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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00595.2001
Submitted on September 28, 2001
Accepted on December 12, 2001
1 Hannah Research Institute, Ayr, Ayrshire, United Kingdom
2 Appetite and Energy Balance Division, Rowett Research Institute, Aberdeen, Aberdeenshire, United Kingdom
3 Sciences Animales, ENSAIA-INPL, Vandoeuvre les Nancy, France
* To whom correspondence should be addressed. E-mail: vernonr{at}hri.sari.ac.uk.
Peripheral and hypothalamic mechanisms underlying the hyperphagia of lactation have been investigated in sheep. Sheep were fed ad libitum and killed at 6 and 18 days of lactation; ad libitum-fed non-lactating sheep were killed as controls. Despite increased food intake, lactating ewes were in negative energy balance. Lactation decreased plasma leptin and adipose tissue leptin mRNA concentrations. OB-Rb gene expression, determined by in situ hybridisation, was increased in the hypothalamic ARC and VMH at both stages of lactation. NPY was increased by lactation in both ARC and DMH, although increased gene expression in the DMH was only apparent at day 18 of lactation. Gene expression was decreased for CART in ARC and VMH, and POMC in ARC during lactation. AGRP gene expression was increased in ARC, and MC3-R expression was unchanged in both ARC and VMH with lactation. Thus the hypoleptinaemia of lactation may activate NPY orexigenic pathways and attenuate anorexigenic melanocortin and CART pathways in the hypothalamus to promote the hyperphagia of lactation.
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