Role of hypothalamic neuropeptide Y and orexigenic peptides in anorexia associated with experimental colitis in the rat.

Feb 15, 2001Clinical science (London, England : 1979)

How hunger-related brain chemicals in the hypothalamus relate to appetite loss during gut inflammation in rats

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Abstract

Food intake in rats with colitis decreased by 30-80% below control values for 5 days.

Increased release of neuropeptide Y (NPY) in the hypothalamus is associated with the normal response to starvation.
Rats with experimental colitis exhibit persistent anorexia, suggesting a failure in the adaptive feeding response.
NPY levels in the paraventricular nucleus were significantly higher in both colitic and pair-fed rats compared to healthy controls.
Administration of NPY, melanin-concentrating hormone (MCH), or hypocretin did not stimulate feeding in colitic rats, unlike healthy controls.
The findings suggest a potential suppression of feeding in colitic rats, possibly due to inhibition of a common neuronal pathway or the action of anorexigenic agents.

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Neuropeptide Y (NPY) is thought to play a crucial role in the normal hypothalamic response to starvation. After a period of food restriction, increased release of NPY induces hunger and hyperphagia, and helps to restore body weight to its set point. Persistent anorexia in rats with experimental colitis implies failure of this adaptive feeding response. In vivo NPY release and regional hypothalamic NPY concentrations were measured in rats with trinitrobenzenesulphonic acid (TNBS)-induced colitis, healthy controls and animals pair-fed to match the food intake of the colitic group. Food intake in the colitic group was assessed after administration of NPY and two other potent orexigenic peptides: melanin-concentrating hormone (MCH) and hypocretin (orexin-A). Food intake was decreased by 30-80% below control values for 5 days in the colitic rats. In both the pair-fed and colitic groups, release of NPY in the paraventricular nucleus was significantly increased compared with free-feeding controls. Intraventricular or intrahypothalamic administration of NPY, MCH or hypocretin elicited a feeding response in healthy controls, but not in the colitic group. In summary, animals with TNBS-colitis and anorexia show an appropriate increase in hypothalamic NPYergic activity. However, the failure of NPY and other orexigenic peptides to increase feeding in the colitic group indicates suppression of feeding, either by inhibition of a common downstream hypothalamic neuronal pathway or by induction of one or more potent anorexigenic agents.

Role of hypothalamic neuropeptide Y and orexigenic peptides in anorexia associated with experimental colitis in the rat.

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