Figure 4. Central and peripheral sites at which the long-acting adiposity hormone leptin potentiates the actions of short-acting GI satiation factors.

Leptin-receptor signaling within the hypothalamus indirectly augments hindbrain neuronal responses to gut satiation signals, such as CCK, through hypothalamus-hindbrain projections involving oxytocin and other neuropeptides (10, 11). Central responses to CCK are also augmented by leptin acting directly on the hindbrain. In the periphery, leptin potentiates GI satiation signals both by enhancing gut-peptide secretion (for example, GLP1 release from distal-intestinal L cells) and by heightening vagal-afferent responsiveness to gut peptides (for example, to CCK from proximal-intestinal I cells). LepR, leptin receptor.