Greenspan's Basic and Clinical Endocrinology, 8th Ed.
Pathophysiology of the Counterregulatory Response to Neuroglycopenia
Sections: Pathophysiology of the Counterregulatory Response to Neuroglycopenia, Counterregulatory Response to Hypoglycemia, Insulin, Catecholamines, Glucagon, Corticotropin and Hydrocortisone, Growth Hormone, Cholinergic Neurotransmitters, Maintenance of Euglycemia in the Postabsorptive State, Role of the Kidney, Role of PGC-1 in Regulation of Gluconeogenesis.
Topics Discussed: acetylcholine; catecholamines; corticotropin; glucagon; gluconeogenesis; hydrocortisone; hypoglycemia; insulin; kidney; liver; neuroglycopenia; somatotropin.
Excerpt: "The plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors, such as the status of blood flow to the brain, the integrity of cerebral tissue, the prevailing arterial level of plasma glucose, the rapidity with which plasma glucose concentration falls, and the availability of alternative metabolic fuels.Endogenous insulin secretion is lowered both by reduced glucose stimulation to the pancreatic cell and by sympathetic nervous system inhibition from a combination of alpha-adrenergic neural effects and increased circulating catecholamine levels. This reactive insulinopenia appears to be essential for glucose recovery, because it facilitates the mobilization of energy from existing energy stores (glycogenolysis and lipolysis); increases hepatic enzymes involved in gluconeogenesis and ketogenesis; increases enzymes of the renal cortex, promoting gluconeogenesis; and at the same time prevents muscle tissue from consuming the blood glucose being released from the liver (Chapter 18)...."