Appetite is not only derived from the daily flux of physiology associated with meals and eating behavior but also must respond to the long-term (tonic) energy status of the organism. Factors derived from the processes of energy storage and the status of the body's energy stores must also contribute to appetite and its expression (e.g., indicators of glucose metabolism and fat storage). Blood carries various substances (other than nutrients) generated in organs implicated in nutrient metabolism and energy storage such as the liver, the pancreas and in adipose tissue depots that reflect the body's energy status and that have been shown to have potent effects on food intake (insulin, glucagons, and leptin). The number of potentially active metabolites and by-products produced by energy metabolism of differing nutrients is vast providing a wide range of potential indicator substances.
As noted earlier one of the classical theories of appetite control has involved the notion of a so-called long-term regulation involving a signal that informs the brain about the state of adipose tissue stores. This idea has given rise to the notion of a lipostatic or ponderostatic mechanism. indeed, this is a specific example of a more general class of peripheral appetite (satiety) signals believed to circulate in the blood reflecting the state of depletion or repletion of energy reserves that directly modulate brain mechanisms. Levels of substances such as satietin and adipsin, or cytokine signals such as inter-leukin-6 (IL-6) tumor-necrosing factors (e.g., TNFa) may all be influenced by adipose tissue. Levels of other circulating hormones, for example, gonadal steroids (androgens, estrogens, and progesterone) also reflect the body fat mass, and so its energy status. Gonadal steroids have potent effects on (both increasing and reducing) food intake, meal size and frequency, body weight, and per cent body fat.
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