Postprandial hypoglycemia after upper gastrointestinal tract surgery: prevalence and pathophysiology (part 1)

Abstract

Nowadays obesity is a major health problem worldwide. Surgery is the most promising treatment for morbid obesity. There are two types of bariatric procedures, one to reduce the food intake volume and the other to limit the absorption of nutrients. Despite the indisputable advantages of bariatric surgery for weight loss, it is necessary to remember the potential risk of severe complications, such as hypoglycemic syndrome at 2 to 3 hours after ingestion of rapidly absorbable carbohydrates manifested by adrenergic and neuroglycopenic symptoms. According to the literature, the prevalence of post-bariatric postprandial hyperinsulinemic hypoglycemia (PHH) varies from 10% to 75%. PHH in post-bariatric patients should be differentiated from the syndrome of non-insulinoma pancreatogenic hypoglycemia and from insulinoma; however, these diseases are described also in patients after bariatric surgery.The mechanisms of PHH as an outcome of shunting bariatric procedures are currently not fully clear. According to the recent studies, incretin hypersecretion in response to the accelerated flow of carbohydrates into the small intestine plays a leading role in the inappropriate excess production of insulin by the pancreas. In addition, there are hypotheses on a slower normalization of insulin production during more rapid bodyweight decrease and regression of insulin resistance, the role of alpha-cell dysfunction, disturbed negative feedback between insulin and ghrelin, compensatory hyperplasia and hypertrophy of the remaining enterocytes (including L-cells), changes in gut microflora, bile acids level and composition. A number of other mechanisms have also been proposed that require further studies.