Disturbances of food intake are frequently the first signs observed by owners when an animal is ill. Owners tend to be very observant of their animals at mealtime, since most people associate a good appetite with good health. Many systemic and even localized disease processes affect food intake. Unfortunately, a disturbance of food intake is not definitive of a specific disease process; rather, it represents a clinical finding common to many diseases. To meaningfully approach this problem, one should understand how food intake is regulated in the normal animal.

Definitions

Hunger. Hunger means a craving or a desire to ingest food. It is often associated with intense rhythmic contractions of the stomach. In animals with the stomach removed, the apparent psychic sensations of hunger still occur and the animal still searches for an adequate food supply.

Appetite. In animals, appetite and hunger are often used as synonymous terms; however, appetite actually implies hunger for specific foods. Thus, appetite reflects the quality of food intake, whereas hunger reflects the quantity of food intake.

Satiety. Satiety is the opposite of hunger and results from a filling meal, particularly when the energy and nutritional requirements of the animal are fulfilled.

Neural Regulatory Mechanisms

Hypothalamic Centers for Hunger and Satiety. The hunger or feeding center is located in the lateral hypothalamus. Stimulation of this area causes an animal to eat voraciously. The feeding center directly stimulates the psychic drive to search for and ingest food. Stimulation of the ventromedial nuclei of the hypothalamus causes complete satiety even in the presence of stimuli that would normally incite hunger. It is believed that the satiety center primarily inhibits the feeding (hunger) center. Neuronal lesions that destroy the ventromedial hypothalamic nuclei cause complete disinterest in food and progressive weight loss. The function of the hypothalamic center is to control the quantity of food intake by exciting activity of lower centers.

Other Mechanisms for Neuronal Control of Feeding. Centers higher than the hypothalamus also affect feeding, presumably via their influence on the feeding and satiety centers. These higher centers include the amygdala and the cortical areas of the cortex. They are closely coupled with the hypothalamus. The amygdala is one of the major parts of the olfactory nervous system and probably couples appealing odors with the desire to eat. Although the amygdala may both stimulate and inhibit feeding, its major function appears to be in the area of food discrimination (appetite). The cortical regions of the limbic system function in much the same manner as the amygdala, except that they play a major role in the animal’s drive to search for food when hungry.

Nutritional and Alimentary Regulation of Food Intake

Nutritional Regulation. Nutritional regulation is concerned primarily with maintenance of normal quantities of nutrient stores in the body. The feeding center in the hypothalamus is influenced by the nutritional status of the body. In general, inadequate nutritional stores cause feeding, whereas abundant nutritional stores favor satiety.

Effects of Glucose and Amino Acid Concentrations. The concentration of blood glucose has important effects on feeding. An increased blood glucose concentration increases activity of the satiety center and secondarily decreases activity of the hunger center. The satiety center concentrates glucose, whereas other areas of the hypothalamus do not. Thus, it is assumed that glucose acts to regulate feeding by increasing the degree of satiety. Increased blood amino acid concentrations also reduce feeding, although the effect is less dramatic than that of glucose.

Effects of Fat Metabolites. The degree of adipose tissue in the body inversely affects feeding. As the degree of adipose tissue increases, the rate of feeding decreases. The quantity of free fatty acids and fat metabolites in the blood is directly proportional to the quantity of adipose stores in the body. It is likely that free fatty acids and other fat metabolites have a negative feedback regulatory effect on feeding. This lipostatic mechanism may be a major factor in long-term feeding regulation.

Alimentary Regulation. Several short-term physiologic stimuli affect feeding. Although habits related to eating are important, factors related to the alimentary tract also play important roles.

Distention of the stomach and intestinal tract inhibits feeding. Nervous impulses arising from mechanoreceptors in the wall of the distended tract stimulate the satiety center and inhibit the feeding center. The inhibitory effects of stomach distention are not completely removed by denervating the stomach wall. Therefore, overstretching the abdominal cavity and nutritional signals from the liver may also be involved. These mechanisms are especially important considerations since diseases of the liver, stomach, small intestine, and abdominal cavity are frequently associated with anorexia.

Cephalic Regulation. Various factors related to feeding, such as chewing, salivation, swallowing, and tasting, may also inhibit the feeding center after a certain amount of food has passed through the mouth. These cephalic factors decrease feeding in animals with esophageal fistulas that prevent food from entering the stomach.

Anorexia is the lack of or disinterest in the ingestion of food. In clinical terms, total anorexia is the pathologic absence of hunger. Its presence is associated with many disease processes that either directly inhibit or suppress activity in the hunger center or stimulate activity in the satiety center. Anorexia may be partial or complete, pathologic, physiologic, or psychologic. The major task confronting the veterinary clinician is to determine whether anorexia is pathologic or physiologic/psychologic in origin.

Pathophysiology