Insulin plays a significant role in the postprandial reduction in appetite (here). In its role as a satiety signal, insulin passess through the blood brain barrier and into the central nervous system, where it interacts with receptors in the hypothalamus to reduce the satiety signal. This ensures that under conditions of elevated blood glucose, further energy is not consumed. The pathway by which insulin regulates appetite is likely through downstream changes to melanocortin and neuropeptide Y, which inhibit and activate appetite, respectively. A correctly functioning insulin system may therefore be a requisite of correct appetite regulation. Insulin resistance describes the inability of insulin to correctly facilitate the transport of glucose from the blood to the cells due to a dysfunction in the intracellular signal pathway for insulin. If insulin develops in the hypothalamus, appetite regulation could be detrimentally affected, and this is one theory that explains weight gain.
A number of studies have investigated the association between plasma insulin and appetite regulation. For example, in one study1, researchers investigated the correlation between the area under the curve for insulin with the appetite responses in Pima Indians from North America. The subjects received an oral glucose tolerance test and from this their insulin responses were established. The ad libitum food intake of the subjects was then recorded over the course of three days. The results of the study showed that the area under the curve for insulin was inversely associated with food intake. This suggests that those subjects with the largest area under the curve for insulin had the lowest food intakes, perhaps leading to a more efficient appetite regulatory mechanisms. The higher insulin area under the curve also predicted lower weight gain in a follow up study 8.5 years later. These results support the contention that insulin is a primary appetite regulatory hormone and regulatory of weight change.
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