appetitie regulation Flashcards
neuro humoral appetite control system
periphery + brain linked- adipose tissue, gut + stomach produce different hormomes and cirulate around body
brain integrates signals in hypothalamus and stimulate appetite stimulating effects- reducing appetite
ghrelin- stimulates initiaion of meals and builds up before next meal - hunger hormone
tonic signals
episodic signals- meal to meal signals
circulation
vagus nerve
hypothalamus
theories of appetite control
food intake as a mechanism of temp regulation
relationship between serum aa cocn and fluctuations in appetite
role of depot fat in the hypothalamic control of food intake in the rate
circulating factor theory
circulating factor that controlled appetite and body weight
showed that obesity had biological influence
2 mutant mice models were identiied serendiptuously displaying hyperphagia (excessive eating) and obesity
parabiosis- link systems of animals together to develop shared physiological system
used to test hypothesis tat a CF may be mediated in the obese phenotype
neuro hormal regulation of appeitite
apipose tissues produces leptin (signal)
increased weight- increased leptin= increased energy expenditure- eat less food
reduced weight- decreased leptin- reduce energy expenditure- eat more food
negative feedback
body’s response to negative energy balance is stronger than positive (undereating compared to over)
dual intervention point model
suggests systems only comes into play when body mass is elevated or reduced
upper and lower boundaries of physiological regulation- lower boundary imposed by starvation and infection pressure
upper boundary imposed by predation - weak UB
passive control in between
different people will have diff boundaries meaning some people are more prone to weight gain than others
RMR
resting metabolic rate is associated with hunger and energy intake
drives us to eat a certain amount of food each day
positive association between RMR and how much we eat
leptin
signal indicating long term energy balance (along with insulin)- suppresses hunger
circulating leptin correlates positively with body fat and is regulated by energy balance
norhern blot- leptin gene expression in scat is elevated in rodents rendered obese by chemical, HFD and age
western blot- cicrulatifn levels of leptin decline with energy restriction and weight loss
positive correlation between leptin levels, BMI and body fat
greater correlation with body fat as leptin is produced on adipose tissue
recombinant leptin
reduces adiposity in leptin deficient humans
many children who are leptin deficient are obese at a very young age - also susceptible to disease as immune function is lowered as brain turns off energy excess systems
many obese people have high levels of leptin but their brain becomes resistant to leptin, meaning body doesnt respond to leptin- injections/ therapy wouldnt work
insulin
has a role in regulating long term energy storage along with leptin
acts as a key to take up glucose out of circulation
mediates the brain’s sensitivity to episodic glucose
- insulin infused into the 3rd cerebral ventricle, results show bw chnages secondary to altered enegry intake
episodic regulation
coordination of food intake on a meal to meal basis
form inhibitory processes which stop eating and prevent its reoccurance- known as satiety signals
pre prandial metabolism
pre meal
meal anticipation- smell, sight of food, time of day + environmental cues
ghrelin- encourages stomach to produce digestive enzymes which speed up gut movement
insulin levels increase in blood before eating- buffers glucose increase
G1P1 involved
post prandial responses
saciety cascade
when eating, we end a meal due to habitual/psychsocial factors rather than hormonal factors (as they dont work as fast)
over time, feeling of satiety is brought about by mechanoreceptors in stomach, then hormone levels increase and make us feel more satiated
hormone response depends on calories in meal- more released for more calorific meal
ghrelin, appetite and food intake
ghrelin stimulates feeding via arcuate nucleus neurons in hypothalamus
dose response stimulation of feeding in ARC- more ghrelin= increased food intake
intravenoys ghrelin indsion in humans- greater energy intake from ghrelin compared to saline
ghrelin levels decrease in individuals with obesity- not associated with pathogenesis of obesity
is important in regulaing appetite in most
peptide YY
released from L cells in distal intestine and colon
active form PYY3-36
circulating levels rise after eating- direct and indirect trigger, is energy and macronutrient dependent
inhibit GE ileal break
suppreses appetitie- inhibits release of NPY in arc nucleus
G1P1
suppresses appetite
used to treat T2D and obesity as it improves glucose regulation
promotes health of pancreas which is often declined in individuals with T2D
semaglutide
94% homology to native G1P1
binds to albumin- allowing it to circulate in the body for up to a week (half life ~ 1 week)
tirzepatide
liscenced in uk for diabetes
mimics 2 gut hormones- G1P1 and GIP
coagonist for hormones
decreases BW by 23% looking at studies
weight surgery
gastric sleeve- removes sections of the stomach which helps to lose weight
ensures hormone levels are normal so that regulation of appetite is regular too
central brain appetite circuit
hypothalamus arcuate nucleus
NPY- neuro peptide Y
AgRP- agouti related peptide
a-MSH- alpha melonocyte stimulaing hormone
CART- cocaine + amphetamine related transcript
PVN- paraventricular nucleus
NPY interact with Y15 receptors on PVN
agrp, amsh, cart all interact with mc-34 receptors on pvn which inhibit food intake
interactions
between homeostatic signals and hedonic processes
studies
- leptin reversible changes in the activation of brain centres linked to the emotional control of eating
- G1P1 therapy decreases the frequency, strength and control of food craving, decreases pleasentness of meals
- in the fed state, ghrelin infsuion increasws the appeal of high energy foods + activation of hedonic appetite centres- as occurs when fasted
non homeostatic (hedonic) influences
pleasure
exercise and appetite regulation
low intensity exercise doesnt impact exercise
exercise > 60% vo2 max suppresses appetite transiently (30-60min)
delays voluntary request for a meal
doesnt effect energy or macronutrient intake
