Hypoglycemia is a condition characterized by CNS symptoms, such as confusion, aberrant behavior, or coma, along with a blood glucose level ≤50 mg/dl, which can be resolved within minutes after administering glucose (Fig. 23.13). It is considered a medical emergency because the CNS requires a constant supply of glucose as fuel. Transient hypoglycemia can lead to cerebral dysfunction, while severe and prolonged cases can cause brain damage. To prevent or correct hypoglycemia, the body has multiple overlapping mechanisms in place. The primary hormonal changes involved in combating hypoglycemia are increased glucagon and catecholamine secretion, accompanied by decreased insulin secretion.

The symptoms of hypoglycemia can be categorized into two groups. Adrenergic symptoms, such as anxiety, palpitation, tremor, and sweating, are mediated by the release of catecholamines (mainly epinephrine), regulated by the hypothalamus in response to hypoglycemia. Adrenergic symptoms typically occur when blood glucose levels rapidly decline. The second category of symptoms is neuroglycopenic, resulting from the impaired delivery of glucose to the brain (neuroglycopenia). This impairs brain function and leads to symptoms like headache, confusion, slurred speech, seizures, coma, and even death. Neuroglycopenic symptoms usually arise from a gradual decline in blood glucose, often below 50 mg/dl. In such cases, the slow decline in glucose does not trigger an adequate adrenergic response.

Humans possess two glucose-regulating systems that are activated in response to hypoglycemia: the release of glucagon by pancreatic α cells and the activation of glucose receptors in the hypothalamus, which respond to abnormally low blood glucose levels. These hypothalamic glucoreceptors can trigger the secretion of catecholamines (mediated by the sympathetic division of the autonomic nervous system) and the release of adrenocorticotropic hormone (ACTH) and growth hormone by the anterior pituitary (see Fig. 23.13). It is important to note that ACTH increases cortisol synthesis and secretion in the adrenal cortex. Glucagon, catecholamines, cortisol, and growth hormone are referred to as counterregulatory hormones because each opposes the action of insulin on glucose utilization.

The most crucial counterregulatory hormones in the acute, short-term regulation of blood glucose levels are glucagon and epinephrine. Glucagon stimulates the breakdown of glycogen in the liver (glycogenolysis) and the production of new glucose (gluconeogenesis). Epinephrine promotes glycogenolysis and lipolysis, inhibits insulin secretion, and prevents the uptake of glucose by muscle and adipose tissues mediated by GLUT-4. Epinephrine assumes a critical role in cases where glucagon secretion is deficient, such as in the late stages of type 1 diabetes mellitus. The prevention or correction of hypoglycemia fails when both glucagon and epinephrine secretion are inadequate.

Cortisol and growth hormone are less significant in the short-term maintenance of blood glucose levels but play a role in the long-term management of glucose metabolism through transcriptional processes.

Regarding types of hypoglycemia, the excerpt does not provide further information.
IV. HYPOGLYCEMIA
Hypoglycemia is characterized by 1) central nervous system (CNS) symptoms, including confusion, aberrant behavior, or coma; 2) a simultaneous blood glucose level ≤50 mg/dl; and 3) symptoms being resolved within minutes following glucose administration (Fig. 23.13). Hypoglycemia is a medical emergency because the CNS has an absolute requirement for a continuous supply of bloodborne glucose to serve as a metabolic fuel. Transient hypoglycemia can cause cerebral dysfunction, whereas severe, prolonged hypoglycemia causes brain damage. Therefore, it is not surprising that the body has multiple overlapping mechanisms to prevent or correct hypoglycemia. The most important hormone changes in combating hypoglycemia are increased secretion of glucagon and the catecholamines, combined with decreased insulin secretion.
A. Symptoms
The symptoms of hypoglycemia can be divided into two categories. Adrenergic (neurogenic, autonomic) symptoms, such as anxiety, palpitation, tremor, and sweating, are mediated by catecholamine release (primarily epinephrine) regulated by the hypothalamus in response to hypoglycemia. Adrenergic symptoms typically occur when blood glucose levels fall abruptly. The second category of hypoglycemic symptoms is neuroglycopenic. The impaired delivery of glucose to the brain (neuroglycopenia) results in impairment of brain function, causing headache, confusion, slurred speech, seizures, coma, and death. Neuroglycopenic symptoms often result from a gradual decline in blood glucose, often to levels <50 mg/dl. The slow decline in glucose deprives the CNS of fuel but fails to trigger an adequate adrenergic response.
B. Glucoregulatory systems
Humans have two overlapping glucose-regulating systems that are activated by hypoglycemia: 1) the pancreatic α cells, which release glucagon, and 2) receptors in the hypothalamus, which respond to abnormally low concentrations of blood glucose. The hypothalamic glucoreceptors can trigger both the secretion of catecholamines (mediated by the sympathetic division of the autonomic nervous system) and release of adrenocorticotropic hormone (ACTH) and growth hormone by the anterior pituitary (see Fig. 23.13). [Note: ACTH increases cortisol synthesis and secretion in the adrenal cortex (see p. 239).] Glucagon, the catecholamines, cortisol, and growth hormone are sometimes called the counterregulatory hormones because each opposes the action of insulin on glucose use.
1.
Glucagon and epinephrine: Secretion of these counterregulatory hormones is most important in the acute, short-term regulation of blood glucose levels. Glucagon stimulates hepatic glycogenolysis and gluconeogenesis. Epinephrine promotes glycogenolysis and lipolysis. It inhibits insulin secretion, thereby preventing GLUT-4–mediated uptake of glucose by muscle and adipose tissues. Epinephrine assumes a critical role in hypoglycemia when glucagon secretion is deficient, for example, in the late stages of type 1 diabetes mellitus (see p. 340). The prevention or correction of hypoglycemia fails when the secretion of both glucagon and epinephrine is deficient.
2.
Cortisol and growth hormone: These counterregulatory hormones are less important in the short-term maintenance of blood glucose concentrations. They do, however, play a role in the long-term (transcriptional) management of glucose metabolism.
C. Types