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  • Review Article
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The endocrinology of food intake

Abstract

Many questions must be considered with regard to consuming food, including when to eat, what to eat and how much to eat. Although eating is often thought to be a homeostatic behaviour, little evidence exists to suggest that eating is an automatic response to an acute shortage of energy. Instead, food intake can be considered as an integrated response over a prolonged period of time that maintains the levels of energy stored in adipocytes. When we eat is generally determined by habit, convenience or opportunity rather than need, and meals are preceded by a neurally-controlled coordinated secretion of numerous hormones that prime the digestive system for the anticipated caloric load. How much we eat is determined by satiation hormones that are secreted in response to ingested nutrients, and these signals are in turn modified by adiposity hormones that indicate the fat content of the body. In addition, many nonhomeostatic factors, including stress, learning, palatability and social influences, interact with other controllers of food intake. If a choice of food is available, what we eat is based on pleasure and past experience. This article reviews the hormones that mediate and influence these processes.

Key Points

  • Endocrine influences over eating are complex and include factors related to the body's energy needs (homeostatic factors) and to experience, habits and opportunity (nonhomeostatic factors)

  • Meal-anticipatory endocrine responses that are initiated by food cues before eating start the digestive process and reduce the incidence of meal-associated hyperglycaemia and other metabolic challenges

  • Although satiation hormones such as cholecystokinin and glucagon-like peptide 1 (GLP-1) determine how much a person eats, they have not proven efficacious as clinical treatments for reducing body weight

  • Adiposity hormones, such as leptin and insulin, change the sensitivity of the brain to satiation signals, thereby helping maintain stable levels of body fat and body weight over time

  • Stress, reproductive regulatory hormones and cardiovascular regulatory hormones interact with adiposity signals in complex ways to influence food intake

  • Although chronically altered levels of GLP-1, ghrelin and other gastrointestinal hormones are thought to underlie metabolic improvements following bariatric surgery, supporting evidence is lacking

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Figure 1: Meal-fed rats that habitually receive food at time 0 begin making anticipatory responses >1 h before the anticipated meal.
Figure 2: Homeostatic controls determine meal size and are based on satiation signals such as cholecystokinin and glucagon-like peptide-1, adiposity signals such as leptin and insulin, and local nutrient levels reaching the ARC and other hypothalamic areas from the blood, including glucose and some fatty acids and amino acids.
Figure 3: Hormonal signals arising in the periphery influence areas of the brain involved in food intake in many ways.

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Begg, D., Woods, S. The endocrinology of food intake. Nat Rev Endocrinol 9, 584–597 (2013). https://doi.org/10.1038/nrendo.2013.136

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