S Canivell1, M Mohaupt2, D Ackermann2, M Pruijm3, I Guessous4,5, G Ehret6, G Escher2, A Pechère-Bertschi7, B Vogt2, O Devuyst8, M Burnier9,10, P-Y Martin11, B Ponte11, M Bochud12. 1. Institute of Social and Preventive Medicine, Lausanne University Hospital, Lausanne, Switzerland. scanivell@gmail.com. 2. University Clinic for Nephrology, Hypertension and Clinical Pharmacology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 3. Service of Nephrology and Hypertension, University Hospital of Lausanne (CHUV), Lausanne, Switzerland. 4. Department of Community Medicine, Primary Care and Emergency Medicine, University Hospital of Geneva, Geneva, Switzerland. 5. Institute of Social and Preventive Medicine, University Hospital of Lausanne, Lausanne, Switzerland. 6. Cardiology Service, Department of Specialties of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland. 7. Unit of Hypertension, Departments of Specialties of Medicine and Community Medicine and Primary Care and Emergency Medicine, Geneva University Hospitals, Geneva, Switzerland. 8. Institute of Physiology, University of Zurich, Zurich, Switzerland. 9. Nephrology Service, University Hospital of Lausanne, Lausanne, Switzerland. 10. Department of Clinical Research, University of Bern, Bern, Switzerland. 11. Nephrology Service, Department of Specialties of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland. 12. Institute of Social and Preventive Medicine, Lausanne University Hospital, Lausanne, Switzerland.
Abstract
PURPOSE: Arginine vasopressin (AVP) may be involved in metabolic syndrome (MetS) by altering liver glycogenolysis, insulin and glucagon secretion, and pituitary ACTH release. Moreover, AVP stimulates the expression of 11β-hydroxysteroid-dehydrogenase-type 2 (11β-HSD2) in mineralocorticosteroid cells. We explored whether apparent 11β-HSD2 activity, estimated using urinary cortisol-to-cortisone ratio, modulates the association between plasma copeptin, as AVP surrogate, and insulin resistance/MetS in the general adult population. METHODS: This was a multicentric, family-based, cross-sectional sample of 1089 subjects, aged 18-90 years, 47% men, 13.4% MetS, in Switzerland. Mixed multivariable linear and logistic regression models were built to investigate the association of insulin resistance (HOMA-IR)/fasting glucose and MetS/Type 2 Diabetes with copeptin, while considering potential confounders or effect modifiers into account. Stratified results by age and 11β-HSD2 activity were presented as appropriate. RESULTS: Plasma copeptin was higher in men [median 5.2, IQR (3.7-7.8) pmol/L] than in women [median 3.0, IQR (2.2-4.3) pmol/L], P < 0.0001. HOMA-IR was positively associated with copeptin after full adjustment if 11β-HSD2 activity was high [β (95% CI) = 0.32 (0.17-0.46), P < 0.001] or if age was high [β (95% CI) = 0.34 (0.20-0.48), P < 0.001], but not if either 11β-HSD2 activity or age was low. There was a positive association of type 2 diabetes with copeptin [OR (95% CI) = 2.07 (1.10-3.89), P = 0.024), but not for MetS (OR (95% CI) = 1.12 (0.74-1.69), P = 0.605), after full adjustment. CONCLUSIONS: Our data suggest that age and apparent 11β-HSD2 activity modulate the association of copeptin with insulin resistance at the population level but not MeTS or diabetes. Further research is needed to corroborate these results and to understand the mechanisms underlying these findings.
PURPOSE:Arginine vasopressin (AVP) may be involved in metabolic syndrome (MetS) by altering liver glycogenolysis, insulin and glucagon secretion, and pituitary ACTH release. Moreover, AVP stimulates the expression of 11β-hydroxysteroid-dehydrogenase-type 2 (11β-HSD2) in mineralocorticosteroid cells. We explored whether apparent 11β-HSD2 activity, estimated using urinary cortisol-to-cortisone ratio, modulates the association between plasma copeptin, as AVP surrogate, and insulin resistance/MetS in the general adult population. METHODS: This was a multicentric, family-based, cross-sectional sample of 1089 subjects, aged 18-90 years, 47% men, 13.4% MetS, in Switzerland. Mixed multivariable linear and logistic regression models were built to investigate the association of insulin resistance (HOMA-IR)/fasting glucose and MetS/Type 2 Diabetes with copeptin, while considering potential confounders or effect modifiers into account. Stratified results by age and 11β-HSD2 activity were presented as appropriate. RESULTS: Plasma copeptin was higher in men [median 5.2, IQR (3.7-7.8) pmol/L] than in women [median 3.0, IQR (2.2-4.3) pmol/L], P < 0.0001. HOMA-IR was positively associated with copeptin after full adjustment if 11β-HSD2 activity was high [β (95% CI) = 0.32 (0.17-0.46), P < 0.001] or if age was high [β (95% CI) = 0.34 (0.20-0.48), P < 0.001], but not if either 11β-HSD2 activity or age was low. There was a positive association of type 2 diabetes with copeptin [OR (95% CI) = 2.07 (1.10-3.89), P = 0.024), but not for MetS (OR (95% CI) = 1.12 (0.74-1.69), P = 0.605), after full adjustment. CONCLUSIONS: Our data suggest that age and apparent 11β-HSD2 activity modulate the association of copeptin with insulin resistance at the population level but not MeTS or diabetes. Further research is needed to corroborate these results and to understand the mechanisms underlying these findings.
Authors: Sofia Enhörning; Joachim Struck; Elisabet Wirfält; Bo Hedblad; Nils G Morgenthaler; Olle Melander Journal: J Clin Endocrinol Metab Date: 2011-04-13 Impact factor: 5.958
Authors: Belén Ponte; Menno Pruijm; Daniel Ackermann; Philippe Vuistiner; Ute Eisenberger; Idris Guessous; Valentin Rousson; Markus G Mohaupt; Heba Alwan; Georg Ehret; Antoinette Pechere-Bertschi; Fred Paccaud; Jan A Staessen; Bruno Vogt; Michel Burnier; Pierre-Yves Martin; Murielle Bochud Journal: Hypertension Date: 2013-10-14 Impact factor: 10.190
Authors: Umer Saleem; Mahyar Khaleghi; Nils G Morgenthaler; Andreas Bergmann; Joachim Struck; Thomas H Mosley; Iftikhar J Kullo Journal: J Clin Endocrinol Metab Date: 2009-04-14 Impact factor: 5.958
Authors: Don T Li; Estifanos N Habtemichael; Omar Julca; Chloe I Sales; Xavier O Westergaard; Stephen G DeVries; Diana Ruiz; Bhavesh Sayal; Jonathan S Bogan Journal: Yale J Biol Med Date: 2019-09-20