerebral ventricular of rats for 3 days. To distinguish
between direct leptin effects and those secondary to leptin-induced
anorexia, we studied vehicle-infused rats with food available ad
libitum and those that were pair-fed to leptin-treated animals.
Although body weight was comparably reduced (
8%) and plasma
glycerol was comparably increased (142 and 17%, respectively) in
leptin-treated and pair-fed animals relative to controls, increases in
plasma fatty acids and ketones were only detected (132 and 234%,
respectively) in pair-fed rats. Resting energy expenditure
(15%) and gastrointestinal fill (50%) were reduced by
pair-feeding relative to the ad libitum group, but they were not
reduced by leptin treatment. Relative to controls, leptin increased
hypothalamic mRNA for corticotropin-releasing hormone (CRH; 61%) and
for proopiomelanocortin (POMC; 31%) but did not reduce mRNA for
neuropeptide Y. These results suggest that CNS leptin prevents
metabolic/gastrointestinal responses to caloric restriction by
activating hypothalamic CRH- and POMC-containing pathways and raise the
possibility that these peripheral responses to CNS leptin
administration contribute to leptin's anorexigenic action.
OB protein; sympathetic nervous system; corticotropin-releasing hormone; proopiomelanocortin; food intake
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