Abstract
A hormonal short-term satiety mechanism involving cholecystokinin (CCK) has recently been proposed. We attempted to manipulate endogenous CCK levels in rats by administering oral preloads at varying time intervals before a test meal. Support for the CCK hypothesis was equivocal. In addition, there was little support for other hypothesized satiety mechanisms, such as regulation of volume or calories, or glucose-related mechanisms. The results are discussed in terms of the necessity of considering the total “ecological” situation (diet composition, diet palatability, diet availability, and training) when studying food intake and body weight.
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