Digestion Control

The gastrointestinal tract has its own intrinsic nervous system. It can regulate secretory and motor functions of digestive organs independently of the extrinsic, autonomous nervous system but is nevertheless strongly influenced by the latter. The afferent neurons receive their signals from mechano-and chemoreceptors; these are most common in the duodenum. Efferent neurons may supply smooth musculature, as well as glands. Acetylcholine functions as the neurotransmitter for the preganglionic fibers of the vagus nerve. A multitude of bioactive peptides function as neurotransmitters for the postganglionic nerve fibers.

Various cell types embedded in the gastrointestinal mucosa secrete specific gastrointestinal hormones and pep-tides (A) upon contact with food components. The classical hormones gas-trin, secretin, and cholecystokinin (CCK) are released into the blood in response to their respective stimuli. Some of the peptides diffuse into neighboring tissues and act upon effector cells there. Others are released at the nerve endings and function as neurotransmitters. These substances may have agonistic or synergistic effects on various cell types of different organs.

Hormonal regulation has a decisive influence on all digestive functions and sets in early, i. e., even before actual food intake.

Secretion of saliva, for instance, begins with the expectation of a meal and is not controlled by conditioned (oral or gastrointestinal) reflexes (Pavlov). The function of this early secretion is to enable starch breakdown by salivary amy-lase and to release antibacterials

(thiocyanate), as well as somatostatin and growth factors (IGF, NGF).

In the stomach, vagal stimulation (expectation of food and stress) and/or actual ingestion of food triggers acid secretion. The latter also causes localized histamine and gastrin release, which in turn causes parietal cells to release H+ ions. Pepsinogen is released by the chief cells in the same fashion, leading to digestion of proteins, enhanced by their denaturation in an acidic environment.

The arrival of fat and proteins in the stomach and upper small intestine stimulates CCK release into the blood. CCK release is a preparatory and coordinating step for the digestion of most nutrients in the duodenum and jejunum and also influences nutrient distribution after their absorption into the bloodstream. CCK quickly reduces the gastric emptying rate and stimulates the secretion of bile and pancreatic fluids into the duodenum. CCK appears to effect gall bladder contractions by stimulating acetylcholine release. CCK also enhances insulin secretion into the blood.

i- A. Gastrointestinal Hormones: Sites of Production and Effects

Sites of production and effects

Gastrointestinal hormones

Site of hormone production

Effects on secretory activity

Effects on motor activity

Gastrin

Stomach and duodenum

Stomach (HCl, pepsin) •••• Liver (bile) • Pancreas (enzymes) •

Stomach Gall bladder

Cholecystokinin

Duodenum and jejunum

Pancreas

Small and large intestine •

Stomach ••

Secretin

Duodenum and jejunum

Pancreas •••• (HCO3 and enzymes) Bile duct ••

Small and large intestine •/• Stomach ••

Vasoactive intestinal peptide

Small and large intestine

Pancreas •••• (enzymes) Liver (bile) ••

(enzymes)

Stomach ••

Stomach ••• Small intestine

Enteroglucagon

Small and large intestine

Pancreas • (insulin)

Small and large intestine •••

Gastrointestinal inhibitory peptide

Small and large intestine

Small and large intestine •

(enzymes)

Pancreas • (insulin)

Motilin

Small and large intestine

Stomach •••• Small and large intestine ••••

Pancreatic polypeptide

Pancreas • ?

?

Somatostatin

Small and large intestine

?

Bombesin

Upper small intestine

GI tract • ? Release of gastrin

?

Neurotensin

Lower small intestine

?

?

Glucagon-like peptide

Lower small intestine and colon

?

Stomach ••

Neuromedin K Substance P

Small intestine (neuronal and endocrine cells)

(atropine-resistant contractions)

Enkephalins

Small intestine

?

?

  • Stimulatory effect • Inhibitory effect • No effect
  • Stimulatory effect • Inhibitory effect • No effect

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