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)

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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.

Glucagon

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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.

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)

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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)

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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.

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Normal hypoglycemic counterregulation.

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Table. Sulfonylurea exposures reported to the American Association of Poison Control Centers' National Data Collection System from 2006-2021

Table. Sulfonylurea exposures reported to the American Association of Poison Control Centers' National Data Collection System from 2006-2021

Year	Exposures	< 6 Years	≥6 Years	Unintentional Exposures	Overall Mortality*	Pediatric Mortality
2006	1951	974	903	1647	1	0
2007	1975	991	890	1666	0	0
2008	1850	987	808	1571	0	0
2009	1769	922	769	1515	1	0
2010	1712	898	745	1453	0	0
2011	1687	804	807	1404	1†	-
2012	1753	850	798	1449	1†	-
2013	1590	778	762	1340	0	0
2014	1584	778	769	1316	2	0
2015	1659	807	852	1413	2	0
2016	1582	677	905	1295	2†	-
2017	1471	693	778	1240	2†	-
2018	1512	613	899	1199	1†
2019	1370	570	800	1113	0
2020	1189	482	707	957	1†
2021	1084	410	674	844	2†
*Overall mortality includes adult and pediatric cases † Patient age not noted

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Author

David Tran, MD Attending Physician, Department of Emergency Medicine, North Shore-LIJ Plainview Hospital

David Tran, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Received salary from Merck for employment.

Chief Editor

Stephen L Thornton, MD Associate Clinical Professor, Department of Emergency Medicine (Medical Toxicology), University of Kansas Hospital; Medical Director, University of Kansas Hospital Poison Control Center; Staff Medical Toxicologist, Children’s Mercy Hospital

Stephen L Thornton, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Additional Contributors

Michael E Mullins, MD Assistant Professor, Division of Emergency Medicine, Washington University in St Louis School of Medicine; Attending Physician, Emergency Department, Barnes-Jewish Hospital

Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians

Disclosure: Received stock ownership from Johnson & Johnson for none; Received stock ownership from Savient Pharmaceuticals for none.

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Michael Lucchesi, MD, to the original writing and development of this article.