Internal Regulation

three types of heredibility for obesity

1) syndromal: when a gene causes a medical problem that includes obesity 2) monogenic obesity: occurs when a signle gene leads to obesity without other physical or mental abonromalities 3) Polygenic or common obesity: relates to many genes, each of which slightly increases probability of obesity (FTO gene)

leptin

A hormone produced by adipose (fat) cells that acts as a satiety factor in regulating appetite. Only in vertebrates more fat cells, more leptin Leptin signals to the brain about fat reserves, when fat reserves decrease so does leptin, and you react by eating more and becoming less active, to save energy

Type one diabetes

Diabetes which is caused when the pancreas cannot make insulin. Low insulin, so higher than normal levels of blood glucose People with diabetes eat more because their cells are starving but excrete most of their glucose and lose weight

production of fever

Immune system: that react to an infection by sending prostaglandins and histamines to the preoptic area or anterior hypothalamus Chemcials cause shivering, increases metabolism, and produce a fever

Satiety signals

Leptin (fat cells)( long term) Insulin (pancreas)( intermediate) CCK (duodenum) (short term) Glucose (short term) Excite satiety motive which releases: glutamate and melanocortin (facilitate that inhibition (??) excitatory on PVN)

hunger sensitive set of cells in arcuate nucleus

NT ghrelin Stomach releases ghrelin during a period of food deprivation, and triggers stomach contractions Ghrelin also acts on the hypothalamus to increase appetite Most output goes to periventricular nucleus (PVN) of the hypothalamus Certain types of PVN inhibit lateral hypothalamus (important for eating) Inhibitory NTs: GABA, neuropeptide Y and agouti related peptide Increase in heating and arousal and hunger: inhiting an inhibitory so net excitation If the inhibition of PVN is strong enough, rats eat huge meals (inhibit the PVN to inhibit the lateral hypothalamus- so eats large meals?)

the amygdala sends two kinds of input to the lateral hypothalamus

One path inhibits eating during illness and mediates aversion to foods Other path stimulates eating in response to highly tasty foods

Vassopressin or ADH

Osmotic thirst (Increase vasopressin increases thirst When vasopressin is not present, excrete lots of fluid (urination))

lateral hypothalamus

The part of the hypothalamus that produces hunger signals Output from the PVN acts on this Controls insulin secretion, alters taste responsiveness, facilitates feeding in other ways Stimulation of this area increases drive to eat

homeostasis

Walter Cannon Temperature regulation and other biological processes that keep body variables within a fixed range

sodium specific hunger

a strong craving for salty foods -develops automatically to restore solute levels in the blood Depends partly on hormones: adrenal glands produce aldosterone

hypovolemic thirst

a thirst resulting from loss of fluids due to bleeding or sweating Osmotic pressure stays the same, still need fluid Heart has trouble pumping blood to the head, and nutrients do not flow as easily as usual to cells Receptors on your kidneys and blood vessels react to decreased blood pressure by sending a messages to the brain to release vasopressin, which constricts blood vessels and conserves the fluid you still have Kidneys also release renin, which splits a portion off angiotensinogen (large protein in the blood) to form angiotensin I which is then converted to angiotensin II which constrict blood vessels, compensating for the drop in blood pressure Thirst based on low volume, need to restore lost salts not just water So drink saltier waters, water would just dilute your blood volume and not restore the lost salts and other things (DC).

ectohermic

amphibians, reptiles, and most fish They depend on external sources for body heat instead of generating it themselves Lack shivering and sweating Use behavioral mechanisms

bulimia nervosa

an eating disorder characterized by episodes of overeating, usually of high-calorie foods, followed by vomiting, laxative use, fasting, or excessive exercise Goes between binging and strict dieting People with bulimia have increase production of ghrelin after treatment: body grehlin goes back to normal

ways in which the lateral hypothalamus promote eating

axons from lateral hypothalamus to the nucleus of the tractus solitarius, part of the taste pathway, alter the taste sensation and the salivation response to the tastes: hunger makes food taste better Axons from the lateral hypothalmus extend to several parts of cerebral cortex: facilitates ingestion and swallowing, causing cortical cells to increase response to taste, smell , sight of food Lateral hypothalmus increases pituitary gland's secretion of hormones that increase insulin Lateral hypothalmus sends axons to spinal cord: controls autonomic responses such as digestive secretions

Digestive steps

begins in the mouth where enzymes in salvia break down carbohydrates. Swallowed: down to stomach where it mixes with hydrocholoric acid and enzymes that digest protein Spinchter opens at end of stomach to release food into small intestine. Small intestine has enzymes that digest proteins, fats, and carbohydrates. Also absorbs digested materials into the blood, which carries those chemicals to body cells that either use them or store them. The large intestine absorbs water and minerals and lubricates the remaining materials to excrete them

eating carbohydrates

body increases secretion of insulin, which moves sugars into storage, and also moves phenylalanine into storage

angiotensin and cholecystokinin

body uses same chemicals in the periphery and in the brain for closely related functions

preoptic area/anterior hypothalamus (POA/AH)

brain area important for temperature regulation, thirst, and sexual behavior Send output to the hindbrain's raphe nucleus, which controls the autonomic responses such as shivering sweating, changes in heart rate and metabolism and blood flow to the skin Integrates several types of info: input from temperature receptors in the skin, organs, and hypothalamus (if hot they sweat, pant, seek coolness) Animal reacts most vigorously if the skin and hypothalamus are both too hot or cold Also receives input from immune system: reacts to infection by sending prostaglandins and histamines to here. Receives input from temperature receptors and immune system

Aldosterone and Angiotensin II

change the properties of taste receptors on the tongue, neurons in the nucleus of the tractus solitarius (taste system) and neurons elsewhere in the brain to increase salt intake Aldosterone: indicates low sodium Angiotensin two: indicates low blood volume Combined effect is substantial

supraoptic nucleus and paraventricular nucleus (PVN)

control rate at which the posterior pituitary releases vasopressin (raises blood pressure by constricting blood vessels)

raphe nucleus

controls mechanisms such as shivering, sweating, changes in heart rate and metabolism, and changes in blood flow to the skin. Seretonin

vagus nerve

conveys info to the brain about the stretching of the stomach walls

after meal

decrease glucose, decrease insulin, increase glucagon

glucose

digestion converts most of the meal into glucose, an important source of energy throughout the body and nearly the only fuel for the brain Two pancreatic hormones: insulin and glucagon, regulate the flow of glucose into cells

allostasis

dynamic changes adaptive way in which the body anticiaptes needs depedning on the situation, avoiding errors rather than just correcting them

osmotic thirst

eating salty foods cause this If you eat something salty, sodium ions spread through the blood and extracellular fluid but do not cross the membranes into cells. Results is a higher concentration of solutes (including sodium) outsdie the cells than inside. Which then allows for osmotic pressure to draw water from the cells into the extracellular fluid. Certain neurons detect their own loss of water and trigger this thirst This thirst is a drive for water that helps restore the normal state. Kidneys also excrete more concentrated urine to rid the body of excess sodium and maintain as much water as possible Not life threatening SALT

meals end after distension (swelling) of..

either stomach or duodenum

insulin

enables glucose to enter the cells This is produced before a meal and after From the pancreas Brain cells do not need insulin: glucose can enter without it

Glycogen

excess glucose from a meal enters the liver Stores it.

concentration of all solutes (molecules in solution)

fluid remains at a near constant level of.15 M (molar) Molarity is a measure of number of particles per unit of solution, regardless of size of each particle This is a set point

endothermic

generate enough body heat to remain significantly above the temperature of the environment Mammals and birds Use physiological mechanisms to keep their core temp nearly constant It is costly, especially in small animals. Small mammals or birds have a high surface-to-volume ratio and therefore radiates heat rapidly. How to beat the heat: evaporation of water (sweat, or licking, or panting) Cold: shivering, muscle contractions generate heat. Or decrease blood flow to the skin, prevents blood from cooling too much (warm organs, cold skin) or Goosebumps or fur puffing out. We do use behavioral mechanisms: so we use less energy

2 hunger signals

grehlin (brain and stomach) Taste input PVN inhibits lateral nucleus (motivation of hunger)

Cholecystokinin

hormone released when the duodenum stretches Limits meal size in two ways: First this hormone constricts the spincter muscle between the stomach and duodenum causing the stomoach to hold its contents and fill more quickly than usual. So it quickens stomach distension (primary signal for ending a meal) Second: this hormone stimulates the vagus nerve to send signals to they hypothalamus, causing cells to release NT that is a shorter version of this hormone. This hormone cannot cross the BBB but it stimulates cells to release the similar NT

aldosterone

hormone that causes the kidneys, salivary glands, and seat glands to retain salt Sodium specific hunger depends partly on this hormone from the adrenal glands

OVLT organum vasculosum laminae terminalis

how the brain detects osmotic pressure Receptors around the third ventricle Receives input from receptors in the digestive tract, enabling it to anticipate an osmotic need before the rest of the body experiences it Blood brain barrier is weak in this area Detect osmotic pressure and blood sodium content when more water is needed..

subfornical organ (SFO)

how the brain detects osmotic pressure Receptors around the third ventricle Blood brain barrier is weak in this area Have neurons that increase thirst and another that suppresses it

flow chart in book

hunger motive system: either Ghrelin signals hunger or you have taste input (excitatory to hunger motive -> release either neuropeptide Y, agouti-related peptide , or GABA (all inhibitory) -> PVN of hypothalamus, -> sends further inhibitory the lateral hypothalmus which then-> release Orexin (increases arousal and motivation) or GABA (goes to other areas to increase feeding) Leptin, long term satiety signal decreases hunger motive Insulin: intermediate term satiety signal inhibits hunger motive Satiety motive: Insulin, leptin, cholecystokinin, or glucose excites satiety motive: releases either glutamate and melanocortin (excitatory) to/ from (?) PVN of hypothalmus: limit food intake

arcuate nucleus

hypothalamus One set of neurons senesitve to hunger signals and a second set sensitive to satiety signals Input to these cells (sets of neurons) come from hormones such as insulin and leptin I think this is for hunger cells in the arcuae nucleus Most output goes to periventricular nucleus (PVN) of the hypothalamus Certain types of PVN inhibit lateral hypothalamus (important for eating) Inhibitory NTs: GABA, neuropeptide Y and agouti related peptide Increase in heating and arousal and hunger: inhiting an inhibitory so net excitation If the inhibition of PVN is strong enough, rats eat huge meals (inhibit the PVN to inhibit the lateral hypothalamus- so eats large meals?)

Lateral preoptic area

hypothalmus control drinking

before meal

increase glucose, increase insulin, decrease glucagon (glucagon: released by the pancreas when glucose levels decrease..)

Osmotic thirst mechanism

increase salt intake-> sodium spread in blood (stomach and digestive tract)--> OVLT and SFO--> hypothalamus--- supraoptic nucleus and PVN---> Increase ADH (anti-diuretic hormone: vasopressin) ---> increase h20 retention, and decrease urination (kidneys)

fever

increased set point for body temp Fever is not something an infection does to the body, it is someting the hypothalamus directs the body to produce. Your body works harder to keep its temp at feverish level Fever above 39 celcius (103 F)does more harm than good (109 F) is life threatening and above

Angiotensin II

increases blood pressure Kidney releases enzyme called renin which splits a portion off of angiotensinogen to form angiotensin one and then to angiotensin two. Also helps trigger thirst Different than osmotic thirst because you need to restore lost salts and not just water: hypovolemic thirst: thirst based on low volume When angiotensin two reaches the brain it stimulates neurons in the third ventricle. These neurson go to the hypothalamus where they release angiotensin two as NT

Eating behavior is

inhibited So to motivate hunger is PVN (NPY- neuropeptide Y, agouti related peptide (AgRP), and GABA) to inhibit lateral nucleus Inhibit the inhibition to get eating behavior

basal metabiolism

most of our used energy (2,600 calories a day, 2/3 go to to temperature regulation) used to maintain a constant body temperature at rest Temp regulation uses brown adipose cells, like muscle cells, burn fuel like muscles do, but release it as heat and not muscle contractions

drive theory

motivated behaviors: staying warm (body temp), hunger, thirst Sweating--> losing salty fluid-> biological mechanisms that note homeostasis has been altered (this produces a "drive" which leads to behavior to put homeostasis back in order If you are losing fluid out of the body by sweating, bleeding, vomiting- drinking water will not satisfy that drive (hypovolemic thirst) seak out fluid with electrolytes or salt

lactase

necessary for mebatbolizing lactose, the sugar in milk Most mammals around weaning lose this enzyme Humans are partial exception to this rule. Genes: ability to metabolize lactose in adulthood is common in societies with a long history of domesticated cattle.

ventromedial hypothalamus

output from here inhibits feeding

duodenum

part of the small intestine adjoining the stomach, major site for absorbing nutrients Nerves from here inform brain not only about distension but also about the type and amount of nutrition Distension of here releases hormone cholecystokinin

orexin

pathway from PVN to lateral hypothalmus releases this (involved in narcolepsy too: deficiency of this leads to narcolepsy) Two roles in feeding: first it increases animals' persistence in seeking food 2nd: increases activity and motivation in general

hypothalamus

physiological changes that regulate body temp depend on this

vasopressin

posterior pituitary releases this hormone Raises blood pressure by constricting blood vessels Increased pressure helps compensate for decreased blood volume also known as antidiuretic hormone (ADH: it enables the kidneys to reabsorb water from urine and therefore make the urine more concentrated (Diuresis means urination) Also produced while sleeping so you can preserve body water while you cannot drink Helps you get through the night without needing to go to the bathroom Increase vasopressin increases thirst When vasopressin is not present, excrete lots of fluid (urination)

Allostasis

process by which the body achieves stability through physiological change

negative feedback

processes that reduce discrepancies from the set point are negative feedback Something causes a distrubance and behavior proceeds until it relieves the disturbance

Satiety sensitive cells of the arcuate nucleus

receives several input Distension of intestines triggers neurons to release NT cholecystokinin, short term signal Blood glucose, short term signal, directly stimulates satiety cells in the arcuate nucleus and prompts pancreas to release insulin, which also stimulates satiety cells Leptin from body fat is a long term satiety signal Nicotine also stimulates satiety neurons Axons from the satiety sensitive cells of arcuate nucleus deliver an excitatory message to the PVN releasing melanocortins and glutamate Melanocortin limit food intake

anorexia nervosa

refusal to eat enough to maintain a healthy body weight

two kinds of cells in the arcuate nucleus of hypothalamus

regarded as the master area for controlling appetite Axons extend from the arcuate nucleus to other areas of the hypothalamus

reproductive cells

require cooler temperatures Testes outside the body

set point

single value that the body works to maintain

glucagon

stimulating the liver to convert some of its stored glycogen back to glucose Pancreas increases release of this when hungry

input from temperature receptors

temperature receptors input (skin, organs, hypothalamus) -> POA/AH (can sense own temp)--> raphe nucleus (which controls the autonomic responses such as shivering sweating, changes in heart rate and metabolism, and blood flow to the skin)

Osmotic pressure

tendency of water to flow across a semipermeable membrane from the area of low solute concentration to the area of higher concentration Semipermeable membrane is one through which water can pass but solutes cannot Membrane surrounding a cell is almost a semipermeable membrane because water flows across it freely and various solutes flow either slowly or not at all between the intracellular fluid inside the cell and the extracellular fluid outside it. This pressure occurs when solutes are most concentrated on one side of the membrane than the other Requires energy- going against concentration