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      Effect of moderate alcohol consumption on fetuin-A levels in men and women: post-hoc analyses of three open-label randomized crossover trials

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          Abstract

          Background

          Fetuin-A, a liver-derived glycoprotein that impairs insulin-signalling, has emerged as a biomarker for diabetes risk. Although moderate alcohol consumption has been inversely associated with fetuin-A, data from clinical trials are lacking. Thus, we evaluated whether moderate alcohol consumption decreases circulating levels of fetuin-A.

          Methods

          We analyzed data of three separate open-label, randomized, crossover trials: 1) 36 postmenopausal women consuming 250 ml white wine (25 g alcohol) or white grape juice daily for 6 weeks, 2) 24 premenopausal women consuming 660 ml beer (26 g alcohol) or alcohol-free beer daily for 3 weeks, and 3) 24 young men consuming 100 ml vodka (30 g alcohol) orange juice or only orange juice daily for 4 weeks. After each treatment period fasting blood samples were collected.

          Results

          Circulating fetuin-A concentrations decreased in men after vodka consumption (Mean ± SEM: 441 ± 11 to 426 ± 11 μg/ml, p = 0.02), but not in women after wine (448 ± 17 to 437 ± 17 μg/ml, p = 0.16) or beer consumption (498 ± 15 to 492 ± 15 μg/ml, p = 0.48) compared to levels after each corresponding alcohol-free treatment. Post-hoc power analyses indicated that the statistical power to detect a similar effect as observed in men was 30% among the postmenopausal women and 31% among the premenopausal women.

          Conclusions

          In these randomized crossover trials, moderate alcohol consumption decreased fetuin-A in men but not in women. This sex-specific effect may be explained by the relatively short intervention periods or the low statistical power in the trials among women.

          Trials registration

          ClinicalTrials.gov ID no’s: NCT00285909, NCT00524550, NCT00918918.

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          Most cited references21

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          The role of hepatokines in metabolism.

          The liver is known to be involved in the natural history of the ongoing epidemics of type 2 diabetes mellitus and cardiovascular disease. In particular, the liver has a role in increased glucose production and dysregulated lipoprotein metabolism, conditions that are often found in patients with nonalcoholic fatty liver disease. Additionally, several proteins that are exclusively or predominantly secreted from the liver are now known to directly affect glucose and lipid metabolism. In analogy to the functional proteins released from adipose tissue and skeletal muscle-adipokines and myokines-these liver-derived proteins are known as hepatokines. The first hepatokine that has been proven to have a major pathogenetic role in metabolic diseases is α2-HS-glycoprotein (fetuin-A). Production of this glycoprotein is increased in steatotic and inflamed liver, but not in expanded and dysregulated adipose tissue. Thus, research into this molecule and other hepatokines is expected to aid in differentiating between the contribution of liver and those of skeletal muscle and adipose tissue, to the pathogenesis of type 2 diabetes mellitus and cardiovascular disease.
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            Plasma Fetuin-A Levels and the Risk of Type 2 Diabetes

            OBJECTIVE—The liver-secreted protein fetuin-A induces insulin resistance in animals, and circulating fetuin-A is elevated in insulin resistance and fatty liver in humans. We investigated whether plasma fetuin-A levels predict the incidence of type 2 diabetes in a large prospective, population-based study. RESEARCH DESIGN AND METHODS—A case-cohort study within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study comprising 27,548 subjects was designed. We randomly selected a subcohort of 2,500 individuals of whom 2,164 were diabetes free at baseline and had anamnestic, anthropometrical, and metabolic data for analysis. Of the 849 incident diabetic case subjects identified in the full cohort during 7 years of follow-up, 703 remained for analyses after similar exclusions. RESULTS—Plasma fetuin-A levels were positively associated with diabetes risk after adjustment for age (relative risk [RR] for extreme quintiles 1.75 [95% CI 1.32–2.31]; RR for 10 μg/ml 1.04 [1.03–1.06]). The association remained significant after adjustment for sex, BMI, waist circumference, and lifestyle risk factors (RR for 10 μg/ml 1.03 [1.01–1.06]). Adjustment for glucose, triglycerides, HDL cholesterol, A1C, γ-glutamyltransferase, or high-sensitivity C-reactive protein or mutual adjustment for these biomarkers did not appreciably change this result (RR for 10 μg/ml full adjusted model 1.05 [1.02–1.07]). Furthermore, fetuin-A was associated with increased diabetes risk particularly in individuals with elevated plasma glucose. CONCLUSIONS—Our data suggest that fetuin-A is an independent risk factor of type 2 diabetes.
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              Alpha2-Heremans-Schmid glycoprotein/fetuin-A is associated with insulin resistance and fat accumulation in the liver in humans.

              The alpha(2)-Heremans-Schmid glycoprotein (AHSG; fetuin-A in animals) impairs insulin signaling in vitro and in rodents. Whether AHSG is associated with insulin resistance in humans is under investigation. In an animal model of diet-induced obesity that is commonly associated with hepatic steatosis, an increase in Ahsg mRNA expression was observed in the liver. Therefore, we hypothesized that the AHSG plasma protein, which is exclusively secreted by the liver in humans, may not only be associated with insulin resistance but also with fat accumulation in the liver. Data from 106 healthy Caucasians without type 2 diabetes were included in cross-sectional analyses. A subgroup of 47 individuals had data from a longitudinal study. Insulin sensitivity was measured by a euglycemic-hyperinsulinemic clamp, and liver fat was determined by (1)H magnetic resonance spectroscopy. AHSG plasma levels, adjusted for age, sex, and percentage of body fat, were higher in subjects with impaired glucose tolerance compared with subjects with normal glucose tolerance (P = 0.006). AHSG plasma levels were negatively associated with insulin sensitivity (r = -0.22, P = 0.03) in cross-sectional analyses. Moreover, they were positively associated with liver fat (r = 0.27, P = 0.01). In longitudinal analyses, under weight loss, a decrease in liver fat was accompanied by a decrease in AHSG plasma concentrations. Furthermore, high AHSG levels at baseline predicted less increase in insulin sensitivity (P = 0.02). We found that high AHSG plasma levels are associated with insulin resistance in humans. Moreover, AHSG plasma levels are elevated in subjects with fat accumulation in the liver. This is consistent with a potential role of AHSG as a link between fatty liver and insulin resistance.
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                Author and article information

                Contributors
                Journal
                Diabetol Metab Syndr
                Diabetol Metab Syndr
                Diabetology & Metabolic Syndrome
                BioMed Central
                1758-5996
                2014
                18 February 2014
                : 6
                : 24
                Affiliations
                [1 ]TNO (a Dutch acronym for Netherlands Organisation of Applied Scientific Research), Zeist, the Netherlands
                [2 ]Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands
                [3 ]Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands
                Article
                1758-5996-6-24
                10.1186/1758-5996-6-24
                4094276
                24548643
                57bdbd61-413e-4ce2-bef8-4dadf550bb73
                Copyright © 2014 Joosten et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 22 October 2013
                : 14 February 2014
                Categories
                Research

                Nutrition & Dietetics
                alcohol consumption,fetuin-a,insulin sensitivity,liver enzymes,type 2 diabetes mellitus

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