A Lautenbach1, M Wernecke1, N Riedel1, J Veigel1, J Yamamura2, S Keller2, R Jung3, P Busch4, O Mann4, F K Knop5, J J Holst6, J J Meier7, J Aberle1. 1. Department for Endocrinology and Diabetology, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. 2. Department for Diagnostic and Interventional Radiology, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. 3. Institute for Clinical Chemistry and Laboratory Medicine, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. 4. General, Visceral and Thoracic Surgery Department, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. 5. Centre for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark. 6. NNF Centre for Basic Metabolic Research and Department of Biomedical Sciences, The Panum Institute, University of Copenhagen, Copenhagen, Denmark. 7. Diabetes Division, Department of Medicine I, St Josef Hospital, Ruhr University Bochum, Bochum, Germany.
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.
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.
Authors: G Rega-Kaun; C Kaun; G Jaegersberger; M Prager; M Hackl; S Demyanets; J Wojta; P J Hohensinner Journal: Obes Surg Date: 2020-02 Impact factor: 4.129
Authors: Vinciane Rebours; Philippe Garteiser; Lara Ribeiro-Parenti; Jean-Baptiste Cavin; Sabrina Doblas; Gwenaël Pagé; André Bado; Alain Couvineau; Philippe Ruszniewski; Valérie Paradis; Maude Le Gall; Bernard E Van Beers; Anne Couvelard Journal: Sci Rep Date: 2018-11-02 Impact factor: 4.379
Authors: Ahmed Abdallah Salman; Mohamed Abdalla Salman; Mostafa Said; Mohammad El Sherbiny; Hesham Elkassar; Mohamed Badr Hassan; Ahmed Marwan; Mohamed Abdelkader Morad; Omar Ashoush; Safa Labib; Mohamed H Aon; Abeer Awad; Mohamed Sayed; Ahmed E Taha; Ahmed Moustafa; Hossam El-Din Shaaban; Amir Khater; Ahmed Elewa; Adel M Khalaf; Ahmed A Mostafa; Mohamed Matter; Ahmed Youssef Journal: Front Med (Lausanne) Date: 2022-06-06