Comparison of Hormonal Response to a Mixed-Meal Challenge in Hypoglycemia After Sleeve Gastrectomy vs Gastric Bypass.


Journal

The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362

Informations de publication

Date de publication:
28 09 2022
Historique:
received: 10 04 2022
pubmed: 2 8 2022
medline: 30 9 2022
entrez: 1 8 2022
Statut: ppublish

Résumé

Exaggerated postprandial incretin and insulin responses are well documented in postbariatric surgery hypoglycemia (PBH) after Roux-en-Y gastric bypass (RYGB). However, less is known about PBH after sleeve gastrectomy (SG). We sought to compare meal-stimulated hormonal response in those with PBH after SG vs RYGB. We enrolled 23 post-SG (12 with and 11 without PBH) and 20 post-RYGB (7 with and 13 without PBH) individuals who underwent bariatric surgery at our institution. PBH was defined as plasma glucose less than 60 mg/dL on 4-hour mixed-meal tolerance test (MTT). Islet and incretin hormones were compared across the 4 groups. Participants (N = 43) were on average 5 years post surgery, with a mean age of 48 years, mean preoperative body mass index of 48.4, 81% female, 61% White, and 53% post SG. Regardless of PBH, the SG group showed lower glucose, glucagon, and glucagon-like peptide 1 (GLP-1) responses to MTT and similar insulin and glucose-dependent insulinotropic polypeptide (GIP) responses compared to the RYGB group. Among those with PBH, the SG group following the MTT showed a lower peak glucose (P = .02), a similar peak insulin (90.3 mU/L vs 171mU/L; P = .18), lower glucagon (P < .01), early GLP-1 response (AUC0-60 min; P = .01), and slower time to peak GIP (P = .02) compared to PBH after RYGB. Among individuals with PBH, those who underwent SG were significantly different compared to RYGB in meal-stimulated hormonal responses, including lower glucagon and GLP-1 responses, but similar insulin and GIP responses. Future studies are needed to better understand the differential contribution of insulin and non-insulin-mediated mechanisms behind PBH after SG vs RYGB.

Identifiants

pubmed: 35914520
pii: 6653084
doi: 10.1210/clinem/dgac455
pmc: PMC9516126
doi:

Substances chimiques

Blood Glucose 0
Incretins 0
Insulin 0
Gastric Inhibitory Polypeptide 59392-49-3
Glucagon-Like Peptide 1 89750-14-1
Glucagon 9007-92-5
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e4159-e4166

Subventions

Organisme : NIAID NIH HHS
ID : K24 AI120834
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR003098
Pays : United States
Organisme : NIDDK NIH HHS
ID : K23 DK107921
Pays : United States

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Clare J Lee (CJ)

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21287, USA.

Jeanne M Clark (JM)

Division of General Internal Medicine, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21287, USA.
Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21287, USA.

Josephine M Egan (JM)

National Institute On Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.

Olga D Carlson (OD)

National Institute On Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.

Michael Schweitzer (M)

Department of Surgery, The Johns Hopkins University, Baltimore, Maryland 21287, USA.

Susan Langan (S)

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21287, USA.

Todd Brown (T)

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21287, USA.

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Classifications MeSH