Energy Balance and the Fed–Fasted State
Key facts on fuel depots, insulin/glucagon actions and the fasting timeline.
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Questions Covered in This Set
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Why must plasma glucose be defended so tightly?
The brain uses ~120 g glucose/day and cannot use fatty acids, yet the circulating glucose pool is only ~4 g (~45 minutes of brain fuel). Normal range ~4–6 mmol/L (70–110 mg/dL).
Why can only liver glycogen raise blood glucose?
Liver has glucose-6-phosphatase, so it releases free glucose; muscle lacks it, so muscle glycogen (~400 g) is for local use only (indirectly via lactate/alanine).
Why can't fat be converted to net glucose?
Acetyl-CoA cannot go backwards through pyruvate dehydrogenase. Only the glycerol backbone (~5% of a TAG) is gluconeogenic.
Sequence of glucose-stimulated insulin secretion
Glucose → GLUT2 → glucokinase → ATP rise → closure of K_ATP channels → depolarisation → Ca²⁺ entry → biphasic insulin release.
What is the incretin effect?
GLP-1 and GIP from the gut amplify insulin release, so oral glucose evokes far more insulin than the same dose given IV — the basis of GLP-1 agonist drugs.
Four main actions of insulin
1) GLUT4 insertion in muscle/adipose; 2) hepatic glycogen synthesis, lipogenesis, suppressed gluconeogenesis; 3) activates lipoprotein lipase and inhibits hormone-sensitive lipase; 4) amino acid uptake and protein synthesis.
Which tissues take up glucose independently of insulin?
Brain, liver and red blood cells (GLUT1/GLUT2/GLUT3-mediated).
What is the Randle cycle relevance after a meal?
Insulin's potent suppression of lipolysis lowers plasma free fatty acids, removing FFA competition for oxidation so tissues burn the incoming carbohydrate.
Fasting timeline of fuel sources
0–4 h: hepatic glycogenolysis; 4–24 h: gluconeogenesis (lactate, alanine, glycerol); 1–3 days: lipolysis and ketogenesis; >3 days: brain derives ~2/3 energy from ketones (protein sparing).
What is the true metabolic 'switch' in fasting?
The insulin:glucagon ratio — falling insulin is the primary event, with rising glucagon acting via Gs → cAMP → PKA → phosphorylase kinase.
