Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass

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Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass. / Dirksen, C; Jørgensen, N B; Bojsen-Møller, K N; Jacobsen, S H; Hansen, D L; Worm, D; Holst, Jens Juul; Madsbad, S.

In: Diabetologia, Vol. 55, No. 7, 2012, p. 1890-901.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Dirksen, C, Jørgensen, NB, Bojsen-Møller, KN, Jacobsen, SH, Hansen, DL, Worm, D, Holst, JJ & Madsbad, S 2012, 'Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass', Diabetologia, vol. 55, no. 7, pp. 1890-901. https://doi.org/10.1007/s00125-012-2556-7

APA

Dirksen, C., Jørgensen, N. B., Bojsen-Møller, K. N., Jacobsen, S. H., Hansen, D. L., Worm, D., Holst, J. J., & Madsbad, S. (2012). Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass. Diabetologia, 55(7), 1890-901. https://doi.org/10.1007/s00125-012-2556-7

Vancouver

Dirksen C, Jørgensen NB, Bojsen-Møller KN, Jacobsen SH, Hansen DL, Worm D et al. Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass. Diabetologia. 2012;55(7):1890-901. https://doi.org/10.1007/s00125-012-2556-7

Author

Dirksen, C ; Jørgensen, N B ; Bojsen-Møller, K N ; Jacobsen, S H ; Hansen, D L ; Worm, D ; Holst, Jens Juul ; Madsbad, S. / Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass. In: Diabetologia. 2012 ; Vol. 55, No. 7. pp. 1890-901.

Bibtex

@article{49093543abd24d119848cb6bf2e88c2e,
title = "Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass",
abstract = "Roux-en-Y gastric bypass (RYGB) greatly improves glycaemic control in morbidly obese patients with type 2 diabetes, in many even before significant weight loss. Understanding the responsible mechanisms may contribute to our knowledge of the pathophysiology of type 2 diabetes and help identify new drug targets or improve surgical techniques. This review summarises the present knowledge based on pathophysiological studies published during the last decade. Taken together, two main mechanisms seem to be responsible for the early improvement in glycaemic control after RYGB: (1) an increase in hepatic insulin sensitivity induced, at least in part, by energy restriction and (2) improved beta cell function associated with an exaggerated postprandial glucagon-like peptide 1 secretion owing to the altered transit of nutrients. Later a weight loss induced improvement in peripheral insulin sensitivity follows.",
author = "C Dirksen and J{\o}rgensen, {N B} and Bojsen-M{\o}ller, {K N} and Jacobsen, {S H} and Hansen, {D L} and D Worm and Holst, {Jens Juul} and S Madsbad",
year = "2012",
doi = "10.1007/s00125-012-2556-7",
language = "English",
volume = "55",
pages = "1890--901",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "7",

}

RIS

TY - JOUR

T1 - Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass

AU - Dirksen, C

AU - Jørgensen, N B

AU - Bojsen-Møller, K N

AU - Jacobsen, S H

AU - Hansen, D L

AU - Worm, D

AU - Holst, Jens Juul

AU - Madsbad, S

PY - 2012

Y1 - 2012

N2 - Roux-en-Y gastric bypass (RYGB) greatly improves glycaemic control in morbidly obese patients with type 2 diabetes, in many even before significant weight loss. Understanding the responsible mechanisms may contribute to our knowledge of the pathophysiology of type 2 diabetes and help identify new drug targets or improve surgical techniques. This review summarises the present knowledge based on pathophysiological studies published during the last decade. Taken together, two main mechanisms seem to be responsible for the early improvement in glycaemic control after RYGB: (1) an increase in hepatic insulin sensitivity induced, at least in part, by energy restriction and (2) improved beta cell function associated with an exaggerated postprandial glucagon-like peptide 1 secretion owing to the altered transit of nutrients. Later a weight loss induced improvement in peripheral insulin sensitivity follows.

AB - Roux-en-Y gastric bypass (RYGB) greatly improves glycaemic control in morbidly obese patients with type 2 diabetes, in many even before significant weight loss. Understanding the responsible mechanisms may contribute to our knowledge of the pathophysiology of type 2 diabetes and help identify new drug targets or improve surgical techniques. This review summarises the present knowledge based on pathophysiological studies published during the last decade. Taken together, two main mechanisms seem to be responsible for the early improvement in glycaemic control after RYGB: (1) an increase in hepatic insulin sensitivity induced, at least in part, by energy restriction and (2) improved beta cell function associated with an exaggerated postprandial glucagon-like peptide 1 secretion owing to the altered transit of nutrients. Later a weight loss induced improvement in peripheral insulin sensitivity follows.

U2 - 10.1007/s00125-012-2556-7

DO - 10.1007/s00125-012-2556-7

M3 - Journal article

C2 - 22538359

VL - 55

SP - 1890

EP - 1901

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 7

ER -

ID: 38430566