The Pig As A Model Of Omnivorous Mammals

The eating habits of the domestic pig closely resemble those of the human, with respect to both what it eats and the pattern of meals. In young pigs, the pattern of eating consists of periodic meals separated by intermeal intervals of a few hours' duration. Much of the water consumed is drunk in close association with meals.

It is presumed that during the intermeal intervals deficits of nutrients slowly develop as they are consumed in body metabolism. These deficits are then corrected at subsequent meals. The physiological mechanisms using hormonal and neural pathways will be emphasized here as determining how much food will be consumed in the meals. It should be recognized, however, that the body learns through previous experience how much food should be consumed to satisfy the deficit. In other words, eating is calibrated by experience to match the amount eaten with the metabolic need. This learned control of food intake is difficult to evaluate as part of the combination that includes the mechanistic, physiological control of eating.

It is instructive to consider what kinds of signals could be used by the body to initiate satiation, so that the amount eaten as the meal proceeds matches the need (deficit). These physiological feedback signals that are activated by the presence of food in the digestive tract and that determine the size of each meal are summarized for a typical mammal in Fig. 1. The first and most obvious change caused by the foodstuff as it passes into the mouth, pharynx, and esophagus is distention of these structures and tactile stimulation of their inner surfaces. This oropharyngeal metering of food ingestion plays a small role in controlling the amount eaten in the meal. If this metering acted alone to limit the size of the meal, the meal size would be excessive as much as two or three times the normal size. But such metering does not act alone; there are other signals from the mouth and the rest of the gastrointesinal tract. The taste of the food as it is chewed may oppose further eating, or an attractive taste may act as positive feedback and increase the amount eaten in the meal. An extremely bitter or unpleasant taste (perhaps resembling a toxin) may block eating entirely.

The arrival of the ingested meal in the stomach causes further distension, which is detected by the numerous stretch or distension receptors in the mucosa and wall of the stomach. This distension is a powerful inhibitory influence on eating behavior. By the time the foodstuffs arrive at the small intestine much liquification has occurred, with solubilization of many products of digestion. The duodenum is the site of many sensory receptors, as well as endocrine cells. Most important are the release of the hormone cholecystokinin (CCK), the response of osmoreceptive mechanisms to the concentrated intestinal content, and the absorption of glucose from the chyme. All have a satiation effect that generally strengthens as the meal proceeds, until strong enough to bring the meal to an end.[1]

In addition to these rapid, short-term control systems that operate in the time span of a meal, there are long-term controls that operate over days and weeks. An example is the leptin system. Leptin is released from body fat stores and acts centrally to inhibit eating. Over time, as the fat stores slowly increase, the levels of leptin increase. Leptin depresses food intake and limits body weight increase. Note that the controls of food intake are predominantly

Fig. 1 Controls of food intake in the pig.

inhibitory. Eating is a tonic activity interupted periodically by these inhibitory signals that are initiated by the presence of food in the digestive tract.[2] An intermeal interval follows, and not until those satiety signals weaken does the next meal begin.

THE COW AS AN EXAMPLE OF THE LARGE HERBIVORES

contains about the same amount of glucose as an equivalent amount of cornstarch, its glucose is unavailable to the mammals that ingest it.

The herbivores, such as the cow, have solved this problem of the nutritional inaccessibility of cellulose by anatomical and physiological adaptations that permit the development of large populations of microorganisms within the body. Many of these associated microorganisms bacteria and protozoa mainly can synthesize the enzyme cellulase, which can attack the cellulose molecules. Breakdown of these molecules results in making glucose available for absorption and utilization in the metabolic machinery of the animal.

The calorically dilute nature of the plant material consumed by the cow requires that large amounts must be ingested. A cow can spend eight or more hours grazing on pasture or consuming hay in the barn, and then another eight hours in the process of rumination, where the ingesta is retrieved from the rumen and remasticated. This extensive grinding of plant material is necessary to make cellulose and other complex carbohydrates located within the plant structure accessible to microbial action. The unique process of digestion and absorption of nutrients in ruminants requires unique satiety signals, summarized for the cow in Fig. 2 as the following three steps:

In contrast to the eating habits of the omnivorous pig, most herbivores eat food of quite a different character and follow a different pattern of eating. The plant material eaten by herbivores is in large part not digestible by the ordinary mammalian digestive enzymes that is, not by the digestive juices of the salivary glands (amylase), stomach (pepsin), pancreas (amylase, lipase, etc.), intestine (peptidases), and so on. For the usual omnivore or carnivore such as the pig or dog, this means that the enormous store of nutritionally usable chemical energy stored up in plant structure, and originally derived from the energy of the sun, is not available. For access to these stores of energy the cow is dependent upon the enzymes synthesized by the symbiotic microorganisms that inhabit the gastrointestinal tract, particularly the rumen. These microbial digestive enzymes can make much of the plant energy available.

The prime example of these plant materials is cellulose, the most abundant carbohydrate on earth. Cellulose is abundant, but nutritionally inaccessible to the nonherbi-vore. The key problem for the mammal who ingests cellulose is that the usual digestive enzymes do not have the ability to break up the long polymers of glucose that compose the cellulose molecules. Although the starch can be split by the salivary and pancreatic amylases into the component glucose molecules, the mammalian digestive enzymes cannot break the bonds between glucose molecules in cellulose. The result is that although cellulose

1. As the bulky plant material is ingested, the immediate consequence is distension of the GI tract. There are ample stretch receptors located in the wall of the reticulorumen. When distended, they give rise to inhibitory impulses to the CNS, limiting further eating. As indicated in the figure, the degree of distention depends on the amount of bulky food ingested and the rate of removal of the ingesta, either by fermentative breakdown or by passage from the reticulorumen into the omasum.

[DISTENTION] = [FEED INPUT] — [FERMENTATIVE DIGESTION] — [OUTPUT TO OMASUM]

Fig. 2 Controls of food intake in the ruminant.

[DISTENTION] = [FEED INPUT] — [FERMENTATIVE DIGESTION] — [OUTPUT TO OMASUM]

Fig. 2 Controls of food intake in the ruminant.

2. If the food being ingested is of a more concentrated, water-soluble nature, then the osmolality of the ru-minal fluid rises significantly, due to both the solutes in the feed going into solution and the release of ions and molecules in the microbial fermentation of the foodstuffs. This change in the ruminal fluid acts as a satiety signal to the CNS that, as it grows stronger, brings the meal to an appropriate end. The exact site of reception of this hyperosmolality is unclear.

3. The fermentative action of the ruminal microbes results in the endproducts acetic acid, propionic acid, and butyric acid. These short-chain fatty acids are known as volatile fatty acids (VFAs). There is some evidence that these VFAs act at receptor sites either in the ruminal wall (acetic acid) or in the vascular bed of the liver (propionic acid), giving rise to satiety signals to the CNS that inhibit further eating.[3]

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