1) short-term - located in cells of liver and the muscles, filled with glycogen

• insulin prompts the liver to convert glucose to glycogen and store it

• when there is a fall in glucose, brain signals for insulin release from pancreas to be stopped

• instead, the pancreas secretes glucagon which stimulates the conversion of glycogen back to glucose

• found beneath skin and in the abdominal cavity

• cells can expand enormously

• this is what keeps us alive when we are fasting

• glucagon stimulates conversion of triglycerides to fatty acids and glycerol

• When we awake in the morning, our brain is living on the glucose from the liver and everything else is utilizing long-term storage fats which have been converted to fatty acids and glycerol

• cells except the brain can directly metabolize fatty acids, but liver has to convert glycerol to glucose so brain can use it

• insulin must be present for cells to be able to use glucose, as it enters the cell when glucose transporters are activated by insulin - if no insulin, then glucose can’t get in

• exception is the CNS, which doesn’t have insulin receptors triggering its glucose transporters

WHAT STARTS A MEAL?

1) social, environmental factors

• meal times are set, unlike for rats who eat when hungry

• more people present, more we eat

• sensory-specific satiety - if we eat only one food, we soon become tired of it

• conditioned flavor aversion - usually taste and olfaction involved

• hunger inversely related to the amount of nutrients left over from previous meals

• glucoprivation - depriving cells of glucose

• lipoprivation - depriving cells of lipids (fats)

• we have cells which detect falls in glucose (in hindbrain) and others which detect low levels of lipids (in abdominal cavity)

• receptors in liver detect their own rate of metabolism and send "hunger" signals to the brain when metabolism is low - this is why diabetics can have high amounts of blood glucose and still be hungry (glucose can’t get into cells with insulin receptors, as diabetics lack insulin, so cells "starve")

1) head factors

• eyes, nose, tongue, throat

• appearance, odor, taste, texture, and temperature

• we learn to adjust intake of foods based on their caloric value

• stomach has receptors that detect presence of nutrients

• it is not the volume of food

• signals from stomach only effective when the animal is familiar with the food

• so, we learn to combine head factors with gastric factors

• cholecystokinin (CCK) - peptide secreted by the duodenum, controls rate of stomach emptying

• CCK suppresses eating, but may be due to causing nausea

• last stage of satiety

• when liver receives nutrients from intestines, it signals brain to produce satiety (combined with info from intestinal factors)

1) brain stem - decerebrate animals can still eat, distinguish tastes

• nucleus of the solitary tract - interaction between excitatory effects of taste and satiety signals occurs in NST

• ventromedial hypothalamus (VMH) - lesion produces overeating and obesity; liver and adipose tissue are unable to release their nutrients during the fasting phase, so animal has to keep eating in order to maintain supply of nutrients in the blood

• damage to axons of paraventricular nucleus also occurs with such a lesion

• lateral hypothalamus (LH) - abolish eating behavior, animals hardly move, pay little attention to stimuli around them

• damage to dopaminergic pathways also occurs with such a lesion

• neuropeptide Y - neuromodulator, if injected into hypothalamus, causes ravenous eating

• some neurons respond to sight or smell of food if animal is hungry - motivation

• metabolism seems to be the key - most likely genetic

• if metabolism is inefficient, then person is less likely to be obese

• if efficient metabolism, then can get by on less food, more likely to be obese

• starvation causes a body to be more efficient

• drug treatment

• anorexics interested in, possibly obsessed with, food

• anorexics have a fear of being fat - fat phobic?

• fasting results in increased activity (allows breakdown of long-term reserves)

• anorexics have enlarged ventricles and widened sulci on CT scans

• neuropeptide Y may be involved (contributes to obsession with food)