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 longterm 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.