From neuroanatomy to behavior: central integration of peripheral signals regulating feeding behavior

Abstract

Over the past two centuries, prevalent models of energy and glucose homeostasis have emerged from careful anatomical descriptions in tandem with an understanding of cellular physiology. More recent technological advances have culminated in the identification of peripheral and central factors that influence neural circuits regulating metabolism. This Review highlights contributions to our understanding of peripheral and central factors regulating food intake and energy expenditure.

Figure 1. Central regulation of food intake and energy expenditure

(a) Multiple peripheral factors have been shown to modify food intake and energy expenditure through direct effects on the CNS. (b) Evidence suggests that melanocortin signaling regulates these physiological processes by means of distinct projection patterns originating from POMC neurons in the arcuate nucleus (Arc). Ultimately, MC4 receptor (MC4R)-expressing neurons downstream of POMC neurons act to suppress food intake and increase energy expenditure. Hypothalamic NPY/AgRP, paraventricular nucleus of the hypothalamus (PVH) and VMH neurons, as well as hindbrain DVC, parabrachial nucleus (PBN) and spinal cord intermediolateral cell column (IML) neurons, also regulate or counter-regulate these activities. PP, pancreatic polypeptide; PYY, peptide YY; 3V, third ventricle.