14 - Feeding and body weight Flashcards
4 components of energy exposure (4)
- basal metabolic rate
- thermic effect of food
- non-exercise activity thermogenesis
- exercise activity thermogenesis
basal metabolic rate (2)
- energy required to maintain body
- BMR = 50-80%
thermic effect of food (2)
- heat generated in digestion, absorbing and storing nutrients from food
- TEF = 10%
non-exercise activity thermogenesis (2)
- energy required for daily activities
- NEAT = 15%
exercise activity thermogenesis
EAT = 5%
metabolic rates of liver, brain and heart/kidneys (3)
- liver = 200 kcal/kg/day
- brain = 240 kcal/kg/day
- heart & kidneys = 400 kcal/kg/day
short term energy store
glycogen, stored mainly in liver and muscles
long term energy store
fats, in adipose tissue
energy storage
= energy intake - energy expenditure
adipose tissue (2)
- fat = 25% of body weight in healthy adults
- white adipocytes store high-energy fats (triglycerides)
high-energy fats (2)
- triglycerides
- stored in white adipocytes in adipose tissue
white adipocyte functions (3)
- insulin sensitive - energy production/storage
- lipid storage - triglycerides (homeostasis between lipolysis and lipogenesis)
- secretory functions - endocrine hormones (e.g. leptin)
how is body composition estimated?
dual-energy X-ray absorption (DXA) - two different energy X-ray beams to estimate 2 components of body composition
2 components of body composition (2)
- fat mass - adipose tissue, stores energy as fats
- lean mass - everything else, including internal organs, muscle, body fluids and bond
how is adiposity measured
BMI (body mass index) = weight/height (squared)
obesity
excessive weight gain due to greater energy intake than energy expenditure (BMI>30)
how much do gene variants contribute to majority of observed obesity phenotypes?
50-80%
ob gene (2)
- ob gene expressed in adipose tissue
- codes for protein leptin
leptin (3)
- acts as hormone on leptin receivers in brain
- communicates status of energy sources
- mutation in leptin receptor (dp gene) produces similar phenotype to ob gene)
how does the hypothalamus regulate body weight?
controls appetite and food-seeking behaviour
satiety cascade
series of psychological, behavioural and physiological events leading from hunger to feeding to satiety
what triggers food-seeking behaviour and initiation of feeding?
blood glucose levels dip a few minutes before food-seeking behaviour begins
metabolism during feeding/fasting? (3)
- rapid response after meal to take up nutrients and energy during absorptive phase
- gradual switch to fasting phase (nutrients in food depleted)
- glycogen acts as short term energy store and fat in adipose tissue as longer term storage
what should feeding behaviour be sensitive to?
stores of glycogen and fat within adipose tissue
signals of satiety following meal initiation (2)
- insulin - short term signal
- leptin - long term signal
peptides released after meal to decrease appetite and feeding behaviours (4)
- leptin
- insulin
- cholecystokinin (CCK)
- glucagon-like peptide-1 (GLP-1)
where is leptin secreted?
white adipose tissue
where is insulin secreted?
B-cells in pancreas
where is cholecystokinin (CCK) secreted?
cells in lining of small intestine
where is glucagon-like peptide-1 secreted?
cells in lining of small and large intestines (and other organs)
autonomic satiety signals to brain (2)
- Cholecystokinin (CCK)
- glucagon-like peptide-1
endocrine satiety signals to brain (3)
- leptin
- insulin
- glucagon-like peptide-1
how are endocrine satiety signals sent to the brain?
bind to receptors on neurons in hypothalamus
(GLP-1, leptin, insulin)
how are autonomic satiety signals sent to the brain?
Act via intestinal vagal afferents to signal satiety to neurons in brain stem (vagus nerve also signals gut digestion (fullness) via stretch receptors in gut wall
(GLP-1, CCK)
neural control of feeding (3)
- leptin
- insulin
- glucagon-like peptide-1
- act via hypothalamus
how does neural control of feeding occur?
bind to receptors on neurons in arcuate nucleus (ARC) to signal satiety. these neurons signal to paraventricular nucleus (PVN) to regulate feeding behaviour
2 key neuron types in arcuate nucleus (2)
- POMC neurons (proopiomelanocortin)
(protein precursor used to synthesise MSH (agonist of MC4R)) - NPY/AgRP neurons
(neuropeptide Y/ agouti-related protein)
role of POMC (proopiomelanocortin) neurons in arcuate nucleus
(activated by leptin, GLP-1 and insulin)
releases melanocyte stimulating hormone (MSH) to increase satiety signal
role of NPY (neuropeptide Y)/AgRP (agouti-related protein) neurons in arcuate nucleus
(activated by hormone ghrelin from the stomach)
released to increase hunger signal. NPY also inhibits POMC neurons to decrease satiety signal
MC4R+ neurons: decrease in feeding
if satiety signal (MSH - melanocyte stimulating hormone) > hunger signal (AgRP - agouti-related protein), signal to other brain regions to cease feeding behaviours and release further anorexigenic (appetite suppressing) hormones
MC4R+ neurons: increase in feeding (2)
- inhibited by AgRP (agouti-related protein) -> block of feeding behaviours reduced.
- AgRP and NPY also activate other neurons in PVN to signal to other brain regions to stimulate feeding behaviours (increase release of further orexigenic (appetite stimulating) hormones
Ghrelin
produced in stomach, stimulates hunger and food intake via vagal afferents to brainstem and as hormone to activate NPY/AgRP neurons in arcuate nucleus of hypothalamus
