Vagotomy and subsequent development of diabetes: A nested case-control study
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Vagotomy and subsequent development of diabetes : A nested case-control study. / Starup-Linde, Jakob; Gejl, Michael; Borghammer, Per; Knop, Filip K; Gregersen, Søren; Rungby, Jørgen; Vestergaard, Peter.
In: Metabolism, Vol. 65, No. 7, 07.2016, p. 954-960.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Vagotomy and subsequent development of diabetes
T2 - A nested case-control study
AU - Starup-Linde, Jakob
AU - Gejl, Michael
AU - Borghammer, Per
AU - Knop, Filip K
AU - Gregersen, Søren
AU - Rungby, Jørgen
AU - Vestergaard, Peter
N1 - Copyright © 2016 Elsevier Inc. All rights reserved.
PY - 2016/7
Y1 - 2016/7
N2 - BACKGROUND: Vagal signaling is involved in gastric emptying and the secretion and effect of a number of hormones regulating gluco-metabolic processes and, thus, crucial for metabolic homeostasis.PURPOSE: We hypothesized that vagotomy would increase the risk of developing type 2 diabetes and examined the association between vagotomy and subsequent development of diabetes.METHODS: A nested case-control study was conducted with information on cases and controls from the Danish National Patient Registry. Cases included individuals with a diabetes diagnosis subsequent (>12months) to the first registration of vagotomy and/or upper gastrointestinal disease in the period 1977-2011. Controls had no subsequent diagnosis of diabetes and were matched by incidence density sampling, age and gender. Logistic regression analyses were conducted.RESULTS: 501,724 diabetes patients and 1,375,567 matched controls were included in the analysis. Vagotomy was performed on 2772 individuals and 148,489 individuals had an upper gastrointestinal diagnosis. In this combined population, 30,902 were diagnosed with diabetes. The mean follow-up was 16years. The unadjusted odds ratio for developing diabetes following vagotomy was 0.64 (95% confidence interval (CI): 0.58-0.71) and did not change in an adjusted analysis (0.64, 95% CI: 0.58-0.70). When restricting the multivariate-adjusted analysis to patients with type 2 diabetes and type 1 diabetes, respectively, the multivariate odds ratios were 0.79 (95% CI: 0.70-0.89) and 0.75 (95% CI 0.53-1.08), respectively.CONCLUSION: Vagotomy was associated with a significantly decreased risk of developing type 2 diabetes in a population of patients with upper gastrointestinal disease.
AB - BACKGROUND: Vagal signaling is involved in gastric emptying and the secretion and effect of a number of hormones regulating gluco-metabolic processes and, thus, crucial for metabolic homeostasis.PURPOSE: We hypothesized that vagotomy would increase the risk of developing type 2 diabetes and examined the association between vagotomy and subsequent development of diabetes.METHODS: A nested case-control study was conducted with information on cases and controls from the Danish National Patient Registry. Cases included individuals with a diabetes diagnosis subsequent (>12months) to the first registration of vagotomy and/or upper gastrointestinal disease in the period 1977-2011. Controls had no subsequent diagnosis of diabetes and were matched by incidence density sampling, age and gender. Logistic regression analyses were conducted.RESULTS: 501,724 diabetes patients and 1,375,567 matched controls were included in the analysis. Vagotomy was performed on 2772 individuals and 148,489 individuals had an upper gastrointestinal diagnosis. In this combined population, 30,902 were diagnosed with diabetes. The mean follow-up was 16years. The unadjusted odds ratio for developing diabetes following vagotomy was 0.64 (95% confidence interval (CI): 0.58-0.71) and did not change in an adjusted analysis (0.64, 95% CI: 0.58-0.70). When restricting the multivariate-adjusted analysis to patients with type 2 diabetes and type 1 diabetes, respectively, the multivariate odds ratios were 0.79 (95% CI: 0.70-0.89) and 0.75 (95% CI 0.53-1.08), respectively.CONCLUSION: Vagotomy was associated with a significantly decreased risk of developing type 2 diabetes in a population of patients with upper gastrointestinal disease.
U2 - 10.1016/j.metabol.2016.04.002
DO - 10.1016/j.metabol.2016.04.002
M3 - Journal article
C2 - 27282866
VL - 65
SP - 954
EP - 960
JO - Metabolism
JF - Metabolism
SN - 0026-0495
IS - 7
ER -
ID: 162291107