Feeding and Satiety Flashcards
what is energy homeostasis
physiological process whereby energy intake is matched to energy expenditure over time via feedback loop - promoting body fuel stability (energy stored as fat)
what is obesity in terms of BMI
small constant mismatch between energy intake and energy expenditure;
>30 - obese
>40 - morbidly obese
factors influencing obesity
genetics - susceptibility genes, increasing the risk of developing disease
environmental
consequences of obesity
stroke (hypertension) respiratory disease - sleep apnea heart disease gallbladder disease osteoarthritis dementia - alzheimer's NAFLD diabetes cancer
obesity’s affect on the brain
alters brain function/brain re-programming - brain views extra weight as normal and dieting as a threat to body survival
how does the CNS influence energy body balance and body weight
behaviour - feeding and physical activity
ANS activity - regulates energy expenditure
neuroendocrine system - secretion of hormones
control centre of the brain for feeding behaviour
hypothalamus;
lesioning ventromedial hypothalamus - obesity
lesioning lateral hypothalamus - leanness
concepts underlying the hypothalamus
satiety signalling - feeling full
adiposity negative feedback signalling - state of being obese
food reward
what are satiation signals
short term processes regulating meal initiation, termination and inter-meal frequency (increase to limit meal size)
different types of satitation signals
cholecystokinin (CCK) peptide YY glucagon-like peptide oxyntomodulin (OXM) obestatin
describe cholecystokinin
secreted from enteroendocrine cells in duodenum and jejunum
Released in proportion to lipids and proteins in meal
Signals via sensory nerves to hindbrain and stimulates hindbrain directly (nucleus of solitary tract (NTS)
describe peptide YY
secreted from endocrine mucosal L-cells of G-I tract
Levels increase rapidly post-prandially
Inhibits gastric motility, slows emptying and reduces food intake (Hypo)
describe glucagon-like peptide (GLP-1)
product of pro-glucagon gene.
released from L cells in response to food ingestion
Inhibits gastric emptying and reduces food intake (Hypo, NTS)
describe oxyntomodulin
from pro-glucagon gene and released from oxyntic cells and L-cells of small intestine after meal.
Acts to suppress appetite – mechanism and site unclear.
describe obestatin
peptide produced from gene that encodes ghrelin and released from cells lining stomach/small intestine.
Suggested to reduce food intake – may act to antagonise the actions of ghrelin – actions unclear at present.
what is ghrelin
a hunger signal
octanoylated peptide produced and secreted by oxyntic cells in stomach
there are ghrelin-containing neurones in the hypothalamus
ghrelin function
levels increases before meals and decreases after meals
levels are raised by fasting and hypoglycaemia
ghrelin in the hypothalamus
control fat metabolism
increase lipogenesis
decreases lipid oxidation (liver and adipose)
peripheral ghrelin
stimulates food intake;
decreasing energy expenditure and fat utilisation –> increasing body weight
central appetite controllers
glutamate, gaba and opiods
monoamines
function of flutamate, gaba and opiods
increase food intake when injected into hypothalamic centres - effects modest/short lasting
function of monamines
suppress food intake - many drugs developed to act on these system (many are withdrawn)
hormones reporting fat stores to the brain
adiposity signals - levels will increase in blood as more fat is stored;
leptin (from fat cells)
insulin (pancreatic beta-cells)
function of the hormones reporting fat stores to the brian
inform the hypothalamus to alter energy balance - eat less and increase energy burn
this malfunctions in obese state
mutation in leptin gene
a reduced leptin will mimic starvation, causing an unrestrained appetite and obesity
biological roles of leptin
food intake.energy expenditure/fat disposition
peripheral glucose homeostasis/insulin sensitivity
maintaince of immune system
maintenance of reproductive system
angiogenesis
tumourigenesis
bone formation
describe the food reward effect on the brain
dopamine pathway activated in foods strongly linked to sugar and fat
describe leptin therapy in obesity
limited by severe leptin resistance present in most obese individuals
how does diet-induced obesity result in leptin resistance
defective leptin transport into brain
altered signal transduction following leptin binding to its receptor
describe adaptive thermogenesis
Thermogenic adipocytes – increase energy expenditure uncoupling of oxidative metabolism from ATP production
