Endo – Glucose

Master answer

BSL normally maintained 4-7mmol/L

• maintained by –ve feeback system
  • detector: islets of Langerhans cells in pancreas
  • stimulus= BSL
  • effector = insulin:glucagon release ratio
  • aim: maintain BSL to provide substrate for obligate glucose metbaolisers (brain + RBC)
• hypoglycaemia = BSL <3mmol/L

Acute hypoglycaemia

• ↓ BSL: compensatory mechanisms not yet activated (hormonal ∆s not yet occurred) → glucagon, cortisol, GH levels minimal initial change
• early sign: hunger
• later signs: neurological impairment → confusion, agitation → progression with ↓ BSL → coma, seizures, death

Physiological consequences of acute hypoglycaemia

• SNS activation → ↑ catecholamine release
  • Central: nausea, agitation, hunger
  • Liver: ↑ glycogenolysis, ↑ glucose release
  • Pancreas: inhibition of insulin release
  • CVS: ↑ HR, ↑ SVR, peripheral shutdown, sweating
• ↓ insulin release: ↑ BSL detected by β cells of islets of Langerhans
  • adipose tissue:
    • ↓ glucose uptake (↓GLUT4 transporters in membrane)
    • ↓ fat uptake (extracellular inhibition of LPL in endothelium)
    • ↑ FFA release (↑ intracelular hormone sensitive lipase)
  • muscle
    • ↓ glucose uptake (↓ GLUT4)
    • ↓ protein synthesis
    • ↓ glucogenesis
    • ↑ FFA metabolism
  • liver
    • ↑ glucose release (glycogenolysis)
    • ↑ FFA release (some ketone body formation)
    • ↑ gluconeogenesis via glycerol (fats) and lactate (RBC metabolism)
• ↑ catabolic hormones: ↓ BSL stimulates hormonal changes which aim to ↑ BSL over sustained period
  • ↑ glucagon → ↑ hepatic gluconeogenesis from aa, lactate, glycerol
  • cortisol, GH → ↑ FFA release from adipose tissue

Kerr 2016

Answer by Kerr