Homeostasis

allostasis

adaptive way body changes set point depending on the situation

MAINTAIN STABILITY via physiological or behavioral processes

seasonal changes in body fat lead to change in set point

in well-fed state

insulin

puts glucose into cells

glucose

stored as glycogen in liver and muscles or oxidized

both lower level of metabolic fuels in blood

in fasting state

brain gets glucose

need to raise blood glucose levels

decrease insulin

increase glucagon

glucagon takes glycogen and glucose out of cells and use it

gluconeogenesis

synthesis of glucose from amino acids (not glycogen)

glycogenolysis

breakdown of stored glycogen from liver

lipolysis

sympathetic stimulation of fat breakdown

hunger/feeding and satiety

hunger

MOTIVATION to find and ingest food

satiety

cessation of eating

other factors

seasonal variation in body mass

prairie dogs and other rodents

reproductive status

e.g. nursing mom

food availability

energetic demands

amenorrhea in athletes and dancers

social/cognitive factors in humans

GI hormones serve as satiety signals that converge on the dorsal hindbrain

hormonal control

orexigenic

increase food intake

GHRELIN

anorexigenic

decreases food intake

INSULIN

LEPTIN

anorexia = loss of appetite; aphagia = absence of feeding behavior

produced in GI tract

levels rise right before a meal

stimulate feeding behavior

produced in adipose tissue

dependent on range of need (overweight super hungry if don't eat because range is higher)

produced in beta cells of pancreas

levels rise in response to food intake

stimulates satiety

function to put glucose into cells

functions to increase satiety (lower food intake) and to increase energy expenditure

GLUCAGON

produced in alpha cells of pancreas

removes glucose from cells SO IT CAN BE USED

does not affect behavior though

ALDOSTERONE

specific hungers for salt

released from adrenals

helps with reabsorption of sodium in kidneys

if levels deficient, seek out salty foods

Diabetes

Type I

autoimmune disorder targets beta-cells of pancreas - INSULIN DEFICIENCY

rapid onset

treat with insulin

Type II

tissues become INSENSITIVE TO INSULIN

not taking up glucose

hyperglycemia

triggers additional insulin secretion

when liver and muscle cells are insensitive to insulin, the glucose gets stored in adipose tissue (LIPOGENSIS)

result

increased appetite

increased food intake

body weight gain

NEED FOR GLUCOSE BECAUSE INSULIN CANNOT TAKE IT OUT OF THE CELLS

characterized by

hyperphagia

excess hunger/appetite

hyperglycemia

if left untreated, can be toxic to nervous and circ systems

increased thirst/urination

hyperinsulinemia

too much insulin

results in

increased glucose uptake into cells

inhibited lipolysis

low blood sugar