Transcript Hunger - Bakersfield College

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 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.