#2 - The neuroendocrine control of nutrient intake - the role of gut - brain signalling Flashcards
(12 cards)
What defines obesity?
Obesity is a clinical condition where excess body fat negatively affects health.
Defined by Body Mass Index (BMI):
BMI > 25: Overweight
BMI > 30: Obese
Obesity is correlated with diseases like Type II diabetes and cardiovascular diseases, but it is not directly fatal.
Body fat composition and distribution are important.
Key gut hormones involved in feeding control
Gastrin (G): Stimulated by amino acids
Secretin (S): Stimulated by pH 2-4.5
Cholecystokinin (CCK): Stimulated by fat/proteins
GIP (K): Stimulated by glucose/fat
Somatostatin (D): Stimulated by pH
Neurotensin (N): Stimulated by fat/carbohydrates
Peripheral systems involved in feeding control
Autonomic nervous system
Enteric nervous system (ENS)
Vagal sensory nervous system
Adipose tissue
How is body weight maintained?
Adult body weight is typically stable, but gaining weight can take years, and losing it through dieting is difficult.
Reflexes regulate food intake and energy expenditure to stabilize body weight.
As weight decreases, hunger increases, and metabolism slows to conserve body mass.
Difference between satiety and satiation
Satiety: Fullness after eating; prevents you from eating again soon.
Satiation: Signals to stop eating; the amount consumed in one sitting.
What is the autonomic nervous system’s role in feeding?
Visual, olfactory, and taste sensations influence feeding behavior.
Cephalic phase: 50% of gastrointestinal (GI) secretions are thought to be stimulated by this phase, mediated by motor neurons through the vagal nerve.
Local control of energy intake by the gastrointestinal tract
The stomach expands to about 4L, storing food, which is later broken down and absorbed in the small intestine.
Enteroendocrine cells in the gut release hormones and neurotransmitters in response to nutrients, signaling the brain to regulate food intake.
What are orexigenic hormones (feeding stimulants)?
Ghrelin: “Hunger hormone”; released from the stomach when empty; stimulates appetite and food intake.
Orexin: Neuropeptides in the hypothalamus and enteric neurons; promote gastric emptying and stimulate feeding.
Hormones that terminate feeding (anorexigenic hormones)
Cholecystokinin (CCK): Released by the duodenum in response to fats/proteins; activates vagal afferents to signal satiation.
Peptide YY (PYY): Released by L cells in the ileum; increases time between meals and promotes satiety.
Glucagon-like peptide 1 (GLP-1): Released from L cells in the colon and small intestine; inhibits food intake and aids weight loss.
Amylin: Released with insulin to suppress food intake.
Leptin: Produced by adipose tissue; inhibits hunger.
CNS control of feeding
Peripheral signals target neurons in the arcuate nucleus (ARC) of the hypothalamus.
NPY/AGRP neurons: Orexigenic, stimulate feeding.
POMC/CART neurons: Anorexigenic, inhibit feeding.
The hypothalamus has projections to the forebrain and the nucleus of the solitary tract, affecting feeding behavior.
How do high-fat diets (HFDs) affect feeding signals?
High-fat diets reduce sensory signals from the stomach.
Loss of response to CCK in the gut → Increased meal sizes and weight gain.
Kappa opioid receptor upregulation in the paraventricular hypothalamic neurons reduces CCK’s effect on food intake.
Treatment options for obesity
Lifestyle changes: Exercise, diet modification, or both.
Drug treatments:
Orlistat: Pancreatic lipase inhibitor; causes fat malabsorption and weight loss. Side effects: anal leakage, oily stools.
GLP-1 agonists: Used to treat obesity and Type II diabetes. Reduce glucagon release and help with weight loss.
Surgery: Gastric bands, stents.
