Hunger Flashcards
homeostasis
maintenance of the body’s internal enviro within a narrow physiological range (there’s an optimal level to maintain)
how does homeostasis occur
negative feedback -change detected & negative feedback elicits compensatory mechanisms
main brain area involved in homeostasis
hypothalamus (Ramsay & woods, 2014)
satiety
feeling full
3 main digestive foods & broken down into what
carbs - glucose
fats - lipids
proteins - amino acids
energy metabolism
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Fasting phase:energy is withdrawn from stores to meet the body’s needs
Cephalic phase & absorptive phase
Glucagon is LOW
Insulin is HIGH
- promotes conversion of excess glucose into glycogen & fats
- promotes use of blood glucose as a source of energy
fasting phase
Glucagon is HIGH
Insulin is LOW
- promotes use of stored energy (glucose isn’t main source of energy anymore)
insulin
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)
what causes hunger?
stomach contractions
chemicals
glucostatic theory of hunger
glucose levels determine set-point (thought to account for meal initiation) - hunger is caused by low levels of glucose
neuropeptides
any of a group of compounds which act as neurotransmitters and are short-chain polypeptides. Feedback to the brain
Cholecystokinin (CKK)
type of neuropeptide SUPRESSESS EATING Released in the small intestine Monitors food intake & inhibits eating Learned flavour aversion
Gherlin
Type of neuropeptide
Released when we are hungry
Produced by stomach cells
Dual centre set point model
Ventromedial Hypothalamus: Satiety centre (inhibits LH)
Lateral hypothalamus: Hunger centre (inhibits VMH)
BUT IT WAS WRONG
Ventromedial lesions - evidence against dual model
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
Role of hypothalamus
Energy metabolism (energy flow)
Reinterpretation of the effects of VMH & LH lesions: Insulin
- 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
lipogenesis
production of body fat
lipolysis
break down of body fat into energy forms
Reinterpretation of the effects of VMH & LH lesions: structure of vmh
may actually be the bundle of fibres under the VMH being lesioned in the process
Reinterpretation of the effects of VMH & LH lesions: LH
cessation of eating can be reversed eventually
force feeding & then should come back
neuropeptide Y
- most prevalent neurop in the brain
- gut hunger peptide
- arcuate nucleus & DMH
neuropeptide Y & arcuate nucleus
Many receptors to Ghrelin
Stimulates production of NPY
Thus, increases hunger
