Post-gastric Bypass Hypoglycaemia: A Review

Prapimporn C. Shantavasinkul; Alfonso Torquati; Leonor Corsino


Clin Endocrinol. 2016;85(1):3-9. 

In This Article

Abstract and Introduction


Bariatric surgery is a highly effective treatment for severe obesity, resulting in substantial weight loss and normalizing obesity-related comorbidities. However, long-term consequences can occur, such as postbariatric surgery hypoglycaemia. This is a challenging medical problem, and the number of patients presenting with it has been increasing. Roux-en-Y gastric bypass (RYGB) is the most popular bariatric procedure, and it is the surgery most commonly associated with the development of postbariatric surgery hypoglycaemia. To date, the pathogenesis of this condition has not been completely established. However, various factors – particularly increased postprandial glucagon-like peptide (GLP)-1 secretion – have been considered as crucial mediator. The mechanisms responsible for diabetic remission after bariatric surgery may be responsible for the development of hypoglycaemia, which typically occurs 1–3 h after a meal and is concurrent with inappropriate hyperinsulinaemia. Carbohydrate-rich foods usually provoke hypoglycaemic symptoms, which can typically be alleviated by strict dietary modifications, including carbohydrate restriction and avoidance of high glycaemic index foods and simple sugars. Few patients require further medical intervention, such as medications, but some patients have required a pancreatectomy. Because this option is not always successful, it is no longer routinely recommended. Clinical trials are needed to further determine the pathophysiology of this condition as well as the best diagnostic and treatment approaches for these patients.


Obesity requires treatment to alleviate obesity-related comorbidities, including type 2 diabetes mellitus (T2DM) and cardiovascular disease. Nonsurgical management can induce modest weight loss and improve cardiovascular health outcomes in severely obese individuals.[1] However, medical treatment failure and weight regain are common. Bariatric surgery has emerged as an effective tool for treating obesity, resulting in long-term weight loss and remission of obesity-related comorbidities.[2] Currently, bariatric surgery is indicated in patients with a body mass index (BMI) ≥40 kg/m2 or ≥35 kg/m2 with one or more obesity-related comorbidity such as T2DM, hypertension, hyperlipidaemia or obstructive sleep apnoea.[3] Additionally, patients with poorly controlled T2DM and a BMI of 30–34·9 kg/m2 (particularly in patients with major cardiovascular risk factors) are considered candidates for bariatric surgery.[4]

Bariatric surgeries alter the anatomy of the gastrointestinal tract to restrict caloric intake or reduce nutrient absorption, and they are usually classified as restrictive or malabsorptive. Several bariatric procedures are currently available: laparoscopic adjustable gastric banding (AGB), laparoscopic sleeve gastrectomy (SG), laparoscopic Roux-en-Y gastric bypass (RYGB) and the biliopancreatic diversion with duodenal switch (BPD-DS).

SG and RYGB are the most common procedures. SG is a purely restrictive procedure that has gained increasing popularity during the last couple of years. In this procedure, the greater curvature of the stomach is dissected, leaving a sleeve-shaped tube that has a volume of approximately 150 ml. RYGB, on the other hand, has a combined restrictive and malabsorptive component; stomach capacity is reduced to 20–30 ml and nutrient contents are bypassed to the distal jejunum. A large proportion of patients who undergo RYGB experience complete resolution of obesity-related comorbidities, including T2DM, prior to any significant weight loss. However, RYGB is the procedure most commonly associated with the development of postbariatric surgery hypoglycaemia. This implies that RYGB, which alters the gastrointestinal anatomy and gut-derived hormones, is not only producing weight loss but is also altering critical pathways of glucose metabolisms.

Glucagon-like peptide (GLP)-1 is an incretin hormone produced in the L-cell of the distal intestine, and after RYGB, it is significantly increased postprandial in response to the more rapid passage of nutrients into the small bowel.[5] In one study, gastric bypass patients had an earlier and higher peak response of glucose and a lower nadir glucose, resulting from increasing GLP-1 and insulin secretion.[6] Postprandial GLP-1 is increased 10-fold in RYGB patients, and it is even higher in those with postbariatric surgery hypoglycaemia. Increased incretin levels may contribute to the amplified insulin secretory response, which results in postprandial hypoglycaemia. Although it is likely that multiple factors contribute to postbariatric surgery hypoglycaemia, GLP-1 is a critical contributor to inappropriate insulin secretion in patients with this condition.

Recently, hypoglycaemia associated with gastric bypass surgery has been described as a consequence of the procedure, and multiple mechanisms and clinical presentations have been reported. The prevalence of postbariatric surgery hypoglycaemia has been reported as <1%;[7,8] however, this might be underestimated. With RYGB being increasingly used to treat obesity, physicians may encounter an increasing incidence of postbariatric surgery hypoglycaemia. Herein, we discuss the potential pathophysiology, clinical manifestations, diagnosis and management of postbariatric surgery hypoglycaemia.