Hunger And Thirst

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Homeostatic systems

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use our behavior to keep things balanced

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Negative feedback systems

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Negative feedback systems are the main homeostatic mechanisms
If a desired set point is deviated from compensatory action begins

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Hypovolemic thirst is stimulated by low extracellular/intravascular volume

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Osmotic thirst is stimulated by high extracellular solute concentration

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Osmotic thirst

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is stimulated by high extracellular solute concentration

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Hypovolemic thirst

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is stimulated by low extracellular/intravascular volume

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Hypovolemic thirst

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Triggered by loss of water volume – concentration is not changed
Baroreceptors in blood vessels and heart detect the initial drop
Brain activates thirst and salt craving
Arteries constrict to raise BP

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Hypovolemia causes release of

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Hypovolemia causes release of vasopressin (antidiuretic hormone) – induces blood vessel constriction and reduces flow to the bladder
In diabetes insipidus, vasopressin is not produced – kidneys send more urine to the bladder, resulting in chronic thirst

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Brain Control of Drinking

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Circulating angiotensin II acts in the subfornical organ to send a signal to other brain sites to initiate drinking

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Angiotensin Cascade

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With decreased blood volume, kidneys release renin, which triggers formation of angiotensin I and II

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Osmotic thirst

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Water can pass;
Salt cannot

Osmosensory neurons in anterior hypothalamus (OVLT) respond to rise in blood osmotic pressure

Their cell membranes shrink, opening mechanical ion channels

Osmosensory neurons in hypothalamus respond to increased osmotic pressure, causing the pituitary to release antidiuretic hormone

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Osmosensory neurons

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in hypothalamus respond to increased osmotic pressure, causing the pituitary to release antidiuretic hormone

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Diets

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Energy expenditure is adjusted in response to nutrition
At the start of a diet, the basal metabolic rate will fall – to prevent losing weight
Restricted food intake does promote longevity, up to 40% in rats! In people?

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Energy Utilization

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Glucose is the principal sugar used for energy

Glycogen is glucose stored for short term in the liver

Glycogenesis: converting glucose to glycogen, using pancreas hormone insulin

Lipids, for longer-term storage, are fat tissue

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What stops a meal?

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Two types of satiety signals:
gastrointestinal tract (short term), adipose tissue (long term)
Head factors
Receptors (eyes, nose, tongue, and throat) provide info about appearance, odor, taste, texture, and temp of food
Gastric factors
When stomach is empty, ghrelin is secreted which activates a hunger signal
Stomach also contains receptors that detect presence of nutrients

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organum vasculosum lamina terminalis (OVLT)

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the reduced water content of the cells that contributes to osmotic this is detected in the OVLT

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subfornical organ

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lowered blood volume is also detected by receptors in the kidneys, which trigger the release of the hormone renin. Renin then increases production of the hormone angiotensin2. angiotensin2 circulating in the blood stream informs the brain in the drop in blood volume. it stimulates the s blood brain barrier

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The brain integrates insulin and glucose levels with other information to decide when to

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start/stop eating

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What stops a meal? Intestinal and liver factors

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Axons in duodenum are sensitive to glucose, amino acids, fatty acids;
Duodenum secretes cholecystokinin (CCK), a stop signal in the brain
Human-glucagon-like peptide-1 (GLP-1) is released into blood by intestine in response to food. GLP-1 reduces appetite

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leptin

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Fat cells produce leptin and secrete it into the bloodstream

Defects in leptin production or sensitivity give a falsely low report of body fat, causing animals to overeat

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Ghrelin

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Ghrelin levels are elevated in Prader-Willi

Released by stomach endocrine cells Appetite stimulant - Rises during fasting; drops after eating
Obese people may have elevated ghrelin levels
For Kate Kane, food is on her mind "all the time" Kate, 26, has Prader-Willi syndrome, a genetic disease that causes a sense of never being full or satisfied Kane, 26, feels so hungry that she begs, steals and even eats out of the garbage to get to food And if someone didn't stop her: "I could eat until I die, basically,"

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Lateral hypothalamus (LH) lesions —refusal to eat – a hunger center

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Ventromedial hypothalamus lesions cause obesity – a satiety center

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Two sets of neurons in hypothalamus have opposing effects

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1) NPY/AgRP neurons produce neuropeptide Y and agouti-related peptide
stimulate appetite and lower metabolism weight gain

2) POMC/CART neurons produce pro-opiomelanocortin and cocaine- and amphetamine-related transcript (CART)
- inhibit appetite and raise metabolism weight loss

Leptin inhibits secretion
of AgRP

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Ghrelin: appetite stimulant

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Insulin, Obestatin, PYY3-36, appetite suppressants

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POMC/CART-inhibit weight gain

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AgRP/NPYneuron-enhance weight gain

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Anorexia Nervosa

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Refusal to maintain body weight
Fear of weight gain
Body image disturbance
Amenorrhea
Restricting or Binge-Eating/Purging type

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Bulimia

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Recurrent binge eating
Recurrent inappropriate compensatory behavior
At least 2x/wk for 3 months

Other symptoms of anorexia
thinning of the bones
brittle hair and nails, dry and yellowish skin
mild anemia, muscle weakness and loss, lethargy
severe constipation
low blood pressure, slowed breathing and pulse
drop in body temperature

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Anorexia and Bulimiadrug treatment

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Both anorexics and bulimics show altered serotonin levels
Serotonin is low in bulimics; antidepressants provide some benefit
Serotonin is low in purging anorexics while ill but rises to normal after weight gain. Drugs that reduce serotonin impair treatment

Dopamine may also be involved. Olanzapine, an anti-schizophrenic drug that blocks dopamine receptors, produces some benefit

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Treatment of Obesity (FYI)

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Use drug therapy: Only drugs approved by FDA
Topamax causes anorexia by blocking neuronal monoamine uptake.
Orlistat decreases fat absorption OTC, but weight loss avg 5 pounds a year
Get surgery if morbidly obese and nothing else helps
Gastric bypass to channel food directly into mid intestine thus decreasing absorption
Gastric banding to shrink the stomach – 50% loss of excess wt
Fact: Even weight loss of 5% decreases medical complications significantly

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treat obesity as an addiction

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They have reduced numbers of dopamine D2 receptors and associated decreases in prefrontal metabolism.
Peptides that induce eating target dopamine neurons.
Anti-addiction drugs are somewhat effective in weight loss.

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Obesity and Reduced Metabolism

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Basal metabolic rate (BMR):
energy required to fuel the brain/body and maintain temperature
75% of energy expenditure in average sedentary student




Of women on a diet, the 1/3 who failed to lose weight had low BMRs
Heredity accounts for 40% of a person’s BMR. But, spontaneous activity is important in resisting obesity

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Treatment of Obesity (What Works)

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Eat less: A daily deficit of 500 to 1000 calories is reasonable. This is the most important partt of therapy and most difficult to adhere to.

Exercise. A lot: Strenuous aerobic activity for over 200 minutes per week maintained for a long time with calorie restriction works.
Sad Fact: Moderate exercise like walking 45 minutes a day 5 days a week has minimal effect on weight loss. Exercise does raise your metabolic rate though. Some is better than none.

Modify behavior to avoid temptation to pig out. This means lifestyle change. Self-monitoring and social support are essential.

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Gastric bypass surgery

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Weight loss averages 25%, compared to 5%-10% with dieting and relapse within a year
Reduces ghrelin and increases PYY and GLP-1, reducing hunger.
Reduces mortality and has many health benefits.

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Leptin and Ghrelin

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They have antagonistic effects. Leptin increases the feeling of being full, or satisfied, while ghrelin increases your appetite.

People who are obese may have either deficient leptin levels or elevated ghrelin levels. They always feel hungry.