NUTR BIG TOPICS

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Author:
emmayarewhy
ID:
189450
Filename:
NUTR BIG TOPICS
Updated:
2012-12-14 02:59:11
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  1. How does insulin affect carbohydrate metabolism?
    What tissues are affected the most?
    Liver, muscle, adipose tissue.

    1. Glycogenesis in liver & muscle: Activates PP1 which destroys cAMP and activates glycogen synthase. 

    2. Increase in glucose uptake in muscle & tissue via GLUT 4: Insulin activates GLUT 4 transporters --> glycerol 3P for fat synthesis. 
  2. How does insulin affect lipid metabolism? (2)
    Adipose tissue responds within minutes to insulin, significantly decreasing release of FAs.

    • 1. Decreases TAG degradation - inhibits HSLby breaking down cAMP, decreasing PKA, thus decreasing activation of HSL. WHILE, p'lating HSL. 
    • 2. Increased TAG synthesis  - increases transport & metabolism of glucose into adipocytes, providing substrate glycerol 3-P for TAG synthesis. Insulin also increases LPL activity, allowing VLDL/chylomicrons to provide FAs for esterification. 
  3. How does insulin affect protein synthesis?
    In most tissues, insulin stimulates entry of amino acids into cells and protein synthesis. 
  4. What stimulates glucagon secretion? 3
    • 1. Low blood glucose 
    • 2. Amino acids - from a meal stimulate both glucagon and insulin. Glucagon effectively prevents hypoglycemia that would occur as a result of insulin increase.
    • 3. Epinephrine = by adrenal medulla and/or NE. Thus, during periods of stress, trauma, or severe exercise, elevated ep can override. Despite glucose levels in blood, glucagon levels will be raised and insulin will be lowered. 
  5. What inhibits glucagon secretion?
    Elevated blood glucose and by insulin. 

    Both increased after carb-rich meal & ingestion of glucose. 
  6. What are the metabolic effects of glucagon on carb, lipid, and protein metabolism?
    • 1. Carb: Increases glycogenolysis, gluconeogenesis. 
    • 2. Lipids: increases lipolysis (cAMP), B-oxidation (cAMP), and ketogenesis. 
    • 3. Proteins: Increases uptake of AAs by liver --> increased substrates for GNG --> decreases plasma levels of AAs. 

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