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Vasopressin, from Regulator to Disease Predictor for Diabetes and Cardiometabolic Risk

Annals of Nutrition and Metabolism

S. Karger AG

Vasopressin, Hydration, Diabetes mellitus, Copeptin, Cardiovascular disease

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      Background: Type 2 diabetes and its cardiovascular disease complications are the major public health threats of our century. Although physical activity and dietary changes are the cornerstones in prevention of diabetes, their broad implementation is not elementary and other complementary lifestyle regimens are needed. Summary: Vasopressin (VP) is the main regulator of body water homeostasis, and at insufficient water intake, normal plasma osmolality can be maintained by increased pituitary VP secretion through VP-2 receptor mediated renal water reabsorption. During the last 6 years several independent studies have shown that high circulating VP, measured by the stable VP marker copeptin, predicts development of type 2 diabetes as well as the metabolic syndrome, cardiovascular disease and premature mortality. Interestingly, VP stimulates adrenocorticotrophic hormone, and as a consequence cortisol secretion, through pituitary VP-1B receptors, which could explain why the 25% of the middle-aged population with high circulating VP have a mild Cushing's syndrome-like phenotype. In rats, high VP results in deterioration of glucose tolerance whereas low VP, obtained by high water intake, ameliorates the VP associated dysmetabolic state, suggesting that the relationship between high VP and risk of diabetes and cardiometabolic disease in humans may be causal and reversible by increasing water intake. Key Messages: With the emerging evidence that high VP, which is present in 25% of the population, is an independent risk factor for diabetes and cardiometabolic disease, VP reduction through water supplementation appears as an attractive candidate intervention to prevent diabetes and its cardiovascular complications.

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      Most cited references 24

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      Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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          The cardiovascular safety and efficacy of many current antihyperglycemic agents, including saxagliptin, a dipeptidyl peptidase 4 (DPP-4) inhibitor, are unclear. We randomly assigned 16,492 patients with type 2 diabetes who had a history of, or were at risk for, cardiovascular events to receive saxagliptin or placebo and followed them for a median of 2.1 years. Physicians were permitted to adjust other medications, including antihyperglycemic agents. The primary end point was a composite of cardiovascular death, myocardial infarction, or ischemic stroke. A primary end-point event occurred in 613 patients in the saxagliptin group and in 609 patients in the placebo group (7.3% and 7.2%, respectively, according to 2-year Kaplan-Meier estimates; hazard ratio with saxagliptin, 1.00; 95% confidence interval [CI], 0.89 to 1.12; P=0.99 for superiority; P<0.001 for noninferiority); the results were similar in the "on-treatment" analysis (hazard ratio, 1.03; 95% CI, 0.91 to 1.17). The major secondary end point of a composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, coronary revascularization, or heart failure occurred in 1059 patients in the saxagliptin group and in 1034 patients in the placebo group (12.8% and 12.4%, respectively, according to 2-year Kaplan-Meier estimates; hazard ratio, 1.02; 95% CI, 0.94 to 1.11; P=0.66). More patients in the saxagliptin group than in the placebo group were hospitalized for heart failure (3.5% vs. 2.8%; hazard ratio, 1.27; 95% CI, 1.07 to 1.51; P=0.007). Rates of adjudicated cases of acute and chronic pancreatitis were similar in the two groups (acute pancreatitis, 0.3% in the saxagliptin group and 0.2% in the placebo group; chronic pancreatitis, <0.1% and 0.1% in the two groups, respectively). DPP-4 inhibition with saxagliptin did not increase or decrease the rate of ischemic events, though the rate of hospitalization for heart failure was increased. Although saxagliptin improves glycemic control, other approaches are necessary to reduce cardiovascular risk in patients with diabetes. (Funded by AstraZeneca and Bristol-Myers Squibb; SAVOR-TIMI 53 number, NCT01107886.).

            Author and article information

            Department of Clinical Sciences, Lund University and Department of Internal Medicine, Skåne University Hospital, Malmö, Sweden
            Ann Nutr Metab
            Annals of Nutrition and Metabolism
            Ann Nutr Metab
            S. Karger AG (Basel, Switzerland karger@ )
            June 2016
            16 June 2016
            : 68
            : 2
            : 24-28
            Ann Nutr Metab 2016;68(suppl 2):24-28
            © 2016 The Author(s) Published by S. Karger AG, Basel

            This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

            Figures: 1, Tables: 1, References: 40, Pages: 5


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