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Such a glucose level also stimulates the secretion of adrenaline, whereas slightly lower levels are needed to elicit autonomic warning symptoms, such as sweating, palpitations, trembling and feeling hungry .
When insulin is given to experimentally induce hypoglycemia in people without diabetes, glucose levels at or below ~3.8 mmol/L will induce a glucagon response, the secretion of which by pancreatic alpha-cells is probably controlled by the neighboring beta-cells .
Hypoglycemia is the most frequent complication of insulin therapy in patients with type 1 diabetes.
Since the brain is reliant on circulating glucose as its main source of energy, hypoglycemia poses a threat for normal brain function.
This inability is known as the clinical syndrome of impaired awareness of hypoglycemia and increases the risk of particularly severe hypoglycemia, defined as those events requiring assistance from another person .
Both the attenuated adrenaline response and impaired awareness of hypoglycemia are usually the result of (recurrent) antecedent hypoglycemia rather than of autonomic neuropathy, for which the term ‘hypoglycemia-associated autonomic failure’ (HAAF) has been introduced .
In patients with longer diabetes duration and more frequent exposure to hypoglycemia, adrenaline responses to hypoglycemia become attenuated, in part due to a shift of these responses to lower glucose values .
Disappearance of these symptoms interferes with the ability to timely and accurately perceive, interpret and respond to falling plasma glucose levels.Since the brain’s energy stores are small, normal brain function depends on a continuous supply of glucose from the bloodstream.Under normal conditions, the human body takes great effort and is very efficient in avoiding hypoglycemia in almost all circumstances to maintain sufficient glucose delivery to the brain.The underlying mechanism(s) explaining the attenuating effect of prior hypoglycemia on responses to subsequent events have not been fully elucidated.However, there is agreement that alterations in the brain play a pivotal role.Unfortunately, therapeutic insulin is still poor at mimicking the pharmacology of endogenous insulin.