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The hormonal control of food intake.

Coll AP, Farooqi IS, O'Rahilly S - Cell (2007)

Bottom Line: Numerous circulating peptides and steroids produced in the body influence appetite through their actions on the hypothalamus, the brain stem, and the autonomic nervous system.These hormones come from three major sites-fat cells, the gastrointestinal tract, and the pancreas.In this Review we provide a synthesis of recent evidence concerning the actions of these hormones on food intake.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge CB2 2XY, United Kingdom.

ABSTRACT
Numerous circulating peptides and steroids produced in the body influence appetite through their actions on the hypothalamus, the brain stem, and the autonomic nervous system. These hormones come from three major sites-fat cells, the gastrointestinal tract, and the pancreas. In this Review we provide a synthesis of recent evidence concerning the actions of these hormones on food intake.

Show MeSH
Hormones from the Gut and Endocrine Organs Affect Food IntakeHormonal signals derived from the gut and classical endocrine organs, such as the pancreas, thyroid, and adrenal glands act in synergy to effect changes in feeding behavior.CCK, cholecystokinin; OXM, oxyntomodulin; GLP-1, glucagon-like peptide 1; PYY3–36, peptide YY3–36.
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fig2: Hormones from the Gut and Endocrine Organs Affect Food IntakeHormonal signals derived from the gut and classical endocrine organs, such as the pancreas, thyroid, and adrenal glands act in synergy to effect changes in feeding behavior.CCK, cholecystokinin; OXM, oxyntomodulin; GLP-1, glucagon-like peptide 1; PYY3–36, peptide YY3–36.

Mentions: Cholecystokinin (CCK) is a gut peptide that has long been established to act as a postprandial satiety signal (Chaudhri et al., 2006). It is released into the circulation from enteroendocrine cells of the duodenum and jejunum in response to fatty acids (Figure 2). CCK acts at receptors on peripheral vagal afferent terminals, which transmit signal to appetite centers, such as the nucleus of the solitary tract, contained within the brainstem. Peripheral administration of CCK also activates mouse POMC neurons in the nucleus of the solitary tracts with signaling via MC4Rs in this region appearing to be crucial in bringing about the satiety effects of CCK. This peptide is ineffective in reducing food intake in mice lacking MC4R and in mice in which brainstem melanocortin receptors are blocked pharmacologically (Fan et al., 2004). Thus in addition to integrating long-term adipostatic signals like leptin, the melanocortin system may also be important in integrating short-term gut-derived satiety signals.


The hormonal control of food intake.

Coll AP, Farooqi IS, O'Rahilly S - Cell (2007)

Hormones from the Gut and Endocrine Organs Affect Food IntakeHormonal signals derived from the gut and classical endocrine organs, such as the pancreas, thyroid, and adrenal glands act in synergy to effect changes in feeding behavior.CCK, cholecystokinin; OXM, oxyntomodulin; GLP-1, glucagon-like peptide 1; PYY3–36, peptide YY3–36.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2202913&req=5

fig2: Hormones from the Gut and Endocrine Organs Affect Food IntakeHormonal signals derived from the gut and classical endocrine organs, such as the pancreas, thyroid, and adrenal glands act in synergy to effect changes in feeding behavior.CCK, cholecystokinin; OXM, oxyntomodulin; GLP-1, glucagon-like peptide 1; PYY3–36, peptide YY3–36.
Mentions: Cholecystokinin (CCK) is a gut peptide that has long been established to act as a postprandial satiety signal (Chaudhri et al., 2006). It is released into the circulation from enteroendocrine cells of the duodenum and jejunum in response to fatty acids (Figure 2). CCK acts at receptors on peripheral vagal afferent terminals, which transmit signal to appetite centers, such as the nucleus of the solitary tract, contained within the brainstem. Peripheral administration of CCK also activates mouse POMC neurons in the nucleus of the solitary tracts with signaling via MC4Rs in this region appearing to be crucial in bringing about the satiety effects of CCK. This peptide is ineffective in reducing food intake in mice lacking MC4R and in mice in which brainstem melanocortin receptors are blocked pharmacologically (Fan et al., 2004). Thus in addition to integrating long-term adipostatic signals like leptin, the melanocortin system may also be important in integrating short-term gut-derived satiety signals.

Bottom Line: Numerous circulating peptides and steroids produced in the body influence appetite through their actions on the hypothalamus, the brain stem, and the autonomic nervous system.These hormones come from three major sites-fat cells, the gastrointestinal tract, and the pancreas.In this Review we provide a synthesis of recent evidence concerning the actions of these hormones on food intake.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge CB2 2XY, United Kingdom.

ABSTRACT
Numerous circulating peptides and steroids produced in the body influence appetite through their actions on the hypothalamus, the brain stem, and the autonomic nervous system. These hormones come from three major sites-fat cells, the gastrointestinal tract, and the pancreas. In this Review we provide a synthesis of recent evidence concerning the actions of these hormones on food intake.

Show MeSH