Chapter 10 Internal Regulation

2. Chapter 10 Internal Regulation

3. 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.

4. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

14. 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.

15. 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.

17. 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.

19. 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

20. 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.

21. 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: • neurons sensitive to hunger signals. • neurons sensitive to satiety signals.

22. 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.

23. 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.

24. 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.

25. 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.

26. 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.

29. 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.

33. 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.

34. 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.

36. 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.

37. 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.

38. 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.

39. 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.

40. 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.