Regulation of appetite

A substance that increases food intake.

Fat

A substance that inhibits food intake.

CCK; PYY; leptin; GLP-1; oxyntomodulin.

Live microorganisms that, when administered in adequate amounts, confer a health benefit on the host.

Substrates, usually selectively utilised by gut microorganisms, that confer a health benefit on the host.

It allows bidirectional communication between the gastrointestinal tract and the brain through neural pathways, hormones and metabolic signals, helping regulate hunger, satiety and food intake.

The arcuate nucleus.

It carries afferent sensory signals from the gut to the brain and efferent signals from the brain to the gut, helping regulate appetite and gastrointestinal function.

Chemical signals from the gut, including hormones released by enteroendocrine cells, nutrients, pH and osmolality.

Gastric distension caused by food entering the stomach; the degree of distension is influenced by meal size.

To other hypothalamic regions and brainstem centres, including the nucleus tractus solitarius (NTS).

GLP-1 may be released during the cephalic phase of digestion

They detect nutrients and other chemical signals and trigger intracellular signalling pathways that influence hormone release and appetite.

Specialised hormone-secreting cells found throughout the gastrointestinal tract. They detect nutrients and other signals in the gut and release hormones from their secretory granules.

Typically flask-shaped or pyramidal, with an apical surface facing the gut lumen and a basal surface that releases hormones.

A saturated medium-chain fatty acid containing 12 carbon atoms.

Anorexigenic hormones, including gut hormones involved in satiety.

An orexigenic hormone, often called the hunger hormone, that stimulates appetite.

Orexigenic.

Food intake, particularly after a meal.

Mainly by P/D1 cells in the fundus of the stomach.

Hyperphagia, meaning increased food intake.

Anorexigenic.

Ghrelin levels are often lower in people with obesity than in lean individuals, and appetite regulation involves multiple overlapping pathways. Targeting ghrelin alone may therefore have limited effects.

Promotes satiety, slows gastric emptying and stimulates gallbladder contraction and pancreatic enzyme secretion.

It is released by I cells, mainly in the duodenum and jejunum, in response to nutrients, particularly fats and proteins.

L cells, mainly in the ileum and colon.

Nutrient stimulation, particularly following a meal containing fat or protein.

Enhances satiety and reduces appetite; it can also slow gastrointestinal motility.

Semaglutide; liraglutide.

They mimic GLP-1, increasing glucose-dependent insulin secretion, reducing glucagon secretion, slowing gastric emptying and decreasing appetite and food intake.

An anorexigenic gut hormone released after meals that reduces appetite and may suppress ghrelin secretion.

It is stored in secretory granules and released by intestinal L cells, particularly in the ileum and colon.

An incretin hormone released after nutrient intake that stimulates glucose-dependent insulin secretion. It also has effects on fat metabolism and energy balance.

It is stored in secretory granules and released by K cells, mainly in the duodenum and proximal jejunum.

A hormone produced mainly by adipocytes. It signals energy stores to the hypothalamus, suppressing appetite and increasing energy expenditure.

The arcuate nucleus.

NPY/AgRP neurons, which stimulate appetite; POMC/CART neurons, which suppress appetite.

Activated by ghrelin and inhibited by leptin, insulin and PYY. They release neuropeptide Y (NPY), which stimulates appetite through Y1 and Y5 receptors. AgRP antagonises melanocortin receptors, particularly MC4R, reducing satiety signalling and increasing food intake.

Activated by signals including leptin and insulin. They reduce food intake by releasing melanocortins, such as alpha-MSH, which activate melanocortin receptors, particularly MC4R.

It can enhance enteroendocrine hormone secretion, including anorexigenic hormones such as GLP-1 and PYY, promoting satiety and reducing food intake.