Abstract
ObjectiveRoux-en-Y gastric bypass (RYGB) surgery is currently the most effective treatment for diabetes and obesity. An increasingly recognized and highly disabling complication of RYGB is postprandial hypoglycaemia (PPH). The pathophysiology of PPH remains unclear with multiple mechanisms suggested including nesidioblastosis, altered insulin clearance and increased glucagon-like peptide-1 (GLP-1) secretion. Whilst many PPH patients respond to dietary modification, some have severely disabling symptoms. Multiple treatments are proposed, including dietary modification, GLP-1 antagonism, GLP-1 analogues and even surgical reversal, with none showing a more decided advantage over the others. A greater understanding of the pathophysiology of PPH could guide the development of new therapeutic strategies.MethodsWe studied a cohort of PPH patients at the Imperial Weight Center. We performed continuous glucose monitoring to characterize their altered glycaemic variability. We also performed a mixed meal test (MMT) and measured gut hormone concentrations.ResultsWe found increased glycaemic variability in our cohort of PPH patients, specifically a higher mean amplitude glucose excursion (MAGE) score of 4.9. We observed significantly greater and earlier increases in insulin, GLP-1 and glucagon in patients who had hypoglycaemia in response to an MMT (MMT Hypo) relative to those that did not (MMT Non-Hypo). No significant differences in oxyntomodulin, GIP or peptide YY secretion were seen between these two groups.ConclusionAn early peak in GLP-1 and glucagon may together trigger an exaggerated insulinotropic response to eating and consequent hypoglycaemia in patients with PPH.
Highlights
The Roux-en-Y gastric bypass (RYGB) operation results in a rapid improvement in any pre-existing type 2 diabetes mellitus (T2DM) that occurs shortly after the operation prior to any significant weight loss [1, 2]
Some studies have shown elevated glucagon-like peptide-1 (GLP-1) levels in patients with postprandial hypoglycaemia (PPH) relative to patients without PPH whilst others have failed to confirm this [16, 17, 18]. Both GLP-1 receptor antagonists and agonists have been shown to improve PPH, which is difficult to reconcile [19, 20]. To address these areas of uncertainty regarding the pathophysiology of PPH, we report our experience within the Imperial Weight Centre (IWC)
We describe the dynamics of gut hormone secretion, notably peptide YY (PYY), GLP-1, glucagon and oxyntomodulin (OXM) and glycaemic variability in a cohort of patients referred to the IWC with PPH who underwent a mixed meal test (MMT) and Continuous glucose monitoring (CGM)
Summary
The Roux-en-Y gastric bypass (RYGB) operation results in a rapid improvement in any pre-existing type 2 diabetes mellitus (T2DM) that occurs shortly after the operation prior to any significant weight loss [1, 2]. Beyond a reduction in fasting and postprandial plasma glucose levels, there is a change in the glucose tolerance curve. Glycaemic variability (GV) is broadly defined as the fluctuations between hyper and hypoglycaemia that typically occur in diabetes [4]. Increased GV is not exclusive to RYGB patients with diabetes but is observed in patients who are considered euglycaemic both before and after surgery [3, 10]. It is recognised that a proportion of patients after surgery develop disabling symptoms of postprandial hypoglycaemia (PPH) that are associated with this increased GV
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