MCP unit 8 reveiw Flashcards
Which BMI values correspond to which weight categories?
< 18.5: underweight
18.5 - 24.9: healthy, normal
25.0 - 29.9: Grade 1 overweight
30.0 - 39.9: Grade 2 overweight(30-34.9, Grade 1 obesity; 35-39.9, Grade 2 obesity)
≥ 40.0: Grade 3 overweight (Morbidly obese/Grade 3 obesity)
How is BMI calculated?
BMI = Kg/ height in meters ^ 2
How is resting energy expenditure (REE) calculated?
Men:
(900 + 10w) * activity coefficient
Women:
(700 + 7w) * activity coefficient
w = weight in meters
Activity Coefficients:
- 2 = Sedentary
- 4 = Moderately active
- 8 = Very active
What is the caloric content of 1 kg of fat?
7,650 calories
Fat is 15 percent water, so caloric content of 1 kg of fat = 850g * 9Cal/g = 7,650 calories.
What types of fat should be distinguished from each other and why?
These types raise the risk of CHD:
saturated, trans-unsaturated
These types lower the risk of CHD:
monounsaturated, polyunsaturated, ω-3
How should the various carbohydrate sources be distinguished form each other?
Readily digested carbohydrates should be distinguished from those with lower glycemic index (readily digested -> blood sugar spike)
Fructose-rich, and starchy foods should also be differentiated (high fructose -> fatty liver)
Summarize the 2015 USDA guidelines.
- Eat a diet rich in vegetables, fruits, nuts, legumes, whole grains.
- Try to include more “good fats” such as omega-3s from fish
- Limit your daily percentage of calories from added sugars to < 10%
- Limit red/processed meats, saturated fats and trans-FA.
- Partially limit on cholesterol (dietary cholesterol is less significant than previously thought.)
- moderate drinking (less than 14 units per week)
- limit sodium
- Coffee and eggs are an acceptable part of a healthy diet.
What is the basic macro-nutrient balance present in the atkins diet? What are the long term effects?
- Low carbo.
- High-fat.
- High protein.
- Long-term effect on CHD and other ilnesses unknown.
Describe the normal detoxification of most of the ethanol one ingests.
- Ethanol enters liver hepatocytes where it is matabolized in the cytoplasm by alchohol dehydrogenase (ADH.)
- The product acetaldehyde enters the mitochondria where it is metabolized by aldehyde dehydrogenase (ALDH.)
- Acetate is produced. It can exit to the blood, and enter cells where it can be metabolized to acetyl-CoA (which can enter TCA cycle.)
What percentage of acetaldehyde is metabolized by ALDH. What happens to unmetabolized acetaldehyde?
90% of the acetaldehyde formed is metabolized by a low Km ALDH. The acetaldehyde which is not further metabolized can damage the liver and can also enter the blood exerting toxic effects on other tissues.
Describe MEOS.
- Microsomal Alcohol Oxidizing System (MEOS) is located in the liver and is induced by a high ethanol concentration.
- Comprised of cyt P450 enzymes (primarily CYP2E1.)
- 10-20% of ingested alcohol is oxidized by MEOS.
- Produced acetaldehyde and Reactive oxygen species (ROS) → oxidative stress.
Describe the molecular basis of the harmful effects of chronic alcohol intake.
- Adduct formation with amino acids.
- Adduct formation with the antioxidant glutathione (GSH).
- Induction of MEOS increases ROS production and oxidative stress.
- Oxidative damage to mitochondrial inner membrane inhibits NADH oxidation and diminishes acetaldehyde conversion to acetate.
- Adduct formation with tubulin → decreased secretion of proteins
- Protein accumulation causes water to enter into hepatocytes with resulting swelling & cell damage.
Describe the molecular basis of the harmful effects of acute alcohol intake.
- High NADH/NAD+.
- Accumulation of free fatty acids.
- FAA→TAGs → fatty liver (hepatitic steatosis) and lipidemia.
- Inhibition of TCA cycle → further increase acetyl CoA
- Increased ketone bodies → ketoacidosis.
- Production of lactate → lactic acidosis.
- Lactate decreases uric acid excretion by the kidney (patients with gout therefore are advised not to drink excessively).
- Drinking alcohol in the fasting state reduces gluconeogenesis and causes hypoglycemia.
What are the 6 common endogenos sources of ROS. Which ROS do they produce?
- Mitochondria (CI & CIII)
- NADPH oxidase (Phagocytes)
- Xanthine oxidase (Endothelial)
- Monoamine oxidase (Neurons)
- Redox cycling (Drugs, fava)
All of the above produce ˙O2¯ (superoxide)
- NO synthase produces NO˙
What are the biomarkers for oxidative damage? Why are they biomarkers?
Damage to DNA from ˙OH produces:
8-OHdG, MDA, 4-HNE
GSH (glutathione) is a defense mechanism against ROS. It is oxidized to GSSG. Thus GSH/GSSG ratio is anindicator of oxidative stress if it is low.
Explain the effects of leptin on neurons in the brain.
- Leptin inhibits neurons that produce orexigenic effectors.
- Leptin stimulates neurons that produce anorexigenic effectors.
Explain the cellular/molecular mechanism Lipotoxicity.
- What are the hallmarks & consequences of Metabolic Syndrome?
-Explain how increased adipocity leads to MetS
