Laboratory Animal Models for Investigating the Mechanisms and Function of Parasite-Induced Anorexia

Abstract

Reduced voluntary food intake, or anorexia, is commonly observed in mammalian hosts infected with parasitic worms. Despite the frequent occurrence of anorexia, the functional significance of reduced food intake is still uncertain. It seems likely that, acutely, anorexia benefits the host, whereas more chronic malnutrition is detrimental. The mechanisms underlying this voluntary excursion into negative energy balance have not been extensively studied. We have investigated the endocrine and neuroendocrine consequences of infection of the laboratory rat with the hookworm-like nematode, Nippostrongylus brasiliensis. This parasite induces a biphasic anorexia in its host. Although elevated levels of the adipocyte hormone, leptin, may be causally implicated in infection-induced anorexia, most of the perturbations in the concentrations of leptin, insulin and corticosterone in the bloodstream, and in expression of the anabolic neuropeptide, neuropeptide Y, in the hypothalamus, appear to be secondary to the state of negative energy balance, and to reflect that state. Other factors, such as cytokines, released during the infection may block the normal response to elevated feeding drive encoded by peripheral feedback and CNS integratory systems. Further investigation of the ways in which parasites manipulate their hosts, and of host responses, will allow intervention strategies to be more appropriately evaluated.