Use of flash glucose monitoring for post-bariatric hypoglycaemia diagnosis and management

Lobato, Carolina B.; Pereira, Sofia S; Guimarães, Marta; Morais, Tiago; Oliveira, Pedro F.; Carvalho, Jorge P. M. de; Nora, Mário; Monteiro, Mariana P.

doi:10.1038/s41598-020-68029-8

Cited by 7 publications

(9 citation statements)

References 43 publications

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“…The very first obstacle is symptoms under-or mis-reporting, due to partial overlap with dumping syndrome and/or hypoglycemia unawareness (31-33). While we have previously shown that selfreported symptoms compatible with PBH might be useful for PBH diagnosis when paired along concurrent flash glucose monitoring data, caution shall be taken when considering symptoms alone for PBH diagnosis (33). Our current data reinforces the limited value of symptom reports, as no correlation was observed between symptoms and the glucose profile prompted by a standardized meal stimulus.…”

Section: Discussionsupporting

confidence: 65%

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

et al. 2020

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Obesity and obesity-related diseases are major public health concerns that have been exponentially growing in the last decades. Bariatric surgery is an effective long-term treatment to achieve weight loss and obesity comorbidity remission. Post-bariatric hypoglycemia (PBH) is a late complication of bariatric surgery most commonly reported after Roux-en-Y gastric bypass (RYGB). PBH is the end result of postprandial hyperinsulinemia but additional endocrine mechanisms involved are still under debate. Our aim was to characterize entero-pancreatic hormone dynamics associated with postprandial hypoglycemia after RYGB. Individuals previously submitted to RYGB (N=23) in a single tertiary hospital presenting PBH symptoms (Sym, n=14) and asymptomatic weight-matched controls (Asy, n=9) were enrolled. Participants underwent a mixed-meal tolerance test (MMTT) to assess glucose, total amino acids (total AA), insulin, C-peptide, glucagon, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and neurotensin (NT). We found that hypoglycemia during the MMTT was equally frequent in Sym and Asy groups (p=1.000). Re-grouped according to glucose nadir during the MMTT (Hypo n=11 vs NoHypo n=12; nadir <3.05 mmol/l vs ≥3.05 mmol/l), subjects presented no differences in anthropometric (BMI: p=0.527) or metabolic features (HbA1c: p=0.358), yet distinct meal-elicited hormone dynamics were identified. Postprandial glucose excursion and peak glucose levels were similar (p>0.05), despite distinct late glycemic outcomes (t=60 min and t=90 min: p<0.01), with overall greater glycemic variability in Hypo group (minimum-to-maximum glucose ratio: p<0.001). Hypo group meal-triggered hormone profile was characterized by lower early glucagon (t=15 min: p<0.01) and higher insulin (t=30 min: p<0.05, t=45 min: p<0.001), C-peptide (t=30 min: p<0.01, t=45 min: p<0.001, t=60 min: p<0.05), and GLP-1 (t=45 min: p<0.05) levels. Hyperinsulinemia was an independent risk factor for hypoglycemia (p<0.05). After adjusting for hyperinsulinemia, early glucagon correlated with glycemic nadir (p<0.01), and prevented postprandial hypoglycemia (p<0.05). A higher insulin to glucagon balance in Hypo was observed (p<0.05). No differences were observed in total AA, GIP or NT excursions (p>0.05). In sum, after RYGB, postprandial hyperinsulinemia is key in triggering PBH, but a parallel and earlier rise in endogenous glucagon might sustain the inter-individual variability in glycemic outcome beyond the effect of hyperinsulinism, advocating a potential pivotal role for glucagon in preventing hyperinsulinemic hypoglycemia.

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Section: Discussionsupporting

confidence: 65%

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

et al. 2020

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“…В ходе исследования был разработан индекс риска развития гипогликемии, который во второй группе был выше, чем в первой. Также флеш-мониторинг позволил найти различия между симптомами гипогликемии и другой вегетативной симптоматикой, причиной которых было не снижение гликемии [45].…”

Section: диагностика и дифференциальная диагностикаunclassified

A view at postbariatric hypoglycemia by endocrinologist

et al. 2022

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The obesity epidemic has led to the growing number of bariatric operations and the expansion of indications for this operation as the most effective method of treatment, that’s why endocrinologists are increasingly faced the challenge of late complications, including postbariatric hypoglycemia. Postbariatric hypoglycemia is a rare but severe metabolic disorder that occurs months or years after upper gastrointestinal surgery. Postbariatric hypoglycemia can be accompanied by severe clinical symptoms and lead to disability and decreasing of the life’s quality. It is difficult to assess the prevalence of hypoglycemia after bariatric surgery due to the lack of clear diagnostic criteria, often a hidden clinical picture and ignorance of doctors and patients about this complication. Hypoglycemia in this case has postprandial and hyperinsulinemic nature. The mechanisms of development of this complication have recently been actively discussed. The exchange of incretins and dysregulation of insulin secretion are the subject of constant research in this area. Understanding the mechanisms of development of this condition makes it possible to develop optimal methods of diagnosis and treatment. The issues of pathophysiology, basic principles of diagnosis and treatment of post-bariatric hypoglycemia will be considered in this review.

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“…Within months to years after metabolic surgery, hypoglycemic symptoms occur 1-3 hours after eating, especially after ingesting high glycemic index carbohydrates [28,29]. Post-bariatric hypoglycemia is mainly reported after RYGB [30]. The actual frequency of post-bariatric hypoglycemia remains undefined because of diagnostic criteria and other causes, and the prevalence of this condition might be higher than initially believed [31].…”

Section: Novel Insight Into the Mechanism Of Metabolic Surgery Causin...mentioning

confidence: 99%

Novel Insight into the Mechanism of Metabolic Surgery Causing the Diversity in Glycemic Status in Type 2 Diabetes

Zhou

Wang

Zhou

et al. 2022

Exp Clin Endocrinol Diabetes

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Metabolic surgery results in diverse glycemic status in patients with type 2 diabetes (T2D), including hyperglycemia without remission, significant amelioration of hyperglycemia with partial remission, complete restoration of euglycemia, or with prolonged remission, hyperglycemia recurrence in relapses after remission, or post-bariatric hypoglycemia. Unfortunately, it is not known how metabolic surgery leads to this diverse consequence. Here, we discuss the diversity of glycemic status associated with metabolic surgery and the potential mechanisms of T2D remission. We also highlight the relationship between the change in low-grade inflammation and T2D remission after metabolic surgery. We hypothesize that the level of inflammatory and anti-inflammatory cytokines controls the efficacy of metabolic surgery in patients with T2D. This hypothesis may provide further insight into the mechanism of the beneficial effects of metabolic surgery patients with T2D.

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Use of flash glucose monitoring for post-bariatric hypoglycaemia diagnosis and management

Cited by 7 publications

References 43 publications

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

A view at postbariatric hypoglycemia by endocrinologist

Novel Insight into the Mechanism of Metabolic Surgery Causing the Diversity in Glycemic Status in Type 2 Diabetes

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