Chapter 10 Internal Regulation

Hunger Animals vary in their strategies of eating, but humans tend to eat more than they need at the given moment. A combination of learned and unlearned factors contribute to hunger and eating behaviors.

Hunger The function of the digestive system is to break down food into smaller molecules that the cells can use. Digestion begins in the mouth where enzymes in the saliva break down carbohydrates. Hydrochloric acid and enzymes in the stomach digest proteins.

Hunger The small intestine has enzymes that digest proteins, fats, and carbohydrates and absorbs digested food into the bloodstream. The large intestine absorbs water and minerals and lubricates the remaining materials to pass as feces.

Hunger The brain regulates eating through messages from the mouth, stomach, intestines, fat cells and elsewhere. The desire to taste and other mouth sensations, such as chewing, are also motivating factors in hunger and satiety. Sham feeding experiments, in which everything an animals eats leaks out of a tube connected to the stomach or esophagus, do not produce satiety.

Hunger The main signal to stop eating is the distention of the stomach. The vagus nerve conveys information about the stretching of the stomach walls to the brain. The splanchnic nerves convey information about the nutrient contents of the stomach.

Hunger The duodenum is the part of the small intestine where the initial absorption of significant amounts of nutrients occurs. Distention of the duodenum can also produce feelings of satiety. The duodenum also releases the hormone cholecystokinin (CCK), which helps to regulate hunger.

Hunger Cholecystokinin (CCK) released by the duodenum regulates hunger by: –Closing the sphincter muscle between the stomach and duodenum and causing the stomach to hold its contents and fill faster. –Stimulating the vagus nerve to send a message to the hypothalamus that releases a chemical similar to CCK.

Hunger Glucose, insulin, and glucagon levels also influence feelings of hunger. Most digested food enters the bloodstream as glucose, an important source of energy for the body and nearly the only fuel used by the brain. When glucose levels are high, liver cells convert some of the excess into glycogen and fat cells convert it into fat. When low, liver converts glycogen back into glucose.

Hunger Insulin is a pancreatic hormone that enables glucose to enter the cell. Insulin levels rise as someone is getting ready for a meal and after a meal. In preparation for the rush of additional glucose about to enter the blood, high insulin levels let some of the existing glucose in the blood to enter the cells. Consequently, high levels of insulin generally decrease appetite.

Hunger Glucagon is also a hormone released by the pancreas when glucose levels fall. Glucagon stimulates the liver to convert some of its stored glycogen to glucose to replenish low supplies in the blood. As insulin levels drop, glucose enters the cell more slowly and hunger increases.

Hunger If insulin levels constantly stay high, the body continues rapidly moving blood glucose into the cells long after a meal. –Blood glucose drops and hunger increases in spite of the high insulin levels. –Food is rapidly deposited as fat and glycogen. –The organism gains weight.

Hunger In people with diabetes, insulin levels remain constantly low, but blood glucose levels are high. –People eat more food than normal, but excrete the glucose unused and lose weight.

Hunger Long-term hunger regulation is accomplished via the monitoring of fat supplies by the body. The body’s fat cells produce the peptide leptin, which signals the brain to increase or decrease eating. Low levels of leptin increase hunger. High levels

Hunger High levels of leptin do not necessarily decrease hunger. –Most people are obese because they are less sensitive to leptin. –Some people are obese because of a genetic inability to produce leptin.

Hunger Information from all parts of the body regarding hunger impinge into two kinds of cells in the arcuate nucleus. The arcuate nucleus is a part of the hypothalamus containing two sets of neurons: 1. neurons sensitive to hunger signals. 2. neurons sensitive to satiety signals.

Hunger Ghrelin is released as a neurotransmitter in the brain and a hormone in the stomach Neurons of the arcuate nucleus specifically sensitive to hunger signals receive input from: –The taste pathways. –Axons releasing the neurotransmitter ghrelin. –also acts in the stomach to trigger stomach contractions.

Hunger Input to the satiety-sensitive cells of the arcuate nucleus include signals of both long- term and short-term satiety: –Distention of the intestine triggers neurons to release the neurotransmitter CCK. –Blood glucose and body fat increase blood levels of the hormone insulin. –Leptin provides additional input.

Hunger Output from the arcuate nucleus goes to the paraventricular nucleus of the hypothalamus. The paraventricular nucleus is a part of the hypothalamus that inhibits the lateral hypothalamus which is important for feelings of hunger and satiety. Axons from the satiety-sensitive cells of the arcuate nucleus deliver an excitatory message to the paraventricular nucleus which triggers satiety.

Hunger Output from the paraventricular nucleus acts on the lateral hypothalamus. –The lateral hypothalamus controls insulin secretion and alters taste responsiveness. Animals with damage to this area refuse food and water and may starve to death unless force fed.

Hunger The lateral hypothalamus contributes to feeding by: –Detecting hunger and sending messages to make food taste better. –Arousing the cerebral cortex to facilitate ingestion, swallowing, and to increase responsiveness to taste, smell and sights of food. –Increasing the pituitary gland’s secretion of hormones that increase insulin secretion. –Increasing digestive secretions.

Hunger Damage to the ventromedial hypothalamus that extends to areas outside can lead to overeating and weight gain. Those with damage to this area eat normal sized but unusually frequent meals. Increased stomach secretions and motility causes the stomach to empty faster than usual. Damage increases insulin production and much of the meal is stored as fat.

Hunger Left here People with a mutated gene for the receptors melanocortin overeat and become obese. –Melanocortin is a neuropeptide responsible for limiting food intake Prader-Willis syndrome is a genetic condition marked by mental retardation, short stature, and obesity. –Blood levels of the peptide ghrelin is five times higher than normal.

Hunger Although a single gene can not be identified, a genetic influence has been established in many factors contributing to obesity. Most cases relate to the combined influences of many genes and the environment.

Hunger Obesity can also be a function of genes interacting with changes in the environment. –Example: Diet changes of Native American Pimas of Arizona and Mexico. Obesity has become common in the United States and has increased sharply since the 1970’s. –Attributed to life-style changes, increased fast-food restaurants, increased portion sizes, and high use of fructose in foods.

Hunger Weight-loss is often difficult and specialist rarely agree. Successful treatments include change of lifestyle, increased exercise and decreased eating. Some appetite-suppressant drugs such as fenfluramine and phentermine block reuptake of certain neurotransmitters to produce brain effects similar to that of a completed meal.

Hunger Sibutramine has replaced fenfluramine and decreases meal size and binge eating by bloking reuptake of serotonin and norepinephrine “Orlistat” is drug that prevents the intestines from absorbing fats. Gastric bypass surgery is the removal or sewing off of part of the stomach. Decreased stomach size allows greater distention of the stomach to produce satiety.

Hunger Anorexia nervosa is an eating disorder associated with an unwillingness to eat as much as needed. Causes and physiological predispositions are not well-understood. Associated with a fear of becoming fat and not a disinterest in food. Biochemical abnormalities in the brain and blood are probably not the cause, but a result of the weight loss.

Hunger Bulimia nervosa is an eating disorder in which people alternate between extreme dieting and binges of overeating. –Some force vomiting after eating. Associated with decreased release of CCK, increased release of ghrelin, and alterations of several other hormones and transmitters. –May be the result and not the cause of the disorder. –Reinforcement areas of the brain associated with addiction also implicated.