Food and Behaviour Research

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Pancreatic signals controlling food intake; insulin, glucagon and amylin

Woods SC, Lutz TA, Geary N, Langhans W (2006) Philos Trans R Soc Lond B Biol Sci.  2006 Jul 29; 361(1471):  1219–1235. Published online 2006 Jun 19. doi: 10.1098/rstb.2006.1858 

Web URL: Read this and related abstracts on PubMed here


The control of food intake and body weight by the brain relies upon the detection and integration of signals reflecting energy stores and fluxes, and their interaction with many different inputs related to food palatability and gastrointestinal handling as well as social, emotional, circadian, habitual and other situational factors.

This review focuses upon the role of hormones secreted by the endocrine pancreas: hormones, which individually and collectively influence food intake, with an emphasis upon insulin, glucagon and amylin. Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue.

Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight.

Amylin reduces meal size by stimulating neurons in the hindbrain, and there is evidence that amylin additionally functions as an adiposity signal controlling body weight as well as meal size.

Glucagon is secreted from A-cells and increases glucose secretion from the liver. Glucagon acts in the liver to reduce meal size, the signal being relayed to the brain via the vagus nerves. To summarize, hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis.

Glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amylin as well act over longer intervals to modulate the amount of fat maintained and defended by the brain. Hormones of the endocrine pancreas interact with receptors at many points along the gut–brain axis, from the liver to the sensory vagus nerve to the hindbrain to the hypothalamus; and their signals are conveyed both neurally and humorally.

Finally, their actions include gastrointestinal and metabolic as well as behavioural effects.


Insulin, produced by beta cells of the pancreas, is well known for its effects on blood sugar regulation - and failures to produce or respond to insulin sufficiently result in diabetes (of Type 1 or Type 2 respectively). 

As this review highlights, insulin also operates in co-ordination with other hormones to influence not only energy metabolism but also appetite, satiety and behaviour - and disruptions of these hormonal signalling systems are therefore an active area of study in relation to obesity (which is strongly associated with, and a risk factor for, Type 2 diabetes).

See also this review, which presents a compelling case that high insulin (which will result from a persistently high-sugar diet) not only drives fat storage and leads to insulin resistance, but also disrupts normal responses to other hormones such as leptin and ghrelin: