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