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Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance.
Am J Physiol Endocrinol Metab. 2012 Jul 01; 303(1):E122-31.AJ

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.

Authors+Show Affiliations

Department of Endocrinology, Hvidovre Hospital, Hvidovre, Denmark. nils.bruun.joergensen@gmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22535748

Citation

Jørgensen, N B., et al. "Acute and Long-term Effects of Roux-en-Y Gastric Bypass On Glucose Metabolism in Subjects With Type 2 Diabetes and Normal Glucose Tolerance." American Journal of Physiology. Endocrinology and Metabolism, vol. 303, no. 1, 2012, pp. E122-31.
Jørgensen NB, Jacobsen SH, Dirksen C, et al. Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance. Am J Physiol Endocrinol Metab. 2012;303(1):E122-31.
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. (2012). Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance. American Journal of Physiology. Endocrinology and Metabolism, 303(1), E122-31. https://doi.org/10.1152/ajpendo.00073.2012
Jørgensen NB, et al. Acute and Long-term Effects of Roux-en-Y Gastric Bypass On Glucose Metabolism in Subjects With Type 2 Diabetes and Normal Glucose Tolerance. Am J Physiol Endocrinol Metab. 2012 Jul 1;303(1):E122-31. PubMed PMID: 22535748.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute and long-term effects of Roux-en-Y gastric bypass on glucose metabolism in subjects with Type 2 diabetes and normal glucose tolerance. AU - Jørgensen,N B, AU - Jacobsen,S H, AU - Dirksen,C, AU - Bojsen-Møller,K N, AU - Naver,L, AU - Hvolris,L, AU - Clausen,T R, AU - Wulff,B S, AU - Worm,D, AU - Lindqvist Hansen,D, AU - Madsbad,S, AU - Holst,J J, Y1 - 2012/04/24/ PY - 2012/4/27/entrez PY - 2012/4/27/pubmed PY - 2012/9/11/medline SP - E122 EP - 31 JF - American journal of physiology. Endocrinology and metabolism JO - Am J Physiol Endocrinol Metab VL - 303 IS - 1 N2 - 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. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/22535748/Acute_and_long_term_effects_of_Roux_en_Y_gastric_bypass_on_glucose_metabolism_in_subjects_with_Type_2_diabetes_and_normal_glucose_tolerance_ L2 - https://journals.physiology.org/doi/10.1152/ajpendo.00073.2012?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -