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Metabolic Fuel Use

  • Diet
    • 1g carb/protein (eg, whey) = 4 kcal
    • 1g alcohol = 7 kcal
    • 1g fatty acid = 9 kcal
    • (# letters = # kcal)
  • Fasting and starvation  – Priorities are to supply sufficient glucose to the brain and RBCs and to reserve protein.
    • Fed state (after a meal)
      • Glycolysis and aerobic respiration. Insulin stimulates storage of lipids, proteins, and glycogen.
    • Fasting (between meals)
      • Hepatic glycogenolysis (major); hepatic gluconeogenesis, adipose release of FFA (minor).
      • Glucagon and epinephrine stimulate use of fuel reserves.
    • Starvation days 1–3
      • Blood glucose levels maintained by:
        • Hepatic glycogenolysis
        • Adipose release of FFA
        • Muscle and liver, which shift fuel use from glucose to FFA
        • Hepatic gluconeogenesis from peripheral tissue lactate and alanine, and from adipose tissue glycerol and propionyl-CoA (from odd-chain FFA—the only triacylglycerol components that contribute to gluconeogenesis)
      • Glycogen reserves depleted after day 1.
      • RBCs lack mitochondria and therefore cannot use ketones.
    • Starvation after day 3
      • Adipose stores (ketone bodies become the main source of energy for the brain). After these are depleted, vital protein degradation accelerates, leading to organ failure and death. Amount of excess stores determines survival time.
  • Symptoms of hypoglycemia fall into 2 broad categories: neurogenic (autonomic) and neuroglycopenic.
    • Neurogenic symptoms are caused by sympathoadrenal activation and are mediated via norepinephrine/epinephrine and acetylcholine released by sympathetic postganglionic nerve fibers.  Symptoms of norepinephrine/epinephrine release include tremulousness, palpitations, and anxiety/arousal, whereas cholinergic symptoms include sweating, hunger, and paresthesias.
    • Neuroglycopenic symptoms include behavioral changes, confusion, visual disturbances, stupor, and seizures.

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