How can molecular signals from

the gastro-intestinal tract enable

the body to communicate appetite
and satiety to the brain?

By Elizabeth Le and Mumina Akthar

 Model depicting signals that influence food intake.

Woods S C Am J Physiol Gastrointest Liver Physiol 2004;286:G7-G13

2004 by American Physiological Society

 Hindbrain
Satiety signals influence eating behaviour by
activating neurons in the nucleus of the
solitary tract in the hindbrain.

Image courtesy of: web.lemoyne.edu

 Satiety: Cholecystokinin (CCK)
The first gut-secreted peptide to be
identified as a satiety factor.
CCK reduces meal size.
It is a hormone which is produced in the
duodenum of the small intestine in
response to nutrients in the lumen.
Administration to rats led to reduction in
meal size Gibbs 1973.
Source: T.J Little, M. Horowitz, C Feinle-Bisset, Obesity reviews: Role of
cholecystokinin in appetite control and body weight regulation
2005
 Peptide YY3-36
Peptide yy3-36 is the major circulating
form of PYY.
It is a short-term regulator of appetite
appetite-suppressing hormone.
Inhibits Neuropeptide Y secretion from
the hypothalamus.
There are other hormones similar to PYY
and CCK secreted by the G.I tract that
act as satiety signals.
Source: Principles of Biochemistry VVP
 Appetite: Ghrelin
28 amino acid peptide synthesized mainly in the
stomach.
It is an appetite-stimulating peptide, it is orexigenic:
increases hunger.
Thought to be a short-term regulator of appetite as
levels increase before meals and decrease immediately
afterward (Cummings, 2004)
Increase in meal number not size. In animals increase
in food seeking behaviour.
Works by boosting levels of neuropeptide Y in
hypothalamus
Source: Principles of Biochemistry VVP and Rexford S. Ahima, Brain Regulation
of Appetite and Satiety 2008 Endocrinology and Metabolism Clinics of North
America
 Figure 1 The classical mechanism under ghrelin orexigenic effect.

Varela L et al. J Mol Endocrinol 2011;46:R43-R63

2011 Society for Endocrinology

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