Sự suy giảm nồng độ glucose trong máu sẽ kích hoạt một hệ thống cấp bậc đặc trưng của phản ứng, bắt đầu với sự đàn áp của tiết insulin nội sinh, phát hành của một số truy cập, điều tiết hormone, và sự phát triển tiếp theo các triệu chứng đặc trưng | 134 DIABETES IN OLD AGE 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 . 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 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 . 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 glycogenolysis releasing glucose from glycogen stored in the liver and also promote gluconeogenesis from Figure Hierarchy of responses to hypoglycaemia in nondiabetic humans Figure 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. .
