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

Post-bariatric hypoglycaemia (PBH) is an increasingly recognised complication of bariatric and metabolic surgery, that 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 post-prandial 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.