hypoglycemia

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hypoglycemia:

see diabetesdiabetes
or diabetes mellitus
, chronic disorder of glucose (sugar) metabolism caused by inadequate production or use of insulin, a hormone produced in specialized cells (beta cells in the islets of Langerhans) in the pancreas that allows the body to use and store
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.

Hypoglycemia

 

a decrease in the sugar content of the blood to below 80-70 mg percent.

Hypoglycemia is found in healthy persons during heightened muscular activity as a result of the considerable expenditure of glucose as an energy source when the body’s energy loss is not replenished with readily assimilable carbohydrates. Hypoglycemia sometimes arises after heavy intake of carbohydrates as a result of the reflex secretion by the pancreas of an excessive amount of insulin. The condition is observed in certain diseases of the insular apparatus of the pancreas, the hypothalamic region of the brain, the other endocrine glands, or the liver (disruption of the liver’s function as the principal glycogen depot), as well as in insulin overdose (hypoglycemic shock). In hypoglycemic shock, after a short period of central nervous system excitation, a condition develops that is accompanied by weakness, drowsiness, hunger, and psychic disturbances. Trembling, loss of consciousness, and convulsions may set in when sugar content is lowered to 40 percent or less. The condition is eliminated by administering glucose. Hypoglycemic or insulin shock may be induced artificially for the treatment of certain diseases.

REFERENCES

Genes, S. G. Gipoglikemiia: Gipoglikemiche skii simptomokompleks. Moscow, 1970. (Bibliography, pp. 224-35.)

hypoglycemia

[¦hī·pō‚glī′sē·mē·ə]
(medicine)
Condition caused by low levels of sugar in the blood.
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Currently, there are six major classes of oral hypoglycemic agents available in the United States: agents that stimulate insulin secretion (sulfonylureas and rapid-acting secretagogues); reduce hepatic glucose production (biguanides); delay digestion and absorption of intestinal carbohydrates ([alpha]-glucosidase inhibitors); improve insulin action (thiazolidin-ediones [TZDs]); or inhibit glucagon release (dipeptidyl-peptidase 4 [DPP-4] inhibitors).
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The procedure maintained its effect through 3 years of follow-up, during which the patients significantly lowered their use of oral hypoglycemic agents and insulin.
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