Physiology: Feeding & Satiety Flashcards
What physiological imbalance leads to obesity?
Small constant mismatch between energy intake and energy expenditure
What is energy homeostasis?
over time energy intake is matched to energy expenditure
Obesity BMI range
Up to 25 -> normal
25 - 29.9 -> overweight
30 - 39.9 -> obese
> 40 -> morbidly obese
Describe obesity as a disease
group of conditions with multiple causes
What are the major factors influencing obesity? (2)
- Genetics (susceptibility genes linked to fat storage and also regulation of energy intake and expenditure)
- Environment (wide variety of high calorie food, reduced physical activity e.g. cars, jobs)
What are some diseases does obesity contributes to? (11)
- Stroke (hypertension)
- Dementia (Alzheimer’s)
- Respiratory disease (sleep apnoea)
- Type 2 Diabetes
- Hypertension
- Cardiovascular disease (lipids, diabetes, hypertension)
- Increased cancer risk (especially colon, breast, uterus, prostate)
- NAFLD (Non-Alcoholic Fatty Liver Disease)
- Gall bladder disease
- Osteoarthritis
- Hyperuricaemia -> gout
Functions of fat (3)
- Energy storage
- Prevention of starvation
- Energy buffer during prolonged illness
How does the brain respond to long-term obesity?
Brain defends body weight because it views the new weight as normal and dieting as threat of starvation.
In what 3 ways does the CNS influence energy balance and body weight? What is the site of integration of these influences and what is the neural centre responsible?
- Behaviour - feeding and physical activity
- ANS - regulates energy expenditure
- Hormonal - secretions of hormones
Site of integration: brain
Neural centre responsible: hypothalamus
Lesioning of which part of the hypothalamus causes obesity?
Ventromedial
Lesioning of which part of the hypothalamus causes leanness?
Lateral (lateral leanness)
Define satiation.
Define satiety.
Define adiposity.
Satiation: sense of fullness generated during a meal. (signals increase during meal time to limit meal size)
Satiety: period of time between meals. (satimety)
Adiposity: the state of being obese.
What 3 concepts underlie the control of energy intake and body weight?
- Satiety signalling
- Adiposity negative feedback signalling
- Food reward
What are the 5 Satiation Signals and discuss their location of secretion, release, and action?
- Cholecystokinin
- secreted from enteroendocrine cells in duodenum and jejenum.
- released in proportion to lipids and proteins in a meal.
- signals via sensory nerves to hindbrain and stimulates hindbrain directly (Nucleus of solitary tract NTS) - Peptide YY (PYY3-36)
- secreted from endocrine mucosal L-cells of GI tract
- release increases post-prandially
- inhibits gastric motility, slows emptying and reduces food intake (hypothalamus) - Glucagon-like Peptide 1 (GLP-1)
- product of pro-glucagon gene
- released from L cells in response to food ingestion
- inhibits gastric emptying and reduces food intake (hypothalamus, NTS) - Oxyntomodulin (OXM)
- from pro-glucagon gene, and small intestinal L cells and oxyntic cells
- released after meal
- acts to suppress appetite - Obestatin
- peptide produced from gene that encodes ghrelin
- released from cells lining the stomach and small intestine
- not sure but may reduce food intake and antagonise action of ghrelin
What is the hunger signal? What produces it? When is it produced? How are its levels raised?
Ghrelin
- produced + secreted by oxyntic cells in stomach
- levels increase before meals and decrease after.
- levels raised by fasting and hypoglycaemia