Abstract
Orexins are synthesized by lateral hypothalamic neurons and are suggested to be implicated in feeding behavior. Recent studies have shown that intracerebroventricular administration of orexin-A increases intake of sweet-tasting solution. Effects of suppressing the orexin system on consumption of sweet-tasting solution and sensory processing with sweet taste inputs, however, have yet to be examined. We examined the effects of orexin deficiency on sucrose solution intake, locomotor activity, and preference for sweet solution using male orexin knockout (OxKO) and littermate wild-type (WT) mice. In the dark and over 24-h periods, OxKO mice showed significantly less sucrose intake and lower locomotor activity than WT mice without alteration in food intake whereas preferences for 100mM sucrose were not different between the genotypes. Moreover, sucrose intake of OxKO mice was significantly less than sucrose intake of a subgroup of WT mice with similar locomotor activity compared to that of OxKO mice. These results suggest that factors other than the lower energy expenditure due to lower locomotor activity are likely responsible for the decreased sucrose intake of OxKO mice. Orexin deficiency may lower the satiety threshold resulting in reduced sucrose intake, without altering food intake.
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