In patients with diabetes, hypoglycemia is the result of the relative or absolute excess of exogenous insulin and the compromised physiological and behavioral defense against falling plasma glucose concentrations. The physiological defense against falling plasma glucose concentrations includes (1) reduced insulin secretion; (2) increased glucagon secretion; (3) and, in the absence of the latter, increased adrenaline secretion. On the other hand, behavioral defense mainly consists of carbohydrates assumption. This behavior is induced by the perception of symptoms, mainly neurogenic, mediated by the neural activation of the sympathetic system. All these defense mechanisms, not only insulin secretion, are impaired in DM1 and, in the long run, also in DM2. In overt DM1, circulating insulin levels does not reduce in response to decreased plasma glucose levels. In addition to the lack pancreatic β-cells response, α-cells also fail to produce glucagon in response to hypoglycemia. In the absence of the primary defense mechanisms (insulin and glucagon), DM1 patients are highly dependent on the third defense mechanism, i.e., the adrenaline secretion. The adrenaline response to hypoglycemia is often attenuated due to mechanisms that are not yet fully defined. In the context of a failure to decrease insulin and increase glucagon, when there is a fall in blood glucose levels in response to therapy- induced hyperinsulinemia, the attenuated adrenaline response causes the clinical syndrome of glycemic counter- regulation deficiency.

Patients with this syndrome have a 25-fold increased risk of developing hypoglycemia. In addition, the attenuated sympathetic neural response causes the clinical syndrome of unconscious hypoglycemia, characterized by the impairment or complete loss of alarm symptoms that trigger behavioral defense. Unconscious hypoglycemia is associated with a sixfold increased risk of developing severe hypoglycemia.

The concept of hypoglycemia-associated autonomic failure in diabetes assumes that recent and antecedent hypoglycemia causes both deficits in glycemic counter regulation (by reducing the response to adrenaline without insulin and glucagon response) and unconscious hypoglycemia (mainly by reducing the sympathetic neural response and the resulting neurogenic symptoms) and, therefore, triggers a vicious cycle of recurrent hypoglycemia. In sub jects with DM1, unconscious hypoglycemia and adrenaline deficiency are reversible after 2–3 weeks of scrupulous attention to avoiding therapy-induced hypoglycemia. The glycemic counter- regulatory deficiency syndrome is primarily due to β-cell deficiency. Thus, DM2 patients may also develop it in the long run. In addition, the threshold for the sympathoadrenal response shifts toward lower plasma glucose concentrations due to antecedent hypoglycemia, similar to DM1. Table 1 shows the main risk factors for hypoglycemia and hypoglycemia- associated autonomic failure in patients with diabetes. There are many variables at stake. Thus, the insulin treatment must be carried out by adequately trained people who can recognize and man age the various and changing factors making the necessary corrections; for example, occasionally changing the insulin dose according to diet or after intense physical exercise. In this case, hypoglycemia can appear from 1–2 h up to 17 h after the end of the physical effort. Aerobic exercise causes:

 1. The increase in the insulin-dependent and -independent muscular glucose uptake

2. The 40–60% reduction in the endogenous insulin secretion

3. The increase in insulin sensitivity in the next 2 h

Therefore, it is always necessary to adjust doses according to glucose consumption.

Table1. Risk factors for hypoglycemia and hypoglycemia-associated autonomic failure associated with hypoglycemia in patients with diabetes mellitus

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مواضيع ذات صلة

Early β-cell dysfunction

Physiological insulin secretion

Mouse genetics reveal tissue- integrated insulin signalling

Heterologous regulation and insulin resistance

Abnormalities of glucagon secretion and action in diabetes

Glucagon intra- islet communication and insulin secretion

Glucagon actions in the liver: amino acid metabolism and the hepatic–α- cell axis

Glucagon actions in the liver: glucose and lipid metabolism

Regulation of α- cell secretion

Regulation of insulin secretion by non- nutrients

Regulation of insulin secretion

Islet structure and function