Week 8: Internal Regulation Flashcards
Homeostasis
An active process to maintain a variable within a fixed range, or to maintain a set point
4 features of regulatory system
1) System variable
2) Set point
3) Detector
4) Correctional mechanism
System variable
variable to manipulate
Set point
optimal value of the variable
Detector
monitors the value of the variable
Correctional mechanism
restores the variable’s value to set point
negative feedback
regulatory process that reduces discrepancies
from the set point
basal metabolism
Energy used to maintain a constant body
temperature while at rest
■ 2/3 of total energy dedicated to maintaining basal metabolism
Endothermic
Controlling temperature by the body’s physiological
mechanisms (e.g., humans)
Ectothermic
Controlling temperature by relying on external sources
of heat or cooling. (e.g., reptiles )
What part of the brain contributes to basic motivational behaviours?
Hypothalamus
Which 2 parts of the hypothalamus receive input from thermoreceptors?
Anterior hypothalamus and preoptic area
Evidence of “Homeostatic Redundancy”
POA: Lesions impair physiological response
Lateral H: Lesions impair behavioral response
(in rats)
Homeothermic
having physiological mechanisms in place to maintain constant body temperature, despite changing environments.
Detectors in thermal system
Hypothalamus, spinal chord, brainstem
Allostasis
“stability through change”
Adaptive processes that maintain homeostasis
Whereas homeostasis waits for errors and then corrects them, allostasis uses prior knowledge to prevent and minimize errors.
Satiety mechanism
A brain mechanism that causes cessation of hunger (or thirst), produced by adequate and available supplies of nutrients/energy (or water/fluid)
– Instead of regulating the system variable (i.e.,
nutrients/energy or water/fluid), it monitors the
correctional mechanism (ingestion)
■ an anticipatory mechanism
Regulation of water in the body is essential for:
- rate of chemical reactions
- Maintenance of blood pressure
Two kinds of thirst:
Osmotic thirst
Hypovolemic thirst
Osmotic thirst
Too much sodium chloride (salt) in the extracellular fluid
(e.g., From eating a big bag of salty chips
Hypovolemic thirst
Loss of volume of extracellular fluid (e.g., from
excessive sweating or bleeding)
osmotic pressure
Tendency of water to move from areas of
low solute concentration to areas of high solute
concentration
What do osmoreceptors detect?
osmotic pressure and salt content in blood
Where are osmoreceptors located?
third ventricle (circumventricular areas of the brain)
- Organum vasculosum laminae terminalis (OVLT) (also
receives info from digestive tract)
– Subfornical organ (SFO)
Vasopressin
an antidiuretic hormone released from the pituitary (therefore retain water)
– Vasopressin regulates the kidneys to reabsorb water from urine and excrete concentrated urine to rid the body of excess sodium while conserving water
What controls rate of vasopressin released from posterior pituitary?
Supraoptic nucleus and PVN
Satiety Mechanism Process (6 steps)
- Body loses water (body fluids)
- Detectors signal loss of water (detectors)
- Drinking occurs (correctional mechanism)
- Stomach fills with water, sends signal to brain (stomach)
- Satiety mechanism inhibits further drinking (satiety mechanism)
- Water is absorbed (stomach), body fluids back to normal (body fluids)
Change in blood pressure is measured by:
baroreceptors of heart, blood vessels, and kidneys
Digestion
the process by which food is broken down to provide energy
Digestion pathway
■ Begins in mouth (enzymes for carbs)
■ Esophagus to stomach (hydrochloric acid and
enzymes for proteins)
■ Small intestine (enzymes for proteins, fats,
and carbs)
■ Absorbed into bloodstream
■ Big intestine absorbs water and minerals
(lubricated and expelled)
2 phases of digestion:
Absorptive/digestive phase
fasting phase
Absorptive/digestive phase
– Nutrients are absorbed from the digestive system
– Insulin is secreted from pancreas
– Glucose feeds cells
– Amino acids aid in protein synthesis
– Excess glucose stored in liver (as glycogen) and adipose tissue (triglycerides)
– Fat is stored in adipose tissue
Fasting phase
– Nutrients not available from the digestive system
– Glucagon secreted from pancreas (short-term)
– Glucose derived from glycogen and triglycerides (fatty acids, glycerol) (long-term)
Insulin
pancreatic hormone that enables glucose to enter the cell
Rise and fall of insulin
■ Insulin levels rise as someone is getting ready for a meal and after a meal
– Cephalic phase (thought, sight, or smell of food)
– Digestive phase (while eating to transport glucose to cells of the PNS)
– Absorptive phase (glucodetectors of liver to send satiety signal to the brain)
■ Consequently, high levels of insulin generally decrease appetite (satiety mechanism - signals that food is on its way)
■ As insulin levels drop, glucose enters the cell more slowly and hunger increases
Glucagon
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
short-term reservoir
– Located in cells of the liver
– Stores glycogen
– Reservoir reserved for CNS
■ During short-term fasting your liver feeds the brain by converting glycogen into glucose (via glucagon) and releases it into the blood to nourish cells of the CNS.
long-term reservoir
– Located in adipose tissue
– Stores triglycerides
– Triglycerides contain glycerol and fatty
acids
– Increase in triglycerides increases fat
cells
– Important during fasting
■ During log-term states of fasting, the
adipose tissue supplies the brain with
glucose and the rest of the body with fatty
acids
Diabetes Mellitus
-> blood glucose increases, but insulin level is low -> glucose does not enter the cells, leaves in urine and feces; thus hunger remains high ->
blood glucose levels stay high but cells are starving -> hunger ->
eating
What causes you to eat?
- signals from the environment
- signals from stomach
- Metabolic signals
Eating signals from the environment
- Sight/smell of food
- Time of day
Eating signals from the stomach
▪ Stomach releases the hormone ghrelin to signal the
brain
▪ Ghrelin increases with fasting
▪ Injection of ghrelin increases food intake
▪ Ghrelin is suppressed by duodenum
Metabolic signals to eat
▪ Glucoprivation = decreased glucose available to cells that causes hunger (hypoglycemia)
▪ Lipoprivation = decreased fatty acids available to cells
Detectors for metabolic variables:
✓ brain monitors glucoprivation
✓ liver monitors both glucoprivation and lipoprivation
What stops eating?
Satiety signals
Short-term satiety signals
- Stomach
– Distention (via vagus nerve to the brain)
– Gastric receptors that detect presence of nutrients in the stomach ( via splanchnic nerve to brain) - Intestinal factors (duodenum):
– Chemoreceptors in the duodenum; send info to brain about amount and type of nutrient;
– CCK hormone in the duodenum when distended; controls rate of stomach emptying
– PYY increases in same proportion of calories that are ingested - Liver receives nutrients from intestines and sends satiety signal to brain
- Insulin receptors in hypothalamus
Long-term satiety signals
■ When fat reserves decrease, leptin levels decline, and you react by eating
more and becoming less active, to save energy.
■ When leptin levels return to normal, you eat less and become more active
■ Ob KO mouse: mutation of Ob gene that disrupts production of leptin
Leptin
hormone released by fat cells of adipose tissue determine long-term satiety cues
Brain mechanism in hunger and satiety:
Hindbrain - Medulla Oblongata
▪ Contains neural circuits that detect hunger and satiety
signals and controls some aspects of food intake
▪ Receive taste info from tongue; info from stomach,
duodenum, & liver; detectors for glucose
▪ hunger increases activity of neurons in the medulla
▪ lesions abolish glucoprivic feeding
Brain mechanism in hunger and satiety:
Hypothalamus - Ventromedial hypothalamus
Inhibits eating (Satiety center)
■ Lesion leads to overeating (frequent eating of normal meals) and weight gain.
■ Eating normal sized meals, but frequently (increased insulin and glucoprivation)
Brain mechanism in hunger and satiety:
Hypothalamus - Lateral hypothalamus
(a.k.a. Hunger/Eating center) controls
eating/drinking behavior
■ Lesion causes cessation of eating and drinking
■ Lesions cause under-eating, weight loss.
■ Communicates with taste pathway of solitary nucleus of medulla.
■ Communicates with cortex to facilitate ingestion, swallowing and perception of food.
■ Communicates with spinal cord for digestion of food.
■ Communicates with pituitary to secrete hormones which further increase insulin
Important hunger-satiety pathway:
Arcuate Nucleus (AN) -> Paraventricular Nucleus (PVN) -> Lateral hypothalamus (LH)
Hunger-satiety pathway: Arcuate Nucleus (AN)
“Master Area” for appetite control
■ has neurons sensitive for hunger (ghrelin) and satiety (cck, insulin)
Hunger-satiety pathway: Paraventricular Nucleus (PVN)
Inhibits the lateral hypothalamus
■ Receives input from arcuate nucleus (excited or inhibited)
■ Important for satiety
■ Lesions cause increased meal size, especially increased intake of carbohydrates
Hunger-satiety pathway: lateral hypothalamus
Hunger/Eating center: controls
eating/drinking behavior
Hunger chemicals in the hypothalamus
■ Production of orexigens (appetite inducing chemicals)
■ In AN: neuropeptide Y (NPY) and agouti-related peptide (AgRP)
– Project to Lateral hypothalamus (+) and PVN (-)
– Inhibit satiety cells of the AN
■ In LH: melanin-concentrating hormone (MCH) & orexin
– Project to brain areas important for feedings (motivation, motor) and to the ANS
(metabolism)
Satiety chemicals in the hypothalamus
■ Production of melanocortins (appetite suppressing chemicals)
■ In AN: Alpha-melanocyte-stimulating hormone (α-MSH)
– Stimulates PVN which inhibits LH
– Inhibit hunger cells of the AN
■ Leptin receptors inhibit NPY/AgRP neurons
– Excitatory effect on melanocortin
■ PYY in gastrointestinal tract inhibit NPY/AgRP of AN
The Hunger system
✓Hunger-sensitive neurons (NPY/AgRP) of the AN are stimulated by Ghrelin from stomach and/or from glucose-sensitive cells of the medulla.
✓Hunger-sensitive neurons of AN inhibit satiety cells of AN (α-MSH) and inhibit project to PVN.
✓AN stimulate orexigens (MCH and Orexin) of the Lateral hypothalamus
✓Projections from LH innervate other brain regions to facilitate motivation and eating behaviors
The Satiety system
✓Hunger-sensitive neurons in AN (NPY/ArGP) are inhibited by PYY and Leptin.
✓Satiety-sensitive neurons in AN (α-MSH) are stimulated by Leptin and insulin.
✓Satiety-sensitive neurons of AN project to PVN and excite satiety action of PVN
Eating disorders
obesity
obesity: Etiology
Syndromal obesity: Prader-Willi syndrome
anorexia nervosa
bulimia nervosa
Obesity
■ Definition: BMI > 30
■ 60% adults and 30% children
■ Increased health problems:
– CHD and Stroke
– Type II Diabetes
– Arthritis
– Cancer
– Cognitive impairment,
– Early mortality
obesity: etiology
■ Epigenetic changes in DNA expression (Dutch famine and Obese parents)
– Children born after maternal bariatric gastrointestinal bypass surgery are less obese and exhibit improved cardiometabolic risk profiles carried into adulthood compared with siblings born before maternal surgery.
■ Genetic mutations
– Heredity Leptin Deficiency
– Recessive leptin gene mutation
■ Intrauterine environment
– Maternal diabetes
■ Lifestyle behaviors
syndromal obesity: Prader-willi syndrome
■ Genetic disruption on chromosome 15 which affects
hypothalamic development and function
■ No satiety signals
■ High ghrelin levels, normal NPY/AgRP, normal leptin
receptors
Anorexia nervosa
Excessive dieting and compulsive exercise due to
exaggerated concern with overweight
bulimia nervosa
binging followed by purging
benefits of Mediterranean/prudent diet
– Decreased risk of cancer, CVD,
Parkinson’s and Alzheimer’s disease
– Reduced risk of depression
– Lower Allostatic Load or Biological
Stress
