Metabolic, gastrointestinal, and CNS neuropeptide effects of brain leptin administration in the rat - PubMed (original) (raw)

. 1999 May;276(5):R1425-33.

doi: 10.1152/ajpregu.1999.276.5.R1425.

R J Seeley, T E Thiele, M I Friedman, H Ji, C W Wilkinson, P Burn, L A Campfield, R Tenenbaum, D G Baskin, S C Woods, M W Schwartz

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Metabolic, gastrointestinal, and CNS neuropeptide effects of brain leptin administration in the rat

G van Dijk et al. Am J Physiol. 1999 May.

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Abstract

To investigate whether brain leptin involves neuropeptidergic pathways influencing ingestion, metabolism, and gastrointestinal functioning, leptin (3.5 micrograms) 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.

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