catabolic
releasing and using energy
anabolic
acquiring and storing energy
set point theory
there is a preferred body weight that the brain defends
orexigenic
substances/signals that stimulate hunger, increase food intake
anorexigenic
substances/signals that suppress hunger, decrease food intake
function of nucleus of solitary tract
integrates visceral sensory information related to hunger/satiety
outline leptin
anorexigenic
Hormone produced by adipose tissue (fat cells) in proportion to body fat stores → the more fat cells you have, the more leptin you produce, starts to slow down how much you eat (it’s a way for your brain to know if you have enough body fat)
outline insulin
anorexigenic
Hormone released by pancreas in response to rising blood glucose levels after a meal
Signals the brain (hypothalamus) about energy availability
Acts on arcuate nucleus
outline ghrelin
orexigenic
Hormone released from stomach when empty
Inject w ghrelin = people feel hungry
Activates reward pathways
GLP-1 - glucagon-like peptide
Oregixenic
Hormone released by small intensive in response to food, esp carbs + fats
Satiety signal,
Slows gastric emptying, stimulates insulin release to aid glucose regulation, acts on hypothalamus and brainstem to promote feelings of fulness
Semaglutide
explain how ghrelin acts on brain
Ghrelin: comes in through stomach, causes arcuate nucleus to stimulate the lateral hypothalamus and inhibit PVN, increasing appetite
explain how leptin, GLP-1, insulin act on brain
cause arcuate nucleus to inhibit lateral hypothalamus and stimulate PVN, decreasing appetite
what does PVN do when it’s hungry
activates pituitary gland (starts HPA axis), fight or flight into medulla → autonomic nervous system
what does LH do when it’s full
sends rest/digest to medulla → autonomic nervous system
outline missed lunch effect (subjective state of hunger)
Subjective state of hunger not always tied to body’s need for energy or how long it’s been since we’ve eaten → more tied to time of day/when we typically get hungry
outline Weingarten’s experiment on external cues role in appetite. what does it indicate overall?
rats given food + CS together randomly throughout day
given free access to food but exposed to CS for 2 minutes
eat 20% pf daily caloric intake during those 2 minutes
Huge amount of eating behaviour is tied to conditioning, not energy needs
what causes dopamine release, in relation to food?
Conditioned stimuli, NOT FOOD
homeostatic signals
internal, energy-driven signals involving PVN –> leptin, insulin (stimulating PVN, inhibiting ARC), ghrelin (inhibits PVN, stimulates ARC)
hedonic signals
external, reward-driven signals involving VTA, NAc, cortex –> external signals → processes of mesolimbocortical dopamine and appetite
role of striatum in food-relevant cues
dopamine centre → learning and behaviour
role of amygdala in food-relevant cues
affective response, assigns emotional value (valence) to food-related stimuli
role of orbitofrontal cortex in food-relevant cues
adjusts stimuli reward and value relative to emotional state
role of insula cortex in food-relevant cues
receives taste information and internal body states
explain the role of the orbitofrontal cortex (OFC) in eating
evaluation of food-related rewards, determines appeal of food, decisions about eating: whether to continue (based on palatability) or stop (based on lower reward with continued consumption)