Hunger Flashcards

1
Q

homeostasis

A

maintenance of the body’s internal enviro within a narrow physiological range (there’s an optimal level to maintain)

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2
Q

how does homeostasis occur

A

negative feedback -change detected & negative feedback elicits compensatory mechanisms

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3
Q

main brain area involved in homeostasis

A

hypothalamus (Ramsay & woods, 2014)

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4
Q

satiety

A

feeling full

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5
Q

3 main digestive foods & broken down into what

A

carbs - glucose
fats - lipids
proteins - amino acids

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6
Q

energy metabolism

A

Cephalic phase: prep phase (stimulated by seeing etc food)
Absorptive phase: when nutrients are taken from the food & excess is stored
Fasting phase:energy is withdrawn from stores to meet the body’s needs

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7
Q

Cephalic phase & absorptive phase

A

Glucagon is LOW
Insulin is HIGH
- promotes conversion of excess glucose into glycogen & fats
- promotes use of blood glucose as a source of energy

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8
Q

fasting phase

A

Glucagon is HIGH
Insulin is LOW
- promotes use of stored energy (glucose isn’t main source of energy anymore)

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9
Q

insulin

A

1)promotes use of glucose as main source of energy in the body
2)promotes conversion of nutrients into forms which can be stored
3)promotes storage of glycogen in body
~~ helps glucose to get into cells so when insulin is LOW glucose cant be main energy store - use reserves
(saves glucose for brain - doesnt need insulin)

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10
Q

what causes hunger?

A

stomach contractions

chemicals

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11
Q

glucostatic theory of hunger

A

glucose levels determine set-point (thought to account for meal initiation) - hunger is caused by low levels of glucose

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12
Q

neuropeptides

A

any of a group of compounds which act as neurotransmitters and are short-chain polypeptides. Feedback to the brain

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13
Q

Cholecystokinin (CKK)

A
type of neuropeptide
SUPRESSESS EATING
Released in the small intestine 
Monitors food intake & inhibits eating 
Learned flavour aversion
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14
Q

Gherlin

A

Type of neuropeptide
Released when we are hungry
Produced by stomach cells

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15
Q

Dual centre set point model

A

Ventromedial Hypothalamus: Satiety centre (inhibits LH)
Lateral hypothalamus: Hunger centre (inhibits VMH)
BUT IT WAS WRONG

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16
Q

Ventromedial lesions - evidence against dual model

A

Eventually after lesioning, eating will stablise
2 phases: dynamic (gross eating) & static period (stabilisation & return to new weight regardless)
AND
animals with VMH seem less bothered about food i.e. wont work for it

17
Q

Role of hypothalamus

A

Energy metabolism (energy flow)

18
Q

Reinterpretation of the effects of VMH & LH lesions: Insulin

A
  • Bilteral VMH lesions: increase in BLOOD INSULIN LEVELS
  • this increases lipogenesis & decreases lipolysis
  • calories are being stored & converted into fat at a v HIGH RATE
  • need more calories for immediate energy stores
19
Q

lipogenesis

A

production of body fat

20
Q

lipolysis

A

break down of body fat into energy forms

21
Q

Reinterpretation of the effects of VMH & LH lesions: structure of vmh

A

may actually be the bundle of fibres under the VMH being lesioned in the process

22
Q

Reinterpretation of the effects of VMH & LH lesions: LH

A

cessation of eating can be reversed eventually

force feeding & then should come back

23
Q

neuropeptide Y

A
  • most prevalent neurop in the brain
  • gut hunger peptide
  • arcuate nucleus & DMH
24
Q

neuropeptide Y & arcuate nucleus

A

Many receptors to Ghrelin
Stimulates production of NPY
Thus, increases hunger

25
Q

neuropeptide Y & DMH (dorsomedial hypothalamus)

A

High number of CCK receptors
Reduces production of NYP
Thus, reduces appetite

26
Q

Leptin

A

Produced by expression of Ob gene only in FAT CELLS
This hormone promotes fat production
Leptin acts as a negative feedback signal (like insulin)

27
Q

other factors influencing hunger

A

1) anticipation
2) positive incentive
3) sensory specific satiety