Chapter 9: Homeostasis Hunger and thirst
Gherlin
hunger hormone released by stomach endocrine cells- appetite stimulant rise during fasting; drop after eating some obese people have elevated gherkin levels
Two sets of neurons in hypothalamus have opposing effects
NPY/AgRP POMC/CART
But the brain can recover , if overeating stops
Newborn hypothalamic cells become NPY/AgRP and POMC neurons these new neurons are responsive to fasting and leptin
Osmotic thirst
Occurs when extracellular fluid becomes too salty
LH lesión destroy?
Or exigen if LHA
angiotensin cascade
*Angiotensinogen (in blood)* Enzyme: Renin (from kidneys) *Angiotensin I* Enzyme: Converting enzyme *Angiotensin II* Enzyme: Aminopeptidase *Angiotensin III*
What does VMH destroy ?
A or exigencia PVN
What receptors does hypovolemic thirst use and define it
Baroreceptors in blood vessels and heart detect the initial drop. Brain activates thirst and salt craving arteries constrict to raise BP
Obesity and reduced metabolism
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 can increase it
Larger ínsula
Brain area active when you experience disgust
Larger órbita frontal cortex
Brain area that tells you your shouldn't do that'
Glycogenesis
Converting glucose to glycogen , using pancreases hormone insulin
What's happened if the leptin production are defects
Defects in leptin production or sensitivity give a falsely low report of body fat, causing animals to overeat obese people are leptin-resistant Overnutrition inflames the hypothalamus - obesity , diabetes , and heart disease
Treatment of obesity
Eat less : 500 to 1000 calories modify behavir exercise Don't eat at night treat as an addiction -they have fewer dopamine D2, receptors and associated lower prefrontal lobe metabolism peptides that induce eating target dopamine neurons anti-addiction drugs are somewhat effect in weight loss
Leptin
Fat cells produce leptin and secrete it into the bloodstream
Lipids
For long term storage are fat tissue
Glucose
Fuel for energy
What are the energy utilization for hunger ?
Glucose glycogen glycogenesis lipids
High calorie diets cause
Hypothalamic scarring and microglial activation , and 15% reduction of proopiomelanocortin (POMC) neurons, which are normally activated by leptin to block eating and increase energy expenditure
osmosensory neurons
In anterior hypothalamus (OVLT) Respond to rise in blood osmotic pressure (causes pituitary to release antidiuretic hormone) Their cell membranes shrink, opening mechanical-gated Na+ channels respond to increased osmotic pressure by causing the pituitary to release antidiuretic hormone
Glycogen
Is glucose stored for short term in the liver
Hypovolemic thirst
Is triggered by a loss of lucid volume: the concentration has not changed- salt and ions are also
ventromedial hypothalamus
Lesions cause obesity Lesiones animals exhibit overeat until they become obese increased weight stabilizes - this weight is maintained even after food manipulations
Overeating causes brain damages
Overeating—> hypothalamic inflammation —> inhibits neurogenesis , reset your set point
*Brain Control of Drinking
SFO- subbfornical organ
Leptin inhibits AgRP
Stimulates POMC neurons
What does hypovolemic cause to release ?
Vasopressin (antidiuretic)- induces blood vessel contraction and so reduces blood glow to the bladder diabetes insípidus- vasopressin is not produced - kidneys send more urine to the bladder, resulting in chronic thirst
gastric bypass surgery
Weight loss average 25% and is long-lasting (compared to 5%-10% with dieting and relapse within a year reduces gherkin and increase PYY and GLP-1, reducing hunger reduces mortality and has many health benefits
lateral hypothalamus (LH)
a brain region that produces hunger when activated lesioned animals stop eating , but resume and stabilize their weight at a new , lower level
Bulimia
an eating disorder characterized by episodes of overeating, usually of high-calorie foods, followed by vomiting, laxative use, fasting, or excessive exercise
anorexia nervosa
an eating disorder in which an irrational fear of weight gain leads people to starve themselves
What are the effects of Angiotensin II??
increases blood pressure by stimulating kidneys to reabsorb more water and by releasing aldosterone 1. Blood vessels constrict 2. Circumventricular organs trigger drinking 3. Vasopressin is released 4.aldosterone is released
Homeostatic
self-regulating System use our behavior to keep things balanced negative feedback systems are the main homeostatic mechanisms if a desired set is deviated from, compensatory action begins.
POMC/CART
when these neurons are stimulated they decrease appetite raise metabolism —> weight loss
NPY/AgRP
when these neurons are stimulated they increase appetite lower metabolism —> weight gain