Post-bariatric hypoglycaemia: from altered gut physiology to targeted therapies

Post-bariatric hypoglycaemia (PBH) is an increasingly recognised complication of bariatric and metabolic surgery, which can markedly impair quality of life and jeopardise the long-term benefits of surgery. This review summarises the current evidence on the epidemiology, pathophysiology, and management of PBH, with a particular focus on mechanism-based treatment strategies. We first point out the limitations of existing epidemiological data and then outline a practical diagnostic framework. We next review the evolving understanding of PBH as a heterogeneous, pathophysiology-driven syndrome arising from rapid nutrient delivery, exaggerated incretin responses, excessive insulin secretion, impaired glucagon secretion, and emerging contributors, such as postprandial serotonin hypersecretion, bile acid signalling, and microbiome change. On this basis, we review therapeutic options by mechanistic target, covering dietary and lifestyle interventions, acarbose, SGLT inhibition, somatostatin analogues, GLP-1 receptor antagonists, diazoxide, glucagon-based approaches, and experimental serotonin receptor antagonism, and briefly discuss agents with limited supportive evidence. Finally, we explore key knowledge gaps and future directions, including the need for long-term prospective data, precision medicine approaches, rational combination therapy, and greater integration of continuous glucose monitoring and digital decision support. Mechanism-based, multidisciplinary care from bariatric physicians, dietitians, and surgeons offers the best prospect of managing PBH, preserving quality of life, and safeguarding the metabolic benefits of bariatric surgery.