Homeostasis - W3 Flashcards
Fothergill et al., (2016)
Fothergill et al., 2016: followed 14 of 16 Biggest Loser participants. 6 years after their dramatic weight loss, contestants had gained back an average of 70% and displayed reduced metabolic rates.
Their brains were directing their bodies to work very hard to regain their former body mass
Obesity:
Fothergill et al., (2016)
suggests?
body develops a ‘set point’ that it defends
Control of Food Intake:
Moran (2009)
Internal/external factors can affect weight
who, when, where & stressors can affect food intake
Hayes et al., (2009)
Elevated leptin levels signals the hypothalamus that fat stores are increasing, which inhibits eating
Wren et al., (2001)
Produced and released by stomach
Injections stimulate food intake and increase body mass in rats
Endocrine Regulators (food): Cholescytokinin - Morley et al., (1985)
administration to hungry animals decreases food intake
Leshner & Collier (1975)
estrogens have catabolic effect
rats who were ovariectomised
increased rats body mass by 20-25%
Specific Hungers:
What do gonadal steroid hormones do?
Promotes fertility & synchronise sexual behaviours (energy intake & storage)
Czaja & Goy (1975)
food intake higher during luteal phase in non-human primates
Leshner & Collier (1975)
estrogens have catabolic effect
ovariectomised rats
increased rats body mass by 20-25%
Wade (1976)
Androgens promoted elevated body mass & energy intake
Bronson (2000)
mechanisms in mammals to inhibit reproduction when in negative energy balance
Where is Leptin released from and what is it best understood as?
released from fat cells
‘starvation’ hormone (when leptin levels fall, stimulates food intake)
Where is Ghrelin produced/released from and what is it best understood as?
Produced and released from the stomach and stimulated food intake
Where is Cholecystokinin (CKK) released/produced from and what is it best understood as?
produced and released by the small intestine and provokes satiety
Three steps for the Analogy of a thermostat?
- set point
- detection mechanism
- mobilisation of behaviour when deviation occurs
osmotic thirst step process:
when there is an increase in osmolarity = water is needed
- osmoreceptors in hypothalamus detect increase in osmolarity and release antidiuretic hormone (ADH) down nerve fibres into the posterior pituitary gland where it is released into the blood stream
- ADH causes increase in re-absorption of fluids into the bloodstream
- lowering osmolarity levels
Hypovolemic Thirst
caused by loss of water, sodium and solutes from sweat, vomiting or diarrhoea = stop drinking
- osmolarity decreases = blood volume decrease
- this is detected and the ADH is released which restricts blood vessels = increasing blood pressure
- kidneys release angiotensin II, which also restricts blood vessels
- leads to the release of aldosterone from adrenal glands = which decreases amount of sodium excreted in urine
