As hypothalamic neurons that express agouti-related protein (AgRP) and neuropeptide Y (NPY) increases during lactation and may promote the hyperphagia that ensues, researcher explored the role of AgRP neurons in reproduction and lactation, using a mouse model in which AgRP-expressing neurons were selectively ablated by the action of diphtheria toxin, according to an article in the February 2008 issue of the Endocrine Society, one of the Endocrinology Journals.

According to the article, the mechanisms that support enhanced maternal feeding during lactation are not well established, but most investigators assume that hypothalamic melanocortin system is involved and that it may be supplemented by additional adaptations.

Colin T. Phillips and Richard D. Palmiter from Howard Hughes Medical Institute and Department of Biochemistry, University of Washington studied that in rodents the combined weights of the pups at weaning can exceed that of the dam by 3-fold. Then, the dam adjusts to this energy demand by increased feeding.

Nevertheless, she remains in negative energy balance throughout lactation. The loss of AgRP neurons shortly after birth does not compromise the ability of females to become pregnant, give birth to a normal number of pups, increase food intake during lactation, or to nourish the pups throughout lactation, according to the article.

Therefore, these experiments suggest that feeding under conditions of extraordinary energy demand, not just basal feeding, depends on AgRP neurons. Consequently, we suggest that neurons are not recruited during lactation that can compensate for the loss of AgRP neurons.

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