FIGURE 6. Neuroanatomical model of pathways by which adiposity signals, leptin (secreted by adipocytes) and insulin (secreted by the endocrine pancreas in proportion to adiposity), interact with central autonomic circuits regulating meal size.

From the following article:

Central nervous system control of food intake

Michael W. Schwartz, Stephen C. Woods, Daniel Porte, Jr, Randy J. Seeley and Denis G. Baskin

Nature 404, 661-671(6 April 2000)

doi:10.1038/35007534

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Leptin and insulin are proposed to stimulate a catabolic pathway (POMC/CART neurons) and inhibit an anabolic pathway (NPY/AGRP neurons) that originates in the arcuate nucleus (ARC). These pathways project to the PVN and LHA/PFA, where they make connections with central autonomic pathways that project to hindbrain autonomic centres that process satiety signals. Afferent input related to satiety from the liver, gastrointestinal tract and from peptides such as CCK are transmitted through the vagus nerve and sympathetic fibres to the nucleus of the solitary tract (NTS), where they are integrated with descending hypothalamic input. Net neuronal output from the NTS and other hindbrain regions leads to the termination of individual meals, and is potentiated by catabolic projections from the PVN and inhibited by input from the LHA/PFA. Reduced input from adiposity signals (for example, during diet-induced weight loss), therefore, increases meal size by reducing brainstem responses to satiety signals. Not shown are ascending projections from hindbrain to forebrain that may also contribute to adaptive changes in food intake.

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