4.9 Appetitive Flashcards

(33 cards)

1
Q

catabolic

A

releasing and using energy

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2
Q

anabolic

A

acquiring and storing energy

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3
Q

set point theory

A

there is a preferred body weight that the brain defends

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4
Q

orexigenic

A

substances/signals that stimulate hunger, increase food intake

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5
Q

anorexigenic

A

substances/signals that suppress hunger, decrease food intake

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6
Q

function of nucleus of solitary tract

A

integrates visceral sensory information related to hunger/satiety

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7
Q

outline leptin

A

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)

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8
Q

outline insulin

A

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

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9
Q

outline ghrelin

A

orexigenic
Hormone released from stomach when empty
Inject w ghrelin = people feel hungry
Activates reward pathways

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10
Q

GLP-1 - glucagon-like peptide

A

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

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11
Q

explain how ghrelin acts on brain

A

Ghrelin: comes in through stomach, causes arcuate nucleus to stimulate the lateral hypothalamus and inhibit PVN, increasing appetite

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12
Q

explain how leptin, GLP-1, insulin act on brain

A

cause arcuate nucleus to inhibit lateral hypothalamus and stimulate PVN, decreasing appetite

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13
Q

what does PVN do when it’s hungry

A

activates pituitary gland (starts HPA axis), fight or flight into medulla → autonomic nervous system

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14
Q

what does LH do when it’s full

A

sends rest/digest to medulla → autonomic nervous system

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15
Q

outline missed lunch effect (subjective state of hunger)

A

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

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16
Q

outline Weingarten’s experiment on external cues role in appetite. what does it indicate overall?

A

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

17
Q

what causes dopamine release, in relation to food?

A

Conditioned stimuli, NOT FOOD

18
Q

homeostatic signals

A

internal, energy-driven signals involving PVN –> leptin, insulin (stimulating PVN, inhibiting ARC), ghrelin (inhibits PVN, stimulates ARC)

19
Q

hedonic signals

A

external, reward-driven signals involving VTA, NAc, cortex –> external signals → processes of mesolimbocortical dopamine and appetite

20
Q

role of striatum in food-relevant cues

A

dopamine centre → learning and behaviour

21
Q

role of amygdala in food-relevant cues

A

affective response, assigns emotional value (valence) to food-related stimuli

22
Q

role of orbitofrontal cortex in food-relevant cues

A

adjusts stimuli reward and value relative to emotional state

23
Q

role of insula cortex in food-relevant cues

A

receives taste information and internal body states

24
Q

explain the role of the orbitofrontal cortex (OFC) in eating

A

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)

25
outline the stimulu-specific satiety BANANA experiment
Before eating, banana odour activated the OFC strongly (i.e. rewarding) After eating as many bananas as they liked, the same banana odour when presented during a scan produced much less OFC activity Vanilla didn’t change much Shows: brain reduces the reward value of a just-consumed food → reward value is encoded relative to motivational state
26
what is the effect of placebo pleasantness?
descriptions of food as “rich”, “fresh”, “delicious” is associated with higher activity in OFC
27
outline experiment explaining how Highly palatable foods disguise effect of satiety:
Soup is refilled through a tube, and participants are unknowingly given a carb or fat preload (i.e. to ensure they’re not hungry) Participants are more of the palatable lunch regardless of how much energy they had already consumed, whereas normally after a high-energy preload people eat less at the next meal
28
changes to WHICH type of mechanisms are most closely associated with obesity?
hedonic
29
3 big changes in regulation in obesity"
Reduced susceptibility to internal satiety signals Reduced dopamine regulation Highly susceptible to external sensory cues and food palatability
30
higher BMI is correlated with lower what receptor
D2
31
similarities between obesity and addiction: both include...
dopamine involvement, reward system activation, cue-induced craving, compulsive behaviour, neuroadaptation → NAc strengthens salience of stimuli and decreases self-regulation
32
what does GLP-1 do for addiction?
reduce addictive behaviour for drugs of abuse, addiction
33
how does (simply) GLP-1 work for addiction?
Targets nucleus accumbens and VTA to dampen dopamine release, making the drug/food feel less rewarding