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Parasite-induced anorexia: leptin, insulin and corticosterone responses to infection with the nematode, Nippostrongylus brasiliensis

Published online by Cambridge University Press:  01 January 1999

H. C. ROBERTS
Affiliation:
Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK Department of Zoology, University of Aberdeen, Tillydrone Avenue, Aberdeen AB24 2TZ, UK Present address: Wellcome Trust Centre for Epidemiology of Infectious Disease, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.
L. J. HARDIE
Affiliation:
Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK Present address: Molecular Epidemiology Unit, Algernon Firth Building, University of Leeds, Leeds LS2 9JT, UK.
L. H. CHAPPELL
Affiliation:
Department of Zoology, University of Aberdeen, Tillydrone Avenue, Aberdeen AB24 2TZ, UK
J. G. MERCER
Affiliation:
Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
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Abstract

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The nematode parasite, Nippostrongylus brasiliensis, induces a biphasic anorexia in its rat host. The mechanisms, underlying this anorexia and its possible advantages to the host or parasite are unknown. We have investigated the effect of acute (12–24 h) and chronic (2–17 days) infections on plasma concentrations of leptin, insulin and corticosterone, and on hypothalamic expression of neuropeptide Y, galanin and corticotrophin-releasing factor genes. Plasma leptin was elevated in infected rats relative to uninfected ad libitum-fed controls and pair-fed controls in 12 h infections initiated at dark onset and in infections of 2 days' duration. At other times prior to parasite expulsion, plasma leptin in infected and pair-fed rats was lower than that of uninfected ad libitum-fed controls, reflecting the existing state of negative energy balance. Elevated plasma leptin concentrations in infected rats at day 2 post-infection were accompanied by reduced neuropeptide Y gene expression in the hypothalamic arcuate nucleus compared with both ad libitum control and pair-fed animals, and by lowered corticotrophin-releasing factor gene expression in the paraventricular nucleus relative to pair-feds. Twelve hour infections were characterized by a substantial increase in plasma corticosterone that was independent of reduced food intake, and in 12 h infections initiated at dark onset, where plasma leptin was elevated, there was also increased plasma insulin concentration in infected rats. In longer infections, differences between the groups in plasma insulin and corticosterone concentration were only observed at day 4 post-infection. In summary, perturbations to leptin, insulin and corticosterone signals early in infection may have a causative role and might feed back onto hypothalamic gene expression, whereas subsequent changes in these parameters are more likely to be secondary to negative energy balance.

Type
Research Article
Copyright
1999 Cambridge University Press