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      Increased copeptin levels in metabolic syndrome from a Romanian population

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          Abstract

          Rationale: Arginine vasopressin (AVP) is secreted under conditions of water deprivation. Since AVP has a low half-life in the plasma, the C-terminal fragment of AVP-precursor (copeptin) was used to estimate the AVP levels. High copeptin levels increase the risk for the development of diabetes mellitus.

          Aim: This study was aimed to measure copeptin levels in the metabolic syndrome (MetS) in Romanians using a competitive enzyme immunoassay.

          Methods and results: Patients prone to present MetS (n = 63) were compared to controls (n = 42). In the MetS group, the syndrome was confirmed in 93.6%. Affected patients displayed 85.7% obesity and insulin resistance (HOMAIR of 4.9 ± 0.4 versus 1.1 ± 0.8 in controls). Low HDL-cholesterol was less represented (47.5%). Copeptin levels were 0.6 ± 0.0 in MetS versus 0.42 ± 0.0 ng/ mL in controls (P < 0.004). Higher copeptin (0.79 to 1.83 ng/ mL) was associated with MetS, P < 0.0018, OR 20, 95%CI [3.03 – 131.7]. In ANOVA, high copeptin was equally explained by MetS or obesity (P < 0.05,α = 3.8). The best correlation was found with high triglyceride levels (P < 0.013,α = 6.3) while the correlation with HOMAIR remained not significant.

          Discussion: These data indicated a concordant correlation between increased copeptin and MetS or its components. In the light of epidemiological data, indicating that more than 50% of the European population has a lower daily water intake and a fraction of 25% displaying high copeptin, our data further sustained that copeptin may be a good biomarker for MetS and/ or obesity, which should be further investigated with other members of the osmoregulation pathway at both pathogenesis and genetic levels.

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          Most cited references22

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          Standards of medical care in diabetes--2006.

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            Vasopressin: mechanisms of action on the vasculature in health and in septic shock.

            Vasopressin is essential for cardiovascular homeostasis, acting via the kidney to regulate water resorption, on the vasculature to regulate smooth muscle tone, and as a central neurotransmitter, modulating brainstem autonomic function. Although it is released in response to stress or shock states, a relative deficiency of vasopressin has been found in prolonged vasodilatory shock, such as is seen in severe sepsis. In this circumstance, exogenous vasopressin has marked vasopressor effects, even at doses that would not affect blood pressure in healthy individuals. These two findings provide the rationale for the use of vasopressin in the treatment of septic shock. However, despite considerable research attention, the mechanisms for vasopressin deficiency and hypersensitivity in vasodilatory shock remain unclear. To summarize vasopressin's synthesis, physiologic roles, and regulation and then review the literature describing its vascular receptors and downstream signaling pathways. A discussion of potential mechanisms underlying vasopressin hypersensitivity in septic shock follows, with reference to relevant clinical, in vivo, and in vitro experimental evidence. Search of the PubMed database (keywords: vasopressin and receptors and/or sepsis or septic shock) for articles published in English before May 2006 and manual review of article bibliographies. The pathophysiologic mechanism underlying vasopressin hypersensitivity in septic shock is probably multifactorial. It is doubtful that this phenomenon is merely the consequence of replacing a deficiency. Changes in vascular receptors or their signaling and/or interactions between vasopressin, nitric oxide, and adenosine triphosphate-dependent potassium channels are likely to be relevant. Further translational research is required to improve our understanding and direct appropriate educated clinical use of vasopressin.
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              Plasma Copeptin, AVP Gene Variants, and Incidence of Type 2 Diabetes in a Cohort From the Community.

              Experimental data support a role for vasopressin in metabolic disorders.
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                Author and article information

                Journal
                J Med Life
                J Med Life
                JMedLife
                Journal of Medicine and Life
                Carol Davila University Press (Romania )
                1844-122X
                1844-3117
                Oct-Dec 2016
                : 9
                : 4
                : 353-357
                Affiliations
                [* ]”Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
                [** ]”C.I. Parhon” National Institute of Endocrinology, Bucharest, Romania
                [*** ]University of Medicine and Pharmacy Craiova, Romania
                [**** ]Laboratory of Molecular Endocrinology, IURC, UMR204, NUTRIPASS (IRD, University of Montpellier, SuprAgro)
                []Passed away in March 2016
                Author notes
                Correspondence to: Vintilă Mădălina, MD, “C. I. Parhon” National Institute of Endocrinology, Bucharest, 34-36 Aviatorilor Blvd., Code 011863, Bucharest, Romania, Mobile phone: +40723 249 516, E-mail: madalina.vintila@yahoo.com
                Article
                JMedLife-09-353
                5141393
                27928437
                a5fe0682-a72a-4825-ba86-fca2be76fa9a
                ©Carol Davila University Press

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 May 2016
                : 27 September 2016
                Categories
                Original Articles

                Medicine
                copeptin,arginine vasopressin,metabolic syndrome,insulin resistance
                Medicine
                copeptin, arginine vasopressin, metabolic syndrome, insulin resistance

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