Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss

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Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss. / Lautenbach, A; Wernecke, M; Riedel, N; Veigel, J; Yamamura, J; Keller, S; Jung, R; Busch, P; Mann, O; Knop, F K; Holst, J J; Meier, J J; Aberle, J.

In: DIABETES-METAB RES, Vol. 34, No. 7, 10.2018, p. e3025.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Lautenbach, A, Wernecke, M, Riedel, N, Veigel, J, Yamamura, J, Keller, S, Jung, R, Busch, P, Mann, O, Knop, FK, Holst, JJ, Meier, JJ & Aberle, J 2018, 'Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss', DIABETES-METAB RES, vol. 34, no. 7, pp. e3025. https://doi.org/10.1002/dmrr.3025

APA

Lautenbach, A., Wernecke, M., Riedel, N., Veigel, J., Yamamura, J., Keller, S., Jung, R., Busch, P., Mann, O., Knop, F. K., Holst, J. J., Meier, J. J., & Aberle, J. (2018). Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss. DIABETES-METAB RES, 34(7), e3025. https://doi.org/10.1002/dmrr.3025

Vancouver

Bibtex

@article{b7f65234419440009011b1ef34007350,
title = "Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss",
abstract = "BACKGROUND: Obesity has been shown to trigger adaptive increases in pancreas parenchymal and fat volume. Consecutively, pancreatic steatosis may lead to beta-cell dysfunction. However, it is not known whether the pancreatic tissue components decrease with weight loss and pancreatic steatosis is reversible following Roux-en-Y gastric bypass (RYGB). Therefore, the objective of the study was to investigate the effects of RYGB-induced weight loss on pancreatic volume and glucose homeostasis.METHODS: Eleven patients were recruited in the Obesity Centre of the University Medical Centre Hamburg-Eppendorf. Before and 6 months after RYGB, total GLP-1 levels were measured during oral glucose tolerance test. To assess changes in visceral adipose tissue and pancreatic volume, MRI was performed. Measures of glucose homeostasis and insulin indices were assessed. Fractional beta-cell area was estimated by correlation with the C-peptide-to-glucose ratio; beta-cell mass was calculated by the product of beta-cell area and pancreas parenchymal weight.RESULTS: Pancreas volume decreased from 83.8 (75.7-92.0) to 70.5 (58.8-82.3) cm3 (mean [95% CI], P = .001). The decrease in total volume was associated with a significant decrease in fat volume. Fasting insulin and C-peptide were lower post RYGB. HOMA-IR levels decreased, whereas insulin sensitivity increased (P = .03). This was consistent with a reduction in the estimated beta-cell area and mass.CONCLUSIONS: Following RYGB, pancreatic volume and steatosis adaptively decreased to {"}normal{"} levels with accompanying improvement in glucose homeostasis. Moreover, obesity-driven beta-cell expansion seems to be reversible; however, future studies must define a method to more accurately estimate functional beta-cell mass to increase our understanding of glucose homeostasis after RYGB.",
keywords = "Adaptation, Physiological, Adiposity, Adult, Female, Follow-Up Studies, Gastric Bypass, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Magnetic Resonance Imaging, Male, Middle Aged, Obesity, Morbid, Pancreas, Weight Loss, Clinical Trial, Journal Article",
author = "A Lautenbach and M Wernecke and N Riedel and J Veigel and J Yamamura and S Keller and R Jung and P Busch and O Mann and Knop, {F K} and Holst, {J J} and Meier, {J J} and J Aberle",
note = "Copyright {\textcopyright} 2018 John Wiley & Sons, Ltd.",
year = "2018",
month = oct,
doi = "10.1002/dmrr.3025",
language = "English",
volume = "34",
pages = "e3025",
journal = "DIABETES-METAB RES",
issn = "1520-7552",
publisher = "John Wiley and Sons Ltd",
number = "7",

}

RIS

TY - JOUR

T1 - Adaptive changes in pancreas post Roux-en-Y gastric bypass induced weight loss

AU - Lautenbach, A

AU - Wernecke, M

AU - Riedel, N

AU - Veigel, J

AU - Yamamura, J

AU - Keller, S

AU - Jung, R

AU - Busch, P

AU - Mann, O

AU - Knop, F K

AU - Holst, J J

AU - Meier, J J

AU - Aberle, J

N1 - Copyright © 2018 John Wiley & Sons, Ltd.

PY - 2018/10

Y1 - 2018/10

N2 - BACKGROUND: Obesity has been shown to trigger adaptive increases in pancreas parenchymal and fat volume. Consecutively, pancreatic steatosis may lead to beta-cell dysfunction. However, it is not known whether the pancreatic tissue components decrease with weight loss and pancreatic steatosis is reversible following Roux-en-Y gastric bypass (RYGB). Therefore, the objective of the study was to investigate the effects of RYGB-induced weight loss on pancreatic volume and glucose homeostasis.METHODS: Eleven patients were recruited in the Obesity Centre of the University Medical Centre Hamburg-Eppendorf. Before and 6 months after RYGB, total GLP-1 levels were measured during oral glucose tolerance test. To assess changes in visceral adipose tissue and pancreatic volume, MRI was performed. Measures of glucose homeostasis and insulin indices were assessed. Fractional beta-cell area was estimated by correlation with the C-peptide-to-glucose ratio; beta-cell mass was calculated by the product of beta-cell area and pancreas parenchymal weight.RESULTS: Pancreas volume decreased from 83.8 (75.7-92.0) to 70.5 (58.8-82.3) cm3 (mean [95% CI], P = .001). The decrease in total volume was associated with a significant decrease in fat volume. Fasting insulin and C-peptide were lower post RYGB. HOMA-IR levels decreased, whereas insulin sensitivity increased (P = .03). This was consistent with a reduction in the estimated beta-cell area and mass.CONCLUSIONS: Following RYGB, pancreatic volume and steatosis adaptively decreased to "normal" levels with accompanying improvement in glucose homeostasis. Moreover, obesity-driven beta-cell expansion seems to be reversible; however, future studies must define a method to more accurately estimate functional beta-cell mass to increase our understanding of glucose homeostasis after RYGB.

AB - BACKGROUND: Obesity has been shown to trigger adaptive increases in pancreas parenchymal and fat volume. Consecutively, pancreatic steatosis may lead to beta-cell dysfunction. However, it is not known whether the pancreatic tissue components decrease with weight loss and pancreatic steatosis is reversible following Roux-en-Y gastric bypass (RYGB). Therefore, the objective of the study was to investigate the effects of RYGB-induced weight loss on pancreatic volume and glucose homeostasis.METHODS: Eleven patients were recruited in the Obesity Centre of the University Medical Centre Hamburg-Eppendorf. Before and 6 months after RYGB, total GLP-1 levels were measured during oral glucose tolerance test. To assess changes in visceral adipose tissue and pancreatic volume, MRI was performed. Measures of glucose homeostasis and insulin indices were assessed. Fractional beta-cell area was estimated by correlation with the C-peptide-to-glucose ratio; beta-cell mass was calculated by the product of beta-cell area and pancreas parenchymal weight.RESULTS: Pancreas volume decreased from 83.8 (75.7-92.0) to 70.5 (58.8-82.3) cm3 (mean [95% CI], P = .001). The decrease in total volume was associated with a significant decrease in fat volume. Fasting insulin and C-peptide were lower post RYGB. HOMA-IR levels decreased, whereas insulin sensitivity increased (P = .03). This was consistent with a reduction in the estimated beta-cell area and mass.CONCLUSIONS: Following RYGB, pancreatic volume and steatosis adaptively decreased to "normal" levels with accompanying improvement in glucose homeostasis. Moreover, obesity-driven beta-cell expansion seems to be reversible; however, future studies must define a method to more accurately estimate functional beta-cell mass to increase our understanding of glucose homeostasis after RYGB.

KW - Adaptation, Physiological

KW - Adiposity

KW - Adult

KW - Female

KW - Follow-Up Studies

KW - Gastric Bypass

KW - Glucose Tolerance Test

KW - Humans

KW - Insulin

KW - Insulin Resistance

KW - Magnetic Resonance Imaging

KW - Male

KW - Middle Aged

KW - Obesity, Morbid

KW - Pancreas

KW - Weight Loss

KW - Clinical Trial

KW - Journal Article

U2 - 10.1002/dmrr.3025

DO - 10.1002/dmrr.3025

M3 - SCORING: Journal article

C2 - 29768729

VL - 34

SP - e3025

JO - DIABETES-METAB RES

JF - DIABETES-METAB RES

SN - 1520-7552

IS - 7

ER -