Cited by 313Bariatric Surgery and OutcomesDiabetes Treatment and ManagementDiabetes, Cardiovascular Risks, and Lipoproteins

Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance

Jørgensen, N. B., Jacobsen, S. H., Dirksen, C., Bojsen-Møller, K. N., Naver, L., Hvolris, L., Clausen, T. R., Wulff, B. S. +4 more·2012·American Journal of Physiology-Endocrinology and Metabolism

Abstract

Our aim was to study the potential mechanisms responsible for the improvement in glucose control in Type 2 diabetes (T2D) within days after Roux-en-Y gastric bypass (RYGB). Thirteen obese subjects with T2D and twelve matched subjects with normal glucose tolerance (NGT) were examined during a liquid meal before (Pre), 1 wk, 3 mo, and 1 yr after RYGB. Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent-insulinotropic polypeptide (GIP), and glucagon concentrations were measured. Insulin resistance (HOMA-IR), β-cell glucose sensitivity (β-GS), and disposition index (D(β-GS): β-GS × 1/HOMA-IR) were calculated. Within the first week after RYGB, fasting glucose [T2D Pre: 8.8 ± 2.3, 1 wk: 7.0 ± 1.2 (P < 0.001)], and insulin concentrations decreased significantly in both groups. At 129 min, glucose concentrations decreased in T2D [Pre: 11.4 ± 3, 1 wk: 8.2 ± 2 (P = 0.003)] but not in NGT. HOMA-IR decreased by 50% in both groups. β-GS increased in T2D [Pre: 1.03 ± 0.49, 1 wk: 1.70 ± 1.2, (P = 0.012)] but did not change in NGT. The increase in DI(β-GS) was 3-fold in T2D and 1.5-fold in NGT. After RYGB, glucagon secretion was increased in response to the meal. GIP secretion was unchanged, while GLP-1 secretion increased more than 10-fold in both groups. The changes induced by RYGB were sustained or further enhanced 3 mo and 1 yr after surgery. Improvement in glycemic control in T2D after RYGB occurs within days after surgery and is associated with increased insulin sensitivity and improved β-cell function, the latter of which may be explained by dramatic increases in GLP-1 secretion.

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Crossref · 10.1152/ajpendo.00073.2012

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Authors
Jørgensen, N. B., Jacobsen, S. H., Dirksen, C., Bojsen-Møller, K. N., Naver, L., Hvolris, L., Clausen, T. R., Wulff, B. S., Worm, D., Lindqvist Hansen, D., Madsbad, S., & Holst, J. J.
Affiliations
  • University of Copenhagen (DK)
  • Hvidovre Hospital (DK)
  • Novo Nordisk (Denmark) (DK)
  • Department of Endocrinology, Hvidovre Hospital, Hvidovre, Denmark;
Corresponding author
Jørgensen, N. B.
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2012-07-01
Volume
303
Issue
1
Pages
E122-E131
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2129549955
Cited by
313
References
49
Citations by year
2026: 6 · 2025: 14 · 2024: 11 · 2023: 15 · 2022: 20 · 2021: 27 · 2020: 17 · 2019: 36 · 2018: 22 · 2017: 30 · 2016: 28 · 2015: 32 · 2014: 16 · 2013: 34 · 2012: 4
FWCI
28.01
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Bariatric Surgery and Outcomes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
Roux-en-Y gastric bypass, type 2 diabetes, glucose metabolism, insulin resistance, beta-cell function, glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, glucagon, C-peptide, insulin secretion, bariatric surgery, obesity, glycemic control, insulin sensitivity
MeSH terms
Adult, C-Peptide, Diabetes Mellitus, Type 2, Female, Follow-Up Studies, Glucagon, Glucose, Humans, Hyperglycemia, Insulin Resistance, Male, Middle Aged, Obesity, Obesity, Morbid, Time Factors, Gastric Bypass, Body Mass Index, Postprandial Period, Insulin-Secreting Cells, Glucagon-Like Peptide 1

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