Literature Review: Drug and Alcohol-Induced Hypoglycaemia

Ethanol metabolism increases NADH, which inhibits two primary steps in gluconeogenesis: conversion of lactate into pyruvate and oxaloacetate into malate.

“Ethanol is metabolized by alcohol dehydrogenase, which reduces NAD+ to NADH in the oxidative process. The increased NADH level inhibits two primary steps in gluconeogenesis: the conversion of lactate into pyruvate and oxaloacetate into malate [18].”

In the setting of poor nutritional status or impaired hepatic function, glycogen stores are likely already depleted, leading to increased risk for hypoglycemia.

“However, in the setting of poor nutritional status or impaired hepatic function, glycogen stores are likely already depleted, leading to an increased risk for hypoglycemia.”

In a healthy individual without risk factors, alcohol usually does not cause hypoglycemia because it also stimulates hepatic glycogenolysis.

“In a healthy individual without risk factors, this usually does not cause issues, as alcohol also stimulates hepatic glycogenolysis [18].”

In patients with diabetes, alcohol ingestion is associated with a reduction in growth hormone levels, which may attenuate counterregulatory responses to hypoglycemia.

“In addition, in patients with diabetes, studies have found that alcohol ingestion is associated with a reduction in growth hormone levels, which may attenuate counterregulatory responses to hypoglycemia [18].”

Sulfonylureas and meglitinides bind to different domains on sulfonylurea receptors expressed on pancreatic β-cells, promoting closure of KATP channels and subsequent insulin release.

“These two classes bind to different domains on sulfonylurea receptors expressed on pancreatic β -cells, promoting closure of KATP channels and subsequent insulin release [18].”