Control of Blood Glucose

Explain the control of blood glucose

Normal blood glucose in the non-diabetic is 4-6 mmol.L-1, though will rise after consumption of carbohydrate. Glucose regulation can be divided into:

  • Short-term
    Regulation via secretion or inhibition of insulin and glucagon from the pancreatic islets.
  • Long-term
    Regulation via both neuronal (SNS activation) and hormonal (cortisol, GH) mechanisms.

Hormonal Mechanisms

Short Term

Glucose levels are sensed directly in the pancreas and will result in insulin release when the BGL is >5.6 mmol.L-1. Pancreatic B cells respond directly to glucose by secreting insulin in a biphasic fashion:

  • An initial, rapid increase in release
    • Glucose enters via the GLUT-2 transporter, and is converted to pyruvate which enters the citric acid cycle and produces ATP
    • ATP inhibits ATP-sensitive K+ channels, reducing K+ efflux and causing depolarisation
    • Depolarisation causes Ca2+ release, resulting in exocytosis of insulin granules
  • A prolonged, slow increase in release
    • Glutamate is produced as a by-product of the citric acid cycle
    • Glutamate stimulates maturation of other insulin granules
    • Release of these granules causes the second phase of insulin release

Conversely, a low glucose level stimulates secretion of glucagon. This is typically less important than the effect of insulin unless in situations of starvation or severe physiological stress.

Long Term

Sustained hypoglycaemia increases fat utilisation and decreases glucose utilisation (limiting further drops in blood glucose), via stimulating release of:

  • GH
  • Cortisol

Neuronal Mechanisms

Hypoglycaemia directly stimulates the hypothalamus, causing:

  • Increased SNS tone
    Adrenaline release in turn stimulates hepatic glucose release.

Organ Effects

Glucose levels are influenced by the:

  • Liver
    Insulin and glucagon act on the liver to continually adjust the relative rates of glycogenolysis and glycogenesis, allowing it to function as an effective buffer of blood glucose.
    • Hepatic disease significantly limits the efficacy of this system, and results in a widely-fluctuating blood glucose level
  • Kidney
    • A transient glycosuria may be seen as hyperglycaemia decreases renal absorption of glucose

Physiological Responses to Hypoglycaemia

BSL (mmol.L-1) Symptoms Endocrine Response
4.6 Insulin secretion inhibited
3.8 Autonomic dysfunction Glucagon, adrenaline, and GH secretion
2.8 CNS dysfunction
2.2 Lethargy, Coma
1.7 Convulsions
0.6 Permanent brain damage, Death


  1. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology. 24th Ed. McGraw Hill. 2012.
  2. Hall, JE, and Guyton AC. Guyton and Hall Textbook of Medical Physiology. 11th Edition. Philadelphia, PA: Saunders Elsevier. 2011.
Last updated 2019-07-18

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