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Acta Physiol Hung. 2014 Dec;101(4):395-407. doi: 10.1556/APhysiol.101.2014.4.1.

The role of gut hormones in appetite regulation (review).

Author information

1
University of Belgrade Institute of Epidemiology, Faculty of Medicine Belgrade Serbia.
2
University of Belgrade Institute of Histology and Embryology, Faculty of Medicine Višegradska 26 11000 Belgrade Serbia.
3
University of Belgrade Institute of Pathology, Faculty of Medicine Belgrade Serbia.
4
University of Nis Institute of Physiology, Faculty of Medicine Nis Serbia.

Abstract

Eating process is an aggregate of complex and different forms of behavior. Its regulation is based on energy homeostasis and appetite control which includes two components: the homeostatic and the hedonistic control. Important signals in appetite regulation are gut-derived hormones. They are produced by enteroendocrine cells in response to nutrient and energy intake, and achieve their effects by influencing brain structures involved in food intake regulation. The key brain structure involved in this process is the hypothalamus. Gut hormones reach the hypothalamus from the circulation or by the vagal nerve via the nucleus of the solitary tract. Among gut peptides, ghrelin is the only orexigenic hormone, leading to an increase in food intake and body weight. All others, such as cholecystokinin, glucagon like peptide-1, oxyntomodulin, peptide tyrosine tyrosine or pancreatic polypeptide, are anorexigenic, leading to decrease in food intake. Also, gut-derived endocannabinoids exert orexigenic effect on appetite. Keeping in mind the growing problem of obesity, the crucial issue when considering gut derived peptides is to understand their mechanisms of acting because of potential role in clinical therapy, and discovering long-lasting gut peptides or their analogues, with no or minimal side effects.

KEYWORDS:

appetite; cholecystokinin; endocannabinoids; ghrelin; glucagon like peptide-1; oxyntomodulin; pancreatic polypeptide; peptide tyrosine tyrosine

PMID:
25532952
DOI:
10.1556/APhysiol.101.2014.4.1
[Indexed for MEDLINE]

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