Counterregulation

The human brain is dependent upon glucose as its principal source of energy and requires a continuous supply of glucose via the cerebral circulation. Depriving the brain of glucose rapidly causes neuro-glycopenia, which has various effects, including impairment of cognitive function.

In humans, several mechanisms have evolved to maintain glucose homeostasis and so protect the integrity and functioning of the brain (Cryer 1993). A decline in blood glucose concentration activates a characteristic hierarchy of responses, commencing with the suppression of endogenous insulin secretion, the release of several counter-regulatory hormones, and the subsequent development of characteristic symptoms (Figure 10.1). These alert the informed individual to the development of hypoglycaemia, so allowing him or her to take early and appropriate action (the ingestion of carbohydrate) to assist recovery. Such protective responses are usually effective in maintaining the arterial blood glucose concentration within a normoglycaemic range (which can be arbitrarily defined as a blood glucose above 3.8 mM), which protects the brain from exposure to neuroglycopenia. Glucose counter-regulation is controlled from centres within the brain (mainly the ventromedial hypothalamus) assisted by activation of hypothalamic autonomic nervous centres with stimulation of the peripheral sympatho-adrenal system. This contributes to glucose counter-regulation through the peripheral actions of catecholamines and by the generation of characteristic autonomic warning symptoms (Figure 10.2). Although glucagon is the most potent counter-regulatory hormone, the role of adrenaline becomes paramount if the secretory response of glucagon is deficient (Gerich 1988). Other counter-regulatory hormones, such as cortisol and growth hormone, have greater importance in promoting recovery from prolonged hypoglycaemia.

Glucagon and adrenaline stimulate hepatic glyco-genolysis, releasing glucose from glycogen stored in the liver, and also promote gluconeogenesis from

Gluconeogenesis Cortisol

Figure 10.1 Hierarchy of responses to hypoglycaemia in non-diabetic humans

Glucose Counterregulation

Figure 10.2 Principal components of glucose counter-regulation in humans

Figure 10.1 Hierarchy of responses to hypoglycaemia in non-diabetic humans

Figure 10.2 Principal components of glucose counter-regulation in humans three-carbon precursors such as alanine, lactate and glycerol. The energy for this process is provided by the hepatic oxidation of free fatty acids that are released by lipolysis. Catecholamines inhibit insulin secretion, diminish the peripheral uptake of glucose, stimulate lipolysis and proteolysis, and promote glycogenolysis in peripheral muscle to provide lactate, which is utilized for gluconeogenesis in the liver and kidney.

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