Hunger and Thirst

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Last updated 10:44 PM on 11/29/25
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27 Terms

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Israel Kamakawiwo’ole

Obese, 757 lbs

Died of heart failure at 38

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Homeostatic systems use our behavior to keep things _________

Balanced

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Negative feedback systems

Main homeostatic mechanisms
Desired set point deviations triggers compensatory actions

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Types of thirst

Hypovolemic:

  • Stimulated by low extracellular/intravascular volume

Osmotic thirst:

  • Stimulated by high extracellular solute concetration

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Hypovolemic thirst

Baroreceptors in blood vessels and heart detect initial drop → brain activates thirst and salt craving → arteries constrict to raise BP

Hypovolemia → vasopressin release

  • Constricts blood vessels and reduces blood flow to the bladder

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Vasopressin deficiency

Kidneys send more urine to the bladder → chronic thirst

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Angiotensin Cascade

Kidneys release renin wen blood volume decreases → formation of angiotensin II

  • Which constrict blood vessels

  • Circumventricular organs trigger drinking

  • Vasopressin is released

  • Aldosterone is released

Angiotensiogen → Angiotensin I → Angiotensin II → angiotensin III

<p>Kidneys release renin wen blood volume decreases → formation of angiotensin II</p><ul><li><p>Which constrict blood vessels</p></li><li><p>Circumventricular organs trigger drinking</p></li><li><p>Vasopressin is released</p></li><li><p>Aldosterone is released</p></li></ul><p></p><p>Angiotensiogen → Angiotensin I → Angiotensin II → angiotensin III<br></p>
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Brain control of drinking

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

<p>Circulating angiotensin II acts in the subfornical organ to signal other brain sites to initiate drinking.</p>
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Osmotic thirst

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

  • Respond to increased osmotic pressure by causing pituitary to release antidiuretic hormone.

Cell membranes shrink → opening mechanical-gated Na+ channels

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Dehydration and rehydration summary

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Why don’t diets work?

Energy expenditure adjusts in response of nutrition
BMR falls at the start of a diet to prevent losing weight

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Obesity and reduced metabolism

BMR:

  • Energy required to fuel brain/body and maintain temperature

  • 75% EE in average sedentary student

Heredity accounts for 40% of BMR

Activity can increase BMR

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Energy storage/Utilization

Glucose: the principal fuel for energy.

Glycogen: glucose stored for short term in the liver

Glycogenesis: Converting glucose to glycogen using pancreas hormone insulin

Lipids: Long term storage, fat tissue

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Metabolic rate variations

Up until age 1 calorie burning is at its peak

From age 1 to about age 20, metabolism gradually slows

From age 20 to 60, it holds steady

After age 60, it declines about 1 percent a year

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Brain ________ insuline and glucose levels with other signals to decide when to start/stop eating.

integrates

<p>integrates</p>
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Leptin

Fat cells produce and secrete them into the bloodstream.
Defects in leptin production/sensitivity give a false low report of body fat.
Obese people are leptin-resistant
Overnutrition inflames the hypothalamus → obesity, diabetes, and heart disease.

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Ghrelin

Appetite stimulant
Released by stomach/gut endocrine cells
Rises during fasting

Drops after eating

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Prader-Willi syndrome

Causes a sense of hunger.

Genetic disease

Ghrelin levels are elevated

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Hypothalamus as the hunger control center

Lateral:

  • Lesions lead to the refusal to eat, destroy hunger-causing LHA

  • Resume and stabilize their weight at new, lower level

Ventromedial:

  • Lesions lead to obesity (eating too much), destroy hunger ending PVN

  • Increased weight stabilizes

  • New weight maintained even after food challenges

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Neurons groups in hypothalamus

NPY/AgRP → neuropeptide Y and agouti-related peptide

  • Stimulate appetite and lower metabolism

  • Ghrelin stimulates them.


POMC/CART → pro-opiomelanocortin & cocaine and amphetamine-related transccript

  • Inhibite appetite

  • Raise metabolism

  • Stimulates by leptin

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Brain damage from overeating

Hypothalamic inflammation → inhibits neurogenesis, resets set point.

Hypothalamic scarring, microglial activation, fewer POMC neurons

Can recover if overeating stops

  • Newborn hypothalamic cells can become POMC neurons.Anore

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Anorexia Nervosa

Restricting or binge eating/purging

  • Refuse to maintain body weight

  • Fear of gaining

  • Body image disturbance

  • Highest mortality rate

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Bulimia

  • Recurrent binge eating

  • Recurrent inappropriate compensatory behavior

  • 2x/wk for 3 months

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Women with anorexia/bulimia

40% childhood anxiety disorders

90% depression

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246 women with eating disorder

30% attempted suicide

5% died

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Teen girls with anorexia

Larger insula → disgust

larger orbitofrontal cortex → you shouldn’t do that

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Obesity treatment

Eat less

  • deficit of 200 calories

Exercise

  • Strenuous aerobic activity for over 200 minutes per week

  • Long time

  • with calorie restriction

  • Walking doesn’t count

Glucagon-like peptide agonists

  • Mounjaro

  • Ozempic