Peripheral signals affecting food intake.

Abstract

Peripheral signals arise from the sequence involving location, selection, ingestion, digestion, and absorption of food. These signals can be anatomically localized to gastrointestinal signals, circulating factors, metabolic signals, nutrient stores, and the sensory capabilities of the nervous system. Since many of the physiologic signals thought to affect feeding are triggered by nutrient ingestion and feeding behavior is influenced by diet composition, it is useful to consider peripheral appetite signals in the context of energy and nutrient balance. Evidence suggests that nutrient metabolism is (directly or indirectly) related to postingestive satiety. Protein is the most satiating macronutrient and has the greatest detectable effect on qualitative intake. Carbohydrates (CHOs) exert potent effects on satiety. Inhibition of CHO metabolism stimulates intake, as do transient declines in plasma glucose. Inhibition of fat metabolism also stimulates intake, but fat is the least readily metabolized macronutrient, and therefore, joule for joule, is less satiating than CHO or protein. High-fat, energy-dense diets lead to excess energy intakes (EIs) and weight gain relative to lower-fat, less energy-dense diets, and fat intake is a risk factor for subsequent weight gain. Earlier models viewed peripheral control of feeding as due to one or more simple negative feedback loops. More recently research has focused on the multiple signalling systems involved in the maintenance of nutrient and energy balance (EB). While protein influences satiety at several levels, relatively little is known about "aminostatic" mechanisms. CHO status appears to be monitored in both the central nervous system (CNS) and periphery; signals relating to fat status largely appear to arise in the periphery. More progress has been made in identifying peripheral signals and some of their connections to the brain than in understanding their quantitative importance for normal feeding.