Appetite Regulation Flashcards
Orexigen
Substance that increases food intake
–> appetite stimulant
Activates specific neurological pathways to increase hunger/food intake
Orexigen forms
Hormones (neuropeptide)
Drugs
Unwanted side effect of medication (increased weight gain)
Desirable outcome of medical therapy (Cachexia treatment, AIDS/cancer)
Anorexigen
Substance that inhibits food intake
–> appetite inhibiting
How food broken down in GI
Mastication Stomach acid Proteases Rhythmic gastric contractions Ingested nutrients pass into duodenum - bile acids, pancreatic enzymes Nutrients sensed by receptors in GI
Mechanical breakdown location
Chewing (mouth)
Churning (stomach)
Segmentation (SI)
Propulsion location
Swallowing (oropharynx)
Peristalsis (oesophagus, stomach, SI, LI)
Digestion locations
Stomach (end)
SI
Absorption location
SI
LI
Into blood vessels + lymph vessels
Enteroendocrine cells
Sense luminal environment Microvilli "taste" nutrient environment Vesicles for endocrine hormone release Specialized cells of the GI tract and pancreas with endocrine function Release peptides + GI hormones
Enteroendocrine cell activation
Nutrients activate GPCR receptors
Release signalling molecules
Vagal Afferent excitation
Vagus nerve appetite regulation
Chemoreceptors on vagus nerve activated by mediator released by EEC
Mechanoreceptors stimulated by stretch- gastric distension causes satiety, meal size
Involved in short term (homeostatic) control of appetite
Arcuate nucleus
Has reciprocal connections with dorsal vagal complex
Nucleus of tractus solitarius, dorsal motor nucleus of vagus, area postrema
Leptin
Satiety factor
Hormone made by adipose tissue- adipokine
Diurnal secretion- not related to food intake
Leptin MOA
Affects organs throughout body Satiety signal --> inhibits NPY/AgRP neurones --> activates POMC/CART neurones Doesn't respond over short term but long term
Leptin functions throughout body
Helps regulate thyroid hormone synthesis Decreases glucose-stimulated insulin secretion Increases HR Regulates bone mass Regulates menstrual cycle Regulates appetite Activation of immune cells Increases BP
Leptin + obesity
Not treatment for obesity
Circulating leptin levels correlated with body fat- adipose tissue produces leptin at constant rate
Obese individuals have high leptin signals –> said to have leptin resistance
Can be due to loss of function mutations in severe obesity
Leptin as treatment
Congenitally leptin deficient children–> leptin injections
Not in diet induced obesity
Defective leptin
ob gene
can’t produce effective leptin
Defective receptor
db gene
can’t detect leptin
Cholecystokinin (CCK)
Anorexigenic
Synthesised in duodenum
Released in response to fat + protein
Slows gastric emptying, releases bile + pancreatic enzymes
Feelings of satiety –> activates vagus nerve
PYY 3-36
Anorexigenic Released from L cells in GI tract Released in response to high fat/protein Inhibits NPY neurones Activates POMC neurones Decrease food intake
Insulin
Acute satiety signal
Inhibits NPY/AgRP neurones
Activates alpha MSH/CART
GLP1
Most powerful incretin
Released in response to food intake
–>decreases blood glucose + food intake
Levels reduced in obese subjects
Pancreatic polypeptide
Released in response to food intake
Proportional to calories
Decreased appetite
Long term energy balance
