Control of Feeding - Anatomy & Physiology

Introduction

Different hormones, neurotransmitters and reflexes are involved in the complicated process of feeding in animals. Secretions and motility of the gastrointestinal tract are stimulated and carefully regulated by numerous factors, including environmental stimuli and the presence of food in different parts of the gastrointestinal tract from the oral cavity right through to the intestines.

When a harmful substance is ingested the body acts to eliminate it in different ways to prevent the animal becoming ill, for example, through vomiting and diarrhoea. If one or more of the pathways in controlling feeding is damaged or inhibited, then problems such as obesity occurs.

Feeding Methods

There are a number of feeding methods, including absorption over the body surface, filter feeding, mucous trapping, fluid feeding, piercing and sucking, cutting and biting, seizing prey, the use of jaws, teeth, beaks and the use of toxins.

Functions of the GIT

The main function of the GIT is to efficiently breakdown feed to the essential nutrients that can then be absorbed. The GIT then acts to propel the waste fed material out of the body. The following constitute this main function:

The secretion of enzymes and co-factors for digestion including water, ions and mucous

Motility for forward propulsion, mechanical breakdown, mixing of ingesta and sphincter tone

Migrating myoelectric complex to prevent debris accumulation

Peristalsis

Haustration

Segmental motility

Blood flow to muscles, submucosa and epithelial surfaces to sustain secretion, motility and the uptake of products of digestion and growth and repair.

Control of the GIT

Endocrine hormones are released into the circulation by cells within the GIT or an accessory organ; paracrine mediators are released by cells within the tract and diffuse locally to act on neighboring target cells; neurotransmitters from nerves and other cells can be used and the autonomic nervous system is superimposed over the local control.

Control of Motility

The control of motility is intrinsic. It uses muscle pacemaker cells (Cajal cells) to set a basic electric rhythm (BER) of 3-20 per minute. It passes through gap junctions and an action potential is created, producing a slow wave of contraction. The likelihood of an action potential is increased through the stretch of food in the lumen and chemical food stimulation.

Endocrine, paracrine or neural signals enter the enteric nervous system via sensory neurones. The neurons interact with plexuses in the GIT wall. The myenteric plexus controls muscle movement and the submucosa plexus controls secretion and blood flow. The two plexuses are connected by interneurones to co-ordinate control. The autonomic nervous system is superimposed.

Excitatory neurotransmitters are parasympathomimetic. They include: ACh (muscarinic M1 and M2), Serotonin and Substance P.

Inhibitory neurotransmitters are sympathomimetic. They include: Vasoactive intestinal polypeptide (VIP), Nitric oxide (NO), ATP and Enkephalins.

Control of GIT Secretions

The presence of food in the GIT is detected by open chemoreceptors. Signals to the endocrine cells or via the autonomic nervous system (ANS) releases gastrointestinal peptide hormones . These hormones act to promote secretion, provide negative feedback or affect motility. Closed mechanoreceptors also act to alter secretions. Conditioned (associative) and unconditioned responses act via the ANS.

Control Method	Neural	Endocrine
Saliva	Yes	No
Stomach	Yes	Yes
Small Intestine	No	Yes

Phases of Gastric Secretion

Cephalic

Cephalic phase of secretion - Copyright RVC 2008

This phase is an unconditioned reflex. It is stimulated by the sight, smell and taste of food. It involves the vagus nerve (CN X) and parasympathetic fibres that synapse in the submucosal plexus. Gastrin is secreted from the endocrine cells in the pyloric mucosa. Postganglionic fibres activate chief, parietal, mucous and G cells. Histamine is secreted due to paracrine action. There is an increase in stomach motility by release of hydrochloric acid and pepsinogen. It is a short phase and overlaps with the gastric phase of secretion. It is inhibited by stress and increased by aggression.

Gastric control of secretion - Copyright RVC 2008

Gastric

Chemical and mechanical receptors in the stomach respond to stretch and chemical stimulation by an increase in the pH of gastric contents. It is a response to undigested materials, especially proteins. Histamine and gastrin are released. It is a negative feedback loop by sympathomimetic somatostatin released by paracrine method to inhibit gastrin secretion (when pH falls below 3). The submucosal and myenteric plexuses are activated in vagus reflex arcs causing the postganglionic release of ACh at parietal cells. The neural response and presence of peptides in chyme stimulates gastrin release. Parietal and chief cells stimulate via gastrin acting in the bloodstream. It is a long response.

Intestinal control of secretion - Copyright RVC 2008

Intestinal

Chyme in the duodenum inhibits acid secretion and motility by decreasing the stomach distension and increasing the stretch of the duodenum leading to the enterogastric reflex. A drop in pH below 4.5 causes release of secretin which inhibits parietal and chief cells and stimulates buffer release from the pancreas. Chyme causes the release of secretin, GIP and CCK decreasing gastric secretions and motility.

Pancretic control of secretion - Copyright RVC 2008

Pancreatic

Involves CCK, secretin and Gastrin. Parasympathetic stimulation during cephalic and gastric phases. Negative feedback occurs from paracrine sympathomimetics (somatostatin and enkephalins).

Biliary

CCK empties the gall bladder and secretin stimulates hydrogencarbonate ions from the bile duct.

Small Intestinal

Involves secretin, GIP and gastrin. Controlled by vagal tone and the parasympathomimetic reflex.

Neuroendocrine Regulation of Feeding

The hypothalamus is the critical region of feeding control. The major hypothalamic nuclei involved are; arcuate, ventromedial hypothalamus, dorsomedial hypothalamus, lateral hypothalamus and paraventricular hypothalamus.

Gut Peptides

Peptide	Site of Release	Effect on Feeding
CCK	Duodenum	Reduces food intake
Ghrelin	Gastric fundus	Increases food intake
GLP-2	Intestine	Reduces food intake
Motilin	Small intestine	Indirectly inhibits food intake
Oxyntomodulin	large intestine	Inhibits food intake
Pancreatic Polypeptide	Pancreas	Inhibits food intake
PYY3-36	Intestine	Inhibits food intake
Somatostatin	Pancreas	Inhibits food intake

Other Peptides

Peptide	Site of Release	Effect on Feeding
Leptin	Adipocyte	Reduces food intake
NPY	Arcuate nucleus	Increases food intake
Agrp	Arcuate nucleus	Increases food intake
MCH	Lateral hypothalamus	Increases food intake
Orexins	Lateral hypothalamus	Increases food intake
CART	Arcuate nucleus	Inhibits food intake
α MSH	Arcuate nucleus	Inhibits food intake
Bdnf	Ventromedial nucleus	Inhibits food intake
Serotonin	Brainstem	Inhibits food intake
Cannabinoids	CNS	Increases food intake

Species Differences

Equine

The anatomy of the equine stomach, the close proximity of the exiting duodenum and the entering oesophagus along with the well developed cardiac sphincter, make it difficult for the horse to vomit. However on rare occasions it does occur.

Click here for more information on The Vomit Reflex.

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