Hypothalamic-brainstem circuits controlling eating.

Abstract

It is now axiomatic that neurons in the hypothalamic arcuate nucleus have a primary role in responding to changes in circulating levels of leptin and transmitting signals to downstream circuits that influence eating and energy expenditure. Signals generated from the gastrointestinal tract during meals reach the brainstem, via the vagus nerve and other routes, and impinge on neural circuits that influence the timing and size of meals and amount of food consumed. One of the mechanisms by which leptin exerts its anorexic effects is by increasing the effectiveness of intestinal signals that cause satiation during a meal. It is clear that the effects of gut satiation signals such as CCK can be amplified by leptin acting in the CNS, and in the arcuate nucleus in particular. The present article describes the state of our knowledge about specific neural circuits between the hypothalamus and brainstem that play a role in the interaction of leptin and meal-control signals to control food intake.