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

Research output: Contribution to journalJournal articlepeer-review

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A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia. / Lobato, Carolina B.; Pereira, Sofia S.; Guimaraes, Marta; Hartmann, Bolette; Wewer Albrechtsen, Nicolai J.; Hilsted, Linda; Holst, Jens J.; Nora, Mario; Monteiro, Mariana P.

In: Frontiers in Endocrinology, Vol. 11, 608248, 2020.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Lobato, CB, Pereira, SS, Guimaraes, M, Hartmann, B, Wewer Albrechtsen, NJ, Hilsted, L, Holst, JJ, Nora, M & Monteiro, MP 2020, 'A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia', Frontiers in Endocrinology, vol. 11, 608248. https://doi.org/10.3389/fendo.2020.608248

APA

Lobato, C. B., Pereira, S. S., Guimaraes, M., Hartmann, B., Wewer Albrechtsen, N. J., Hilsted, L., Holst, J. J., Nora, M., & Monteiro, M. P. (2020). A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia. Frontiers in Endocrinology, 11, [608248]. https://doi.org/10.3389/fendo.2020.608248

Vancouver

Lobato CB, Pereira SS, Guimaraes M, Hartmann B, Wewer Albrechtsen NJ, Hilsted L et al. A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia. Frontiers in Endocrinology. 2020;11. 608248. https://doi.org/10.3389/fendo.2020.608248

Author

Lobato, Carolina B. ; Pereira, Sofia S. ; Guimaraes, Marta ; Hartmann, Bolette ; Wewer Albrechtsen, Nicolai J. ; Hilsted, Linda ; Holst, Jens J. ; Nora, Mario ; Monteiro, Mariana P. / A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia. In: Frontiers in Endocrinology. 2020 ; Vol. 11.

Bibtex

@article{94edbd612a164516ac76ed9d9e9b9af9,
title = "A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia",
abstract = "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), subjects presented no differences in anthropometric (BMI: p=0.527) or metabolic features (HbA(1c): 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: p0.05). 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.",
keywords = "glucagon, glucagon-like peptide-1, hyperinsulinemia, hypoglycemia, Roux-en-Y gastric bypass, INSULIN SENSITIVITY, ORAL GLUCOSE, POSTPRANDIAL HYPOGLYCEMIA, SECRETION, GLP-1, PEPTIDE-1, HORMONES, PLASMA",
author = "Lobato, {Carolina B.} and Pereira, {Sofia S.} and Marta Guimaraes and Bolette Hartmann and {Wewer Albrechtsen}, {Nicolai J.} and Linda Hilsted and Holst, {Jens J.} and Mario Nora and Monteiro, {Mariana P.}",
year = "2020",
doi = "10.3389/fendo.2020.608248",
language = "English",
volume = "11",
journal = "Frontiers in Endocrinology",
issn = "1664-2392",
publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

AU - Lobato, Carolina B.

AU - Pereira, Sofia S.

AU - Guimaraes, Marta

AU - Hartmann, Bolette

AU - Wewer Albrechtsen, Nicolai J.

AU - Hilsted, Linda

AU - Holst, Jens J.

AU - Nora, Mario

AU - Monteiro, Mariana P.

PY - 2020

Y1 - 2020

N2 - 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), subjects presented no differences in anthropometric (BMI: p=0.527) or metabolic features (HbA(1c): 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: p0.05). 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.

AB - 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), subjects presented no differences in anthropometric (BMI: p=0.527) or metabolic features (HbA(1c): 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: p0.05). 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.

KW - glucagon

KW - glucagon-like peptide-1

KW - hyperinsulinemia

KW - hypoglycemia

KW - Roux-en-Y gastric bypass

KW - INSULIN SENSITIVITY

KW - ORAL GLUCOSE

KW - POSTPRANDIAL HYPOGLYCEMIA

KW - SECRETION

KW - GLP-1

KW - PEPTIDE-1

KW - HORMONES

KW - PLASMA

U2 - 10.3389/fendo.2020.608248

DO - 10.3389/fendo.2020.608248

M3 - Journal article

C2 - 33424773

VL - 11

JO - Frontiers in Endocrinology

JF - Frontiers in Endocrinology

SN - 1664-2392

M1 - 608248

ER -

ID: 253730670