Oral Hypoglycemic Agent Toxicity Medication

Updated: Jan 15, 2020
  • Author: David Tran, MD; Chief Editor: Stephen L Thornton, MD  more...
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Dextrose and glucose stimulators

Class Summary

Prompt gluconeogenesis is achieved with glucagon. Emergent blood glucose elevation requires intravenous dextrose. First-line agent for oral hypoglycemic toxicity is dextrose.

Pancreatic alpha cells of the islets of Langerhans produce glucagon, a polypeptide hormone. Exerts opposite effects of insulin on blood glucose. Glucagon elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats (gluconeogenesis). Increases hydrolysis of glycogen to glucose (glycogenolysis) in liver in addition to accelerating hepatic glycogenolysis and lipolysis in adipose tissue. Glucagon increases force of contraction in the heart and has a relaxant effect on the GI tract.

Dextrose (D-glucose)

Used to promptly elevate serum glucose. Monosaccharide absorbed from intestine and then distributed, stored, and used by tissues. Parenterally injected dextrose is used in patients who are unable to sustain adequate oral intake. Direct oral absorption results in a rapid increase in blood glucose concentrations. Effective in small doses. No evidence suggests that it may cause toxicity. Concentrated dextrose infusions provide higher amounts of glucose and increased energy intake in a small volume of fluid.


Extracted from beef and pork pancreas. Chemically unrelated to insulin, glucagon is a single-chain polypeptide with 29 amino acid residues and a molecular weight of 3,483. In patients with insulinoma, IV administration of glucagon produces an initial increase in blood glucose; however, because of glucagon's insulin-releasing effect, it may cause the insulinoma to release its insulin and subsequently cause hypoglycemia. Glucagon increases blood glucose concentration and is used to treat hypoglycemia. It is effective in small doses, and no evidence of toxicity has been reported with its use. Glucagon acts only on liver glycogen, converting it to glucose. Parenteral administration of glucagon produces relaxation of the smooth muscle of the stomach, duodenum, small bowel, and colon. The half-life of glucagon in plasma is approximately 3-6 min, similar to that of insulin.


Insulin secretion inhibiting agents

Class Summary

Insulin secretion may be altered by various mechanisms. Diazoxide inhibits pancreatic secretion of insulin, stimulates glucose release from the liver, and stimulates catecholamine release, which elevates blood glucose levels. It causes a false-negative insulin response to glucagon.

Octreotide is a peptide with pharmacologic action similar to somatostatin, which inhibits insulin secretion.

Diazoxide (Proglycem, Hyperstat)

Increases blood glucose by inhibiting pancreatic insulin release and possibly through an extrapancreatic effect. Hyperglycemic effect begins within an hour and usually lasts a maximum of 8 h with normal renal function.

Octreotide (Sandostatin)

Acts primarily on somatostatin receptor subtypes II and V. A somatostatin analogue, which activates G-protein K channel. Hyperpolarization of the beta cell results in inhibition of Ca influx and insulin release. Octreotide is also used for acromegaly, carcinoid tumors, and Vipomas.