Enterogastrone

A hormone secreted by the duodenal mucosa when fatty food is in the stomach
or small intestine; it is also thought to be released when sugars and proteins are
in the intestine. Enterogastrone is transported by the bloodstream to the
glands and muscles of the stomach, where it inhibits gastric movements and
secretions, possibly by blocking the production or activity of gastrin, the
hormone that initially causes these functions. Enterogastrone may slow down
stomach emptying by reducing the amount of acid produced. High acid content
causes the valve between the stomach and intestine to relax, allowing food
passage.
The chemical identity of enterogastrone is still uncertain. Substances from the
intestine that were thought to be enterogastrone have been shown to be
composed of not one but possibly as many as three independent hormones.
Two of these hormones are now known as secretin and cholecystokinin.
Consequently, many functions originally thought to be performed by
enterogastrone have been reassigned to these other hormones.
"enterogastrone." Encyclopdia Britannica. 2010. Encyclopdia Britannica Online. 29
Jul. 2010 <http://www.britannica.com/EBchecked/topic/188869/enterogastrone>.
How Digestion is Controlled
Since meals vary in timing, size and content, digestion must be controlled so that digestive
juices are not wasted, so that acids and enzymes do not do excessive damage to the system
itself, and so that enzymes have the appropriate time to carry out their work. Regulation
involves the brain, the senses, and a variety of hormones produced in the digestive system
itself.
Various small centres in the brain gauge the state of nutrition and satiation (how full one
feels). If the amount of glucose (blood sugar) drops, a brain centre makes us feel hungry.
When we eat and stretch the stomach wall a different brain centre makes us feel satisfied.
Researchers suspect that in many overweight people, there is a delay or a lack of
sensitivity in the centre that registers satiation. Since the two centres are in slightly
different places, many researchers believe that eating disorders (anorexia, bulimia) occur
when one centre fails to act appropriately. Anorexics may fail to register hunger, even
though they are not satisfied, while bulimics may continue to feel hungry if the satiation
centre does not act to cancel the hunger urge. Of course, these disorders usually have
psycho-social origins, but once they create conditioned patterns in the brain the victim is
rarely able to overcome the problem without outside help.

1. Assuming everything is working properly, the sight, smell, taste, or even thought of
food can start a response in the brain that acts directly on the stomach and makes you
ready to eat. This is much more likely if you are hungry (which is why experts always say
to do grocery shopping after a good meal.) A nervous signal from the brain will start the
stomach churning, which in turn releases acid and pepsin.
2. Peptides released by digestion stimulate cells in the wall of the stomach, which secrete a
hormone called gastrin into the blood. Gastrin stimulates the muscles of the stomach wall
and causes increased secretion - a positive feedback loop. Acids in the stomach inhibit
gastrin secretion (negative feedback). If there are lots of proteins in the stomach, they react
with acids and neutralize them, so gastrin keeps flowing until the protein is gone. If a meal
contains few proteins, the build up of acid in the stomach turns off gastrin secretion.
3. The presence of acid (from the incoming chyme) causes the duodenal wall to release a
hormone called secretin. Secretin travels through the blood to the pancreas, where it
stimulates the release of sodium bicarbonate, which in turn neutralizes the acid.
4. The presence of fat and peptides in the duodenum stimulates the release of another
hormone, CCK (or cholecystokinin). CCK travels in the blood to the gall bladder, where it
stimulates the contractions that pump bile into the duodenum, and to the pancreas, where it
stimulates the release of digestive enzymes. Together, bile and the pancreatic juices
complete most of the digestion of macromolecules.
5. If the chime is very rich in fats, the small intestine releases another hormone,
enterogastrone, which slows down peristalsis in the stomach. This causes the stomach
to release chime more slowly, and allows more time for the intestines to digest the food.
This is one of the things that makes a fatty meal more filling.
The old quip, "I love Chinese food, but I'm hungry again half an hour later" actually has some truth to it,
since traditional Chinese cuisine is usually quite low in fat. Of course, this presents a problem for dieters
and people trying to eat a healthier diet. In reducing fat intake, they may actually make the urge to snack
between meals greater. Obviously, chips and triple thick shakes are NOT the answer! However, judicious
and planned consumption of foods with enough good fats (e.g. unsaturates such as olive oil, omega-3 and
omega-6 rich fats such as flax oil) may improve the chances of sticking to a diet. It is also likely that
increased satiation due to fats accounts for the success some people have had with the low carb, high
protein diets that were all the rage in the early 2000s. Unfortunately, many of these diets were deficient
in other nutrients, some encouraged fat intake well above the accepted healthy level, and most entailed
other risks. The moral is, "Moderation in everything"!

When all the hormones have done their work, the digestive system will release large
amounts of micro molecules to be absorbed into the blood. These will travel, among other
places, to the brain where they will damp down our hunger response until they are used up
by the body and we need to eat once more.
Created by J. David Moffatt
Hillfield-Strathallan College, Hamilton, ON, Canada November2005
Send questions, comments and suggestions to moffatt@hillstrath.on.ca

Gut. 2006 February; 55(2): 148150.

PMCID: PMC1856501
doi: 10.1136/gut.2005.071787.
Copyright 2006 BMJ Publishing Group & British Society of Gastroenterology
To be or not to bean incretin or enterogastrone?
M Horowitz and M A Nauck
M Horowitz, University of Adelaide, Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide,
South Australia 5005, Australia
M A Nauck, Internist/Gastroenterology/Endocrinology, Diabetology (DDG), Diabeteszentrum Bad
Lauterberg, Kirchberg, Bad Lauterberg im Harz, Germany
Correspondence to: Professor M Horowitz
Department of Medicine, North Terrace, Royal Adelaide Hospital, Adelaide, South Australia 5005,
Australia; michael.horowitz@adelaide.edu.au