Lecture 5 Energy Balance & Obesity Flashcards
How is energy balance regulated?
CNS is the controller which receives input from peptides, hormones and vagal afferents and the output from the CNS is changes in food intake and energy expenditure resulting in system energy balance
What is the CNS integration of afferent signals?
- short term signals - meal
- long term signals - adipose tissue storage
What helps to integrate afferent signals from the CNS?
numerous neurotransmitters and neuropeptide systems
redundancy to maintain energy balance
What is the efferent response of food intake?
regulate the level of
* appetite
* energy expenditure (activity)
* nutrient partitioning
* reproduction and growth
* hormones
What are the afferent neurotransmitter signals controlling energy balance?
- Meal: glucose, aa, fatty acids
- Adipose: leptin
- Pancreas: Insulin, amylin, PP
- Stomach: Ghrelin
- SI: CCK, PYY, GLP-1, OXM
Integration of meal related CNS signals in physiological control of food intake
Short-acting
* quantity and quality of food
* The hypothalamus is sensitive to blood concentrations of glucose, aa, and fatty acids
* Mostly negative feedback/inhibitory
Integration of gut signals in physiological control of food intake
mechanical (stretch receptors) and chemical (peptides from GI tract)
* GI-tract receptors act in combination to reduce meal size and lengthen inter-meal satiety
Integration of neuron information in physiological control of food intake
Neuron information is collated by brain stem NTS and is sent onto the hypothalamus.
Gut peptides that reduce meal size vs. increase meal size
Reduce:
* Cholecystokinin
* Bombesin family (BBS, GRP, NMP)
* Glucagon
* Glucagon-like peptide 1, gulcagon-like peptide 2
* Amylin
* Somatostatin
* Enterostatin
* Apolipoprotein A-IV
* Gastric inhibitory peptide
Increase:
* Ghrelin
Most GI peptides involve inhibition
Role of
CCK
Cholecystokinin - SI Duodenum
* Gall bladder contraction
* Gastrointestinal motility
* Pancreatic exocrine secretion
Role of
Secretin
SI Duodenum S cells
* Gall bladder contraction
* Gastrointestinal motility
* Pancreatic exocrine secretion
responds to acidic chyme
Role of
GIP
Gastric inhibitory polypeptide: stomach & SI Duodenum
* Incretin activity
Stimulate decrease in blood glucose levels by releasing insulin
Role of
Motilin
SI-Duodenum
* Gastrointestinal motility
Role of
Ghrelin
Stomach
* Hunger
* Growth Hormone release
Role of
Gastrin
Stomach
* Acid secretion
Role of
Insulin & glucagon
Pancreas
* glucose homeostasis
Role of
pancreatic polypeptide
pnacreas
* gastric motility
* satiation
Role of
Amylin
pancreas
* glucose homeostasis
* gastric motility
role of
GLP-1
Glucagon-like peptide 1: LI
* Incretin activity
* satiation
Role of
GLP-2
Glucagon-like peptide-2: LI
* GI motility and growth
Role of
Oxyntomodulin
LI
* satiation
* acid secretion
Role of
PYY
peptide tyrosine tyrosine - LI ileum and colon
* satiation by slowing gastric emptying
What are the long term signals for integration of food intake?
Long term signals from fat storage and appetite signals the CNS hunger/ food intake need.
* Includes the peptides leptin and insulin.
Role of
Leptin
secreted by adipocytes proportional to size of fat stores
* reduces foot intake
* elevates EE
Role of
Insulin
secreted by B-cells in pancreas and reflect fuel availabilty
* glucose uptake by cells
* reduction in appetite
Insulin resistant
Lack of sensitivity to insulin, more secreted for same effect
How does the CNS converge information?
- short term meal derived signals collated by the NTS in the brainstem
- short and long term signals collated by paraventricular nucleus (PVN) located in the ventromedial hypothalamus
- Lateral hypothalamus (LH); stimulates feeding
- Arc in hypothalamus converges adiposity signals
How do insulin and leptin act on the brain to regulate food intake with energy surplus?
Increased hormone secretion converges at the Arc and inhibits food intake and increases EE
* inhibits NPY and AgRP neurons in ARC thus inhibiting orexigenic (LHA) neurons in stimulation from NPY and preventing anorexigenic (PVN) neuron inhibition from AgRP.
* Stimulates POMC neurons in the ARC which stimulates aMSH which stimulate anorexigenic neurons (PVN)
How do insulin and leptin act on the brain to regulate food intake with energy deficit?
Decreased hormone secretion converges at the Arc and stimualtes food intake and decreases EE
* NPY and AgRP neurons in ARC are stimulated thus orexigenic (LHA) neurons are stimulated from increased NPY and anorexigenic (PVN) neurons are inhibited from increased AgRP.
* Inhibites POMC neurons in the ARC which inhibits aMSH which cannot act on anorexigenic neurons (PVN), thus inhibting them
How do efferent signals control energy balance?
Long term signals
* Energy deficit promotes feeding and energy storage via PNS (vagus nervue)
* Excess energy promotes satiety and EE vis SNS and adrenal medulla
How do the efferent signals from energy deficit promote energy storage?
- stimulates the secretion of digestive enzymes
- stimulates intestinal motility and peristalsis
- relaxes intestinal sphincters
- Increases insulin release
- Increases adipose tissue insulin sensitivity
- Increases substrate partitioning into adipose tissue
How do the efferent signals from excess energy promote EE?
- Increases adaptive thermogenesis by BAT
- Increases movement
- Inhibits insulin release and promotes insulin sensitivity
- Increases glycogenolysis and fatty acid oxidation in skeletal muscle
- Increases lipolysis in adipose tissue
What is eating?
A behaviour controlled by the brain
homeostatic vs. hedonic control of eating
appetite ≠ hunger
environmental and genetic influences can override physiological feedback loops that control set point.
Role of epigenetics in energy balance
interaction of genes and the environment cause changes that effect the way your genes work by changing how your body reads a DNA sequence
What does obesity reflect?
Reflects an imbalance between energy uptake and expenditure that is mediated by behaviour and is excess of adipose tissue accumulation
Classifications of obesity based on BMI
Health risks associated with obesity
- Type 2 diabetes
- Dyslipidemia
- High blood pressure
- Metabolic syndrome
Medical complications of obesity
- Pulmonary disease
- Nonalcoholic fatty liver disease
- Gall bladder disease
- Gynecologic abnormalities
- Osteoarthritis
- Skin problems
- Gout
- Idiopathic intracranial hypertension
- Stroke
- Cataracts
- Coronary heart disease
- Diabetes
- dyslipidemia
- hypertension
- Severe pancreatitis
- Cancer Phlebitis
What is metabolic syndrome
A cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes:
* increased waist circumference
* BMI >30
* increased triacylgyceride level
* decreased HDL-C
* Increased BP
* Increased glucose levels
Treatment for obesity
- Prevention with regulating energy intake
- Manage weight loss
- Lifestyle changes
- Anti-obesity drugs
- Surgery
