Hypothalamic Regulation of Appetite

Katherine A. Simpson; Niamh M. Martin; Steve R. Bloom

Disclosures

Expert Rev Endocrinol Metab. 2008;3(5):577-592. 

In This Article

Interactions Between the Brainstem & Hypothalamus

Although the hypothalamus could be regarded as the 'gate keeper' of appetite signaling, it is important to remember that, in addition to input from higher brain centers, the hypothalamus also receives signals from the periphery (Figures 1 & 2). The deficient blood-brain barrier of the ARC enables circulating factors regulating appetite to communicate directly with the hypothalamus. The brainstem is another key CNS appetite-regulation center [163] and peripheral satiety signals can also act directly on brainstem structures such as the area postrema, which also possesses an incomplete blood-brain barrier. Extensive reciprocal neuronal projections exist between brainstem and hypothalamic feeding circuits to provide an alternative pathway through which circulating satiety factors can communicate with the hypothalamus.[164,165] The vagus nerve is the major neuroanatomical link between the GI tract and the brain. Cell bodies of afferent fibers of the abdominal vagus nerve are located in the nodose ganglia, which project onto the brainstem. Here, the dorsal vagal complex (DVC), consisting of the dorsal motor nucleus, the area postrema and the sensory nucleus of the tractus solitarius (NTS), interfaces with hypothalamic and higher centers.[163] A population of POMC neurons exist in the NTS and it has been shown that over 50% demonstrate activation of STAT-3 in response to peripheral leptin administration.[166] Hence, the vagus nerve provides an additional pathway via which appetite-regulatory signals from the periphery can communicate with the hypothalamus to regulate energy homeostasis.

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