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Hypoglycemia

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Hypoglycemia is a blood glucose level below 70 mg/dL. It commonly occurs in individuals using insulin or insulin-secreting drugs, but may also arise in non-diabetic conditions. People with type 1 diabetes are at the highest risk because they depend on exogenous insulin. People with type 2 diabetes are also at risk, especially when treated with insulin or medications such as sulfonylureas, which increase insulin release regardless of blood glucose levels. It develops when insulin levels exceed...

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...

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Related Experiment Video

Updated: May 13, 2026

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

Methadone-induced hypoglycemia.

Andrew J Faskowitz¹, Vladimir N Kramskiy, Gavril W Pasternak

¹Department of Neurology and The Molecular Pharmacology and Chemistry Program, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10065, USA.

Cellular and Molecular Neurobiology

|March 8, 2013

Summary

High-dose methadone significantly lowers blood glucose in mice, an effect mediated by the mu-opioid receptor. This study highlights the need for careful glucose monitoring in patients on high-dose methadone therapy.

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Area of Science:

Pharmacology
Neuroscience
Endocrinology

Background:

Recent clinical observations noted hypoglycemia in patients receiving high-dose methadone.
The underlying mechanisms for methadone-induced hypoglycemia remain unclear.

Purpose of the Study:

To investigate the effects of methadone and other mu-opioids on blood glucose levels in a mouse model.
To explore the receptor-specific mechanisms of methadone's impact on glucose homeostasis.

Main Methods:

Mice were administered varying doses of methadone and other mu-opioids.
Blood glucose levels were monitored, and the effects were assessed using opioid antagonists (naloxone, β-funaltrexamine, naloxonazine).
Stereoselectivity of methadone's effect was examined using its isomers.

Main Results:

Methadone demonstrated a dose-dependent reduction in blood glucose levels.
The hypoglycemic effect of methadone was antagonized by naloxone and mu-selective antagonists.
The l-isomer of methadone was responsible for the glucose-lowering effect, while the d-isomer was ineffective.
Other mu-opioids like morphine and fentanyl did not significantly alter blood glucose levels.

Conclusions:

Methadone induces hypoglycemia in mice via a stereoselective interaction with the mu-opioid receptor.
This animal model replicates clinical findings, underscoring the need for glucose monitoring in patients on high-dose methadone.
Differences in effects among mu-opioids may involve specific Oprm1 splice variants, warranting further investigation.