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      Low Water Intake and Risk for New-Onset Hyperglycemia

      research-article
      , MD, PHD 1 , 2 , 3 , 4 , , MD, PHD 4 , , PHD 4 , 5 , 6 , , PHD 7 , 8 , , MD, MPH 9 , , MD, PHD 4 , 5 , 6 , 10 , , MD, PHD 1 , 2 , 3 , , PHD 4 , for the D.E.S.I.R. Study Group *
      Diabetes Care
      American Diabetes Association

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          Abstract

          OBJECTIVE

          Water intake alters vasopressin secretion. Recent findings reveal an independent association between plasma copeptin, a surrogate for vasopressin, and risk of diabetes.

          RESEARCH DESIGN AND METHODS

          Participants were 3,615 middle-aged men and women, with normal baseline fasting glycemia (FG), who were recruited in a 9-year follow-up study. Odds ratios (ORs) and 95% CIs for the incidence of hyperglycemia (FG ≥6.1 mmol/L or treatment for diabetes) were calculated according to daily water intake classes based on a self-administered questionnaire.

          RESULTS

          During follow-up, there were 565 incident cases of hyperglycemia. After adjustment for confounding factors, ORs (95% CIs) for hyperglycemia associated with classes of water intake (<0.5 L, n = 677; 0.5 to <1.0 L, n = 1,754; and >1.0 L, n = 1,184) were 1.00, 0.68 (0.52–0.89), and 0.79 (0.59–1.05), respectively ( P = 0.016).

          CONCLUSIONS

          Self-reported water intake was inversely and independently associated with the risk of developing hyperglycemia.

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          Most cited references13

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          Predicting Diabetes: Clinical, Biological, and Genetic Approaches

          OBJECTIVE—To provide a simple clinical diabetes risk score and to identify characteristics that predict later diabetes using variables available in the clinic setting as well as biological variables and polymorphisms. RESEARCH DESIGN AND METHODS—Incident diabetes was studied in 1,863 men and 1,954 women, 30–65 years of age at baseline, with diabetes defined by treatment or by fasting plasma glucose ≥7.0 mmol/l at 3-yearly examinations over 9 years. Sex-specific logistic regression equations were used to select variables for prediction. RESULTS—A total of 140 men and 63 women developed diabetes. The predictive clinical variables were waist circumference and hypertension in both sexes, smoking in men, and diabetes in the family in women. Discrimination, as measured by the area under the receiver operating curves (AROCs), were 0.713 for men and 0.827 for women, a little higher than for the Finish Diabetes Risk (FINDRISC) score, with fewer variables in the score. Combining clinical and biological variables, the predictive equation included fasting glucose, waist circumference, smoking, and γ-glutamyltransferase for men and fasting glucose, BMI, triglycerides, and diabetes in family for women. The number of TCF7L2 and IL6 deleterious alleles was predictive in both sexes, but after including the above clinical and biological variables, this variable was only predictive in women (P < 0.03) and the AROC statistics increased only marginally. CONCLUSIONS—The best clinical predictor of diabetes is adiposity, and baseline glucose is the best biological predictor. Clinical and biological predictors differed marginally between men and women. The genetic polymorphisms added little to the prediction of diabetes.
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            Copeptin, a surrogate marker of vasopressin, is associated with microalbuminuria in a large population cohort.

            Urinary albumin excretion is a powerful predictor of progressive cardiovascular and renal disease. In rats and humans, administration of a synthetic vasopressin analogue, 1-desamino-8-D-arginine-vasopressin, increases urinary albumin excretion; however, it is unknown if endogenous vasopressin levels influence albumin excretion. To determine this we measured copeptin, a marker of endogenous vasopressin levels, and its association with urinary albumin excretion in 7593 patients in the PREVEND study, a prospective population based, observational cohort. Urinary albumin excretion was measured in two consecutive 24-h urine samples by nephelometry while copeptin was measured by an immunoassay. Median copeptin concentrations were significantly higher in males than females and high levels were associated with significantly lower 24-h urine volumes of high osmolarity. With increasing quintiles of copeptin levels, the percentage of microalbuminuric subjects increased from 13 to 25 for males and from 8 to15 for females. This association was independent of age and other potential confounders; however, we found an interaction between age and copeptin in their association with urinary albumin excretion. Our study shows that plasma copeptin levels are associated with microalbuminuria, consistent with the hypothesis that vasopressin is involved in urinary albumin excretion. If future studies show that this association is causal, then drinking more water or pharmacological intervention to decrease plasma vasopressin may have beneficial effects on the kidney, especially in the elderly.
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              Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions.

              1. In hepatocytes from starved rats, vasopressin, angiotensin (angiotensin II) and oxytocin stimulated gluconeogenesis from lactate by 25--50%; minimal effective concentrations were about 0.02pM, 1 nM and 0.2 nM respectively. 2. Vasopressin and angiotensin also stimulated gluconeogenesis from alanine, pyruvate, serine and glycerol. EGTA decreased gluconeogenesis from these substrates. 3. Hormonal stimulation of gluconeogenesis from lactate was abolished in the absence of extracellular Ca2+. 4. Insulin did not prevent stimulation of gluconeogenesis by vasopressin or angiotensin. 5. The potency of the stimulatory effects of vasopressin and angiotensin on hepatic gluconeogenesis suggests they are operative in vivo. Also, the data suggest that Ca2+ plays a role in the stimulation by these hormones.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                December 2011
                14 November 2011
                : 34
                : 12
                : 2551-2554
                Affiliations
                [1] 1Université Paris–Diderot, Paris 7, Paris, France
                [2] 2Département d'Endocrinologie, Diabétologie et Nutrition, Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, Paris, France
                [3] 3INSERM U695, Paris, France
                [4] 4INSERM Unité 872, Centre de Recherche des Cordeliers, Paris, France
                [5] 5Université Pierre et Marie Curie, Paris, France
                [6] 6Université Paris Descartes, Paris, France
                [7] 7INSERM CESP Center for Research in Epidemiology and Population Health, U1018, Epidemiology of Diabetes, Obesity and Chronic Kidney Disease Over the Life Course, Villejuif, France
                [8] 8Université Paris 11, UMRS 1018, Villejuif, France
                [9] 9Institut Inter-Régional pour la Santé, La Riche, France
                [10] 10Département d’Hypertension Artérielle, Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris, France
                Author notes
                Corresponding author: Ronan Roussel, ronan.roussel@ 123456bch.aphp.fr .
                Article
                0652
                10.2337/dc11-0652
                3220834
                21994426
                19504430-d690-4fbf-8c07-78c26378a31c
                © 2011 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 6 April 2011
                : 4 September 2011
                Categories
                Original Research
                Epidemiology/Health Services Research

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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