{"title":"Hypoglycaemia in diabetes","authors":"Simon Heller, Peter Novodvorsky","doi":"10.1016/j.mpmed.2026.07.001","DOIUrl":null,"url":null,"abstract":"<div><div>Hypoglycaemia is a much-feared complication of diabetes treated with insulin or sulfonylureas. Hypoglycaemia prevents people with diabetes from achieving their glycaemic targets. Normal brain function depends on a continuous supply of glucose. Diminished glucose supply to the brain leads to cerebral dysfunction and, if not corrected, confusion and coma. Hypoglycaemia is a direct consequence of the inability of current glucose-lowering therapies to reproduce pancreatic β-cell physiology. This leads to inappropriately high insulin concentrations between meals and at night. Glucagon and adrenaline oppose the glucose-lowering effect of insulin through hepatic glycogenolysis and inhibition of peripheral glucose uptake. In addition, activation of the sympatho-adrenal system provokes symptoms that patients learn to recognize and treat by taking carbohydrates. With an increasing duration of diabetes, and after episodes of hypoglycaemia, these defence mechanisms become impaired. Individuals are increasingly at risk of severe episodes, particularly if they develop ‘impaired awareness of hypoglycaemia’. Structured patient education remains the cornerstone in managing hypoglycaemia. Individualized blood glucose targets prevent recurrent hypoglycaemia. Novel insulin formulations and diabetes technologies such as continuous glucose monitoring and automated insulin delivery systems significantly reduce the burden of hypoglycaemia, but the importance of patient education cannot be overemphasized.</div></div>","PeriodicalId":74157,"journal":{"name":"Medicine (Abingdon, England : UK ed.)","volume":"54 10","pages":"Pages 749-755"},"PeriodicalIF":0.0000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medicine (Abingdon, England : UK ed.)","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S135730392600174X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/8/31 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Hypoglycaemia is a much-feared complication of diabetes treated with insulin or sulfonylureas. Hypoglycaemia prevents people with diabetes from achieving their glycaemic targets. Normal brain function depends on a continuous supply of glucose. Diminished glucose supply to the brain leads to cerebral dysfunction and, if not corrected, confusion and coma. Hypoglycaemia is a direct consequence of the inability of current glucose-lowering therapies to reproduce pancreatic β-cell physiology. This leads to inappropriately high insulin concentrations between meals and at night. Glucagon and adrenaline oppose the glucose-lowering effect of insulin through hepatic glycogenolysis and inhibition of peripheral glucose uptake. In addition, activation of the sympatho-adrenal system provokes symptoms that patients learn to recognize and treat by taking carbohydrates. With an increasing duration of diabetes, and after episodes of hypoglycaemia, these defence mechanisms become impaired. Individuals are increasingly at risk of severe episodes, particularly if they develop ‘impaired awareness of hypoglycaemia’. Structured patient education remains the cornerstone in managing hypoglycaemia. Individualized blood glucose targets prevent recurrent hypoglycaemia. Novel insulin formulations and diabetes technologies such as continuous glucose monitoring and automated insulin delivery systems significantly reduce the burden of hypoglycaemia, but the importance of patient education cannot be overemphasized.