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Saint Louis University

School of Natural Sciences


Department of Biology

Partial Requirement for Animal Physiology:

Regulation of Digestion

Mesina, Andrew James L.


Rabara, Daryl Kim R.
Co, Bianca Marie I.
Garbo, Rodelyn V.
Ignacio, Jannel Olaine N.
Navarro, Ayna Suzane C.

Myrna Lyn M. Castillo

May 04, 2018


I. Hormones and their functions
Major Hormones that control digestion:

1. Gastrin
Stimulus: Distension of stomach, partially digested proteins and caffeine in stomach, and high pH of stomach
chyme
Secreted by: Enteroendocrine G cells,located mainly in mucosa of pyloric antrum of stomach
Major effects: Promotes secretion of gastric juice, increase gastric motility, promotes growth of gastric mucosa
Minor effects: Constricts lower esophageal sphincter, relaxes pyloric sphincter

2. Secretin
Stimulus: Acidic chyme that enters small intestine
Secreted by: Enteroendocrine S cells in the mucosa of duodenum
Major effects: Stimulates secretion of pancreatic juice and bile that are rich in HCO3- (bicarbonate ions)
Minor effects: Inhibits secretion of gastric juice, promotes normal growth and maintenance of pancreas, enhances
effects of CCK

3. Cholecystokinin (CCK)
Stimulus: Partially digested proteins (amino acids), triglycerides, and fatty acids that enter small intestine
Secreted by: Enteroendocrine CCK cells,located mainly in mucosa of small intestine; can also be released in the
brain
Major effects: Stimulates secretion of pancretic juice rich in digestive enzymes, causes ejection of bile from
gallbladder and opening of sphincter of the hepatopancreatic ampulla (Sphincter of Oddi), induces satiety (feeling of
satisfaction)
Minor effects: Inhibits gastric emptying, promotes normal growth and maintenance of pancreas, enhances effects of
secretin

4. Gastric inhibitory peptide (GIP)


Stimulus: Presence of glucose and lipids in the duodenum.
Secreted by: K cells of the duodenum and jejunum.
Major effects: Stimulate insulin secretion that prepares the appropriate tissues for the transport and metabolism of
nutrients obtained from the GI tract, Inhibit gastric secretion and motility.
Minor effects: It decreases stomach churning in order to slow the emptying of the stomach.

Other hormones of Digestive System:

1. Motilin, substance P, and Bombesin


- Stimulate the motility of intestines
2. Vasoactive intestinal polypeptide (VIP)
- Stimulates secretion of ions and water by intestines and inhibits gastric acid secretion
3. Gastrin- releasing peptide
- stimulates release of Gastrin
4. Somatostatin
- Inhibits Gastrin release
II. 3 Phases of Digestive regulation
1. Cephalic phase
2. Gastric phase
3. Intestinal phase

Cephalic phase
 During the cephalic phase, the smell, sight, thought, or initial taste of food activates neural centers in the cerebral
cortex, hypothalamus, and brain stem.
 The brain stem then activates the Facial (VII), Glossopharyngeal (IX), and Vagus (X) nerves.
 The Facial and Glossopharyngeal nerves stimulate the salivary gland to secrete saliva
 The vagus nerves stimulate the gastric gland to secrete gastric juice.
 It prepares the mouth and stomach for food that is about to be eaten.
General effect: Stimulation of salivary glands

Gastric Phase
 The gastric phase is a period in which swallowed food and semi-digested protein ( peptides and amino acids )
activate gastric activity.
 Begins when the food enters the stomach
 About two-thirds of gastric secretion occurs during this phase.
 It is mediated by Neural and hormonal regulation

Neural regulation
– Food of any kind distends the stomach and stimulates stretch receptors in its walls.
– Chemoreceptors in stomach monitor the pH of the stomach chyme.
– When the stomach walls are distended of pH increases because proteins have entered the stomach and buffered
some of the stomach acid, the stretch receptors and chemoreceptors are activated.
– Neural feedback loop is set in motion.
– From the sretch receptors and chemoreceptors, nerve impulse propagate to the submucosal plexus, where they
activate parasympathetic and enteric neurons.
– The nerve impulse cause waves of peristalsis and continue to stimulate the flow of gastric juice from gastric
glands.
– Mixing of food with gastric juice.
– When waves become strong enough, a small quantity of chyme undergoes gastric emptying into the duodenum.
– Decrease of the stomach chyme pH (more acidic).
– Distension of the stomach wall lessens due to the passing of chyme into the small intestine
– Suppression of the secretion of gastric juice.
Hormonal regulation
– Gastric secretion is regulated by gastrin.
– Gastrin enters the bloodstream, makes a round-trip through the body, until it finally reaches its target organs in
the digestive system.
– Gastrin stimulates gastric glands to secrete large amounts of gastric juice.
General effect: Activation of gastric activity

Gastric Secretion
Stimulated chiefly by three chemicals:

1. Acetylcholine (ACh). This is secreted by the parasympathetic nerve fibers of both the short and long reflex
pathways.
2. Histamine. This is a paracrine secretion from the enteroendocrine cells in the gastric glands.
3. Gastrin. This is a hormone produced by enteroendocrine G cells in the pyloric glands.

– All three of these stimulate parietal cells to secrete hydrochloric acid and intrinsic factor.
– The chief cells secrete pepsinogen in response to gastrin and especially ACh, and ACh also stimulates mucus
secretion.

Two types of feedback:

Positive feedback loop


As dietary protein is digested, it breaks down into smaller peptides and amino acids that directly stimulate the G
cells to secrete even more gastrin. This accelerates protein digestion.

Negative feedback loop


Small peptides buffer the stomach acid so the pH does not fall excessively low. As digestion continues and these
peptides empty from the stomach, the pH drops lower and lower. Below pH of 2, stomach acid inhibits the parietal
cells and G cells. It winds down the gastric phase as the need for pepsin and HCl declines.

Intestinal phase
 It begins once the food enters the small intestine
 It has an inhibitory effects that slow down the exit of chyme from the stomach; this prevents the duodenum from
being overloaded with more chyme that it can handle.
 Responses occuring at this stage promotes the continued digestion of foods that have reached the small intestine.
 Regulated by neural and hormonal mechanism

Neural regulation
– Enterogastric reflex: Caused by distension of the duodenum by the presence of chyme
– Stretch receptors in the duodenal wall will send nerve impulse to the medulla oblongata
– Inhibition of the parasympathetic stimulation and stimulate the sympathetic nerves to the stomach
– Gastric motility is inhibited
– Increase in the contraction of the pyloric sphincter, which decreases gastric emptying

Hormonal regulation
– Mediated by two major hormones released by small intestine:
1. Cholecystokinin
2. Secretin

III. Lipid transport across the gut

Neutral fat or triglyceride


– Bulk of dietary lipid
– It is composed of a glycerol backbone with each carbon linked to a fatty acid.

In order for the triglyceride to be absorbed, two processes must occur:

•Large aggregates of dietary triglyceride, which are virtually insoluble in an aqueous environment, must be broken
down physically and held in suspension - a process called emulsification.
•Triglyceride molecules must be enzymatically digested to yield monoglyceride and fatty acids, both of which can
efficiently diffuse or be transported into the enterocyte
The key players in these two transformations:
1. Bile acids
2. Pancreatic lipase

– Both of which are mixed with chyme and act in the lumen of the small intestine.
– Bile acids are also necessary to solubilize other lipids, including cholesterol.

4 processes:
1. Emulsification
2. Hydrolysis
3. Micelle Formation
4. Transport into blood

Emulsification
– Bile acids play their first critical role in lipid assimilation by promoting emulsification.
– As derivatives of cholesterol, bile acids have both hydrophilic and hydrophobic domains (i.e. they are
amphipathic).
– On exposure to a large aggregate of triglyceride, the hydrophobic portions of bile acids intercalate into the lipid,
with the hydrophilic domains remaining at the surface.
– Such coating with bile acids aids in breakdown of large aggregates or droplets into smaller and smaller droplets.

Hydrolysis
– Hydrolysis of triglyceride into monoglyceride and free fatty acids is accomplished predominantly by pancreatic
lipase.
– The activity of this enzyme is to clip the fatty acids at positions 1 and 3 of the triglyceride, leaving two free fatty
acids and a 2-monoglyceride.

Micelle Formation
– As monoglycerides and fatty acids are liberated through the action of lipase, they retain their association with
bile acids and complex with other lipids to form structures called micelles.
– Micelles are essentially small aggregates (4-8 nm in diameter) of mixed lipids and bile acids suspended within
the ingesta.
– As the ingesta is mixed, micelles bump into the brush border of small intestinal enterocytes, and the lipids,
including monoglyceride and fatty acids, are taken up into the epithelial cells.
Transport into Blood
– The major products of lipid digestion - fatty acids and 2-monoglycerides - enter the enterocyte by simple
diffusion across the plasma membrane.
– A considerable fraction of the fatty acids also enter the enterocyte via a specific fatty acid transporter protein in
the membrane.
– Lipids are transported from the enterocyte into blood
– Once inside the enterocyte, fatty acids and monoglyceride are transported into the endoplasmic reticulum, where
they are used to synthesize triglyeride.
– Beginning in the endoplasmic reticulum and continuing in the Golgi, triglyceride is packaged with cholesterol,
lipoproteins and other lipids into particles called chylomicrons.
– Chylomicrons are extruded from the Golgi into exocytotic vesicles, which are transported to the basolateral
aspect of the enterocyte. The vesicles fuse with the plasma membraneand undergo exocytosis, dumping the
chylomicrons into the space outside the cells.

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