What are the possible consequences of obesity?
-Stroke (hypeprtension) -Respiratory disease (sleep apnoea) - Heart Disease (Lipids, diabetes, hypertension) -Gallbladder disease -Osteoarthritis -Dementia -NAFLD -Diabetes -Cancer (uterus, breast, prostate, colon) -Hyperuricemia, gout
Why do we need fat?
-Energy storage -Prevention of starvation -Energy buffer during prolonged illness
Once a person has gained weight it is difficult to lose it. What is the neurological reasoning for this?
Increased body fat alters brain function Long-term obesity induces brain re-programming i.e. your brain views the extra weight (fat) as normal & dieting as threat to body survival and defends the new weight
How does the CNS influence energy balance and body weight?
1) Behaviour- feeding and physical activity 2) ANS Activity- regulates energy expenditure 3) Neuroendocrine System- secretion of hormones Integration (in the hypothalamus) of these determines final output- feeding behaviour e.g. lesioning ventromedial hypothalamus causes obesity e.g. lesioning lateral hypothalamus causes leanness
What three basic concepts underlie the control system of energy homeostasis?
1. Satiety signalling
2. Adiposity Negative Feedback Signalling
3. Food Reward
Define
a) satiation and
b) satiety.
a) Satiation is a sensation of fullness generated during a meal
b) Satiety is the period of time between termination of one meal and the initiation of the next
Define adiposity
Adiposity is the state of being obese
What are the 5 main satiation signals?
- Cholecystokinin
- Peptide YY
- Glucagon-like peptide
- Oxyntomodulin
- 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)
Describe peptide YY
- secreted from endocrine mucosal L-cells of GI tract
- levels increase rapidly post-meal (post-prandially)
- inhibits gastric motility, slows emptyinh and reduces food intake
Describe glucagon-like peptide 1
- product of pro-glucagon gene
- also released from L cells in response to food ingestion
- inhibits gastric empyting and reduces food intake
Describe oxyntomodulin
- also from pro-glucagon gene and released from oxyntic cells of small intestine after meal
- acts to suppress appetite
- mechanism unclear
Describe obestatin
- peptide produced from gene that encodes ghrelin
- released from cells lining stomach/small intestine
- suggested to reduce food intake- may antagonise the actions of ghrelin- actions unclear at present
What is ghrelin?
Octanolyated peptide
- produced and secreted by oxyntic cells in stomach
- ghrelin levels increase before meals and decrease after meals
- levels are raised by fastin and hypoglycaemia
- peripheral ghreli stimulates food intake and decreases fat utlization
What two hormones report fat status to the brain?
- Leptin- made & released from fat cells
- Insulin- made & released from pancreatic cells
Levels in blood increase as more fat is stored.
Function= inform brain (hypothalamus) to alter energy balance- eat less and increase energy burn
This malfunctions in obese states
What deficiencies might an obese human have?