Term
| What are the current BMI classifications of obesity? |
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Definition
1) Underweight (<18.5 kg/m2) Increased health risk
2) Normal (18.5-24.9 kg/m2) Normal
3) Overweight (25-29.9 kg/m2) Increased health risk
4) Obesity (30-34.9, 35-39.9, >40.0) high, very high and extreme |
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Term
| How does fat distribution relate to risk of CV co-morbidities? |
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Definition
| Upper body fat worse than lower (indicted by waste >40 in men and > 35 in women). |
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Term
| What are the 4 mechanisms that can give rise to obesity? |
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Definition
1) Increased energy intake
2) Decreased expenditure
3) Genetics
4) Combinations of 1-3 |
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Term
| What is the molecular basis for "set point theory"? |
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Definition
When fat stores are depleted, adipostat signal (Leptin) is low in hypothalamus.
When fat stores are high, Leptin (Ob gene) is high and hunger is suppressed. |
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Term
| What does average total energy expenditure decrease with weight loss from obesity? |
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Definition
1) Loss of lean body mass
2) Decreased sympathetic activity (decreased thermogenesis) |
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Term
| What are the major excitatory and inhibitory monamines and peptides that affect feeding? |
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Definition
1) Excitatory
- NPY
- Opioids
- Grehlin
- Growth hormone releasing hormone
2) Inhibiting
- Leptin
- CCK
- 5-HT
- CRH, Glucagon-like peptide, Enterostatin. |
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Term
| Why are obese people sometimes called "leptin-resistant"? |
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Definition
| This peptide produced by adipose should signal to hypothalamus and suppress feeding urge in cases of high adipose storage (enhancing thermogenesis). |
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Term
| How does Substance PYY signaling influence diet? |
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Definition
PPY= Illeal break for satiety
Secreted by endocrine L cells lining distal small bowel and colon after meals (postprandially), in proportion to calories taken in.
- decreases food intake through inhibition of gut motility (acting as an “ileal brake” to cause a sense of satiety.
**initially secreted before nutrients hit lumen, but also secreted after nutrients are digested**
**Signals satiety!** |
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Term
| How does Grehlin function to stimulate appetite? |
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Definition
Released pre-perandilly by oxyntic cells in stomach fundus, activating on growth hormone receptors to increase GH release from pituitary (decreases post-parandially)
**Signals hunger!**
- Increases food intake by stimulating Ghrelin receptors on hypothalamic NPY-expressing neurons and agouti-related-protein-expressing neurons. |
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Term
| What diseases are associated with obesity? |
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Definition
Caused by adipose quantity, factors secreted from adipose, or combination.
1) Fat Mass
- Psychosocial depression
- Sleep apnea
2) Bones/connective tissue/skin
- Osteoarthritis
- Stretch marks
3) DM, insulin resistance, metabolic syndrome
4) Cholelithiasis (gallstones)
5) Acute pancreatitis (only severe cases)
6) HTN and Heart disease
7) Cancer (gynecological)
8) Chronic venous insufficiency/varicose veins |
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Term
| How is "metabolic syndrome" defined clinically? |
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Definition
3 of 5
1) Waist circumference (men >40 and women >35)
2) Triglycerides >150 mg/dL
3) HDL (M <40 and W < 50)
4) Fasting blood glucose (>110 mg/dL)
5) BP > 130/85 |
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Term
| How does obesity cause HTN? |
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Definition
SNS activity induces pro-inflammatory state by IL-6 production, leading to systemic inflammation
1) Visceral fat is prone to lipolysis; an effect mediated by catecholamine binding to b3 receptors in intra-abdominal fat
2) Central fat distribution disturbs HPA axis
3) Lower NO in obese people |
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Term
| What is heart disease so common in obese individuals? |
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Definition
Increased cardiac weight= increased cardiac work
HTN in normal people causes concentric hypertrophy, but in obese patients, it is ECCENTRIC dilation, with increased preload and stroke work, leading to thickening and failure. |
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Term
| Describe 2 important signaling molecules released from adipocytes themselves. |
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Definition
1) Leptin is correlated with body fat stores (signals satiety)
2) Adiponectin is anti-inflammatory and is inversely correlated with body fat stores (increases glucose uptake) |
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Term
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Definition
| A constellation of liver abnormalities associated with obesity, including hepatomegaly, elevated liver enzymes, and abnormal liver histology--steatosis, steatohepatitis, fibrosis, and cirrhosis |
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Term
| What are the long-term and short-term molecular signals of satiety/hunger (body-fat stores)? |
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Definition
1) Long-term signals associated
- leptin and insulin.
- also modulate short-term signals that determine meal initiation and termination.
2) Short term:
- Gut hormones, such as cholecystokinin, ghrelin, and PYY
- Signals from vagal afferent neurons within the gastrointestinal tract that respond to mechanical deformation, macronutrients, pH, tonicity, and hormones |
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