Adaptive changes in pancreas post Roux‐en‐Y gastric bypass induced weight loss. Issue 7 (8th June 2018)

• Record Type: Journal Article
• Authors: 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.
• Is Part Of: Diabetes/metabolism research and reviews. Volume 34:Issue 7(2018)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-06-08
• Subjects: beta‐cell -- GLP‐1 -- insulin -- pancreas -- RYGB; Diabetes -- Periodicals; Metabolism -- Periodicals; 616.642
• DOI: 10.1002/dmrr.3025
• Languages: English
• ISSNs: 1520-7552

Abstract

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) cm 3 (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.