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A Helicobacter pylori-associated insulin resistance in asymptomatic sedentary young men does not correlate with inflammatory markers and urine levels of 8-iso-PGF2-α or 1,4-dihydroxynonane mercapturic acid

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posted on 2017-11-06, 12:46 authored by Andriy Cherkas, Sergii Golota, Françoise Guéraud, Orest Abrahamovych, Christoph Pichler, Armen Nersesyan, Volodymyr Krupak, Vira Bugiichyk, Ostap Yatskevych, Mykhaylo Pliatsko, Peter Eckl, Siegfried Knasmüller

A potential contribution of H. pylori contamination to low-grade inflammation, oxidative stress (OS) and insulin resistance as well as correlations between these parameters in asymptomatic sedentary males was analysed. We enrolled 30 apparently healthy asymptomatic young subjects (18 H. pylori negative and 12 positive) and measured whole blood glucose, glycated haemoglobin, insulin, C-peptide, cortisol, aldosterone, testosterone, thyroid stimulating hormone, C-reactive protein, interleukins 6 and 10, TNF-alpha and comet assay. As markers of OS, we used urine levels of iso-PGF2-α and 1,4-dihydroxynonane mercapturic acid (DHN-MA). Twofold elevation of fasting insulin level and HOMA index in H. pylori–positive subjects (p < .05) was shown. Inflammatory parameters and monocyte DNA damage, urine levels of DHN-MA and iso-PGF2-α did not show significant differences between the groups. The early stage of H. pylori-triggered metabolic derangements in sedentary subjects include development of insulin resistance in H. pylori-positive subjects; however, there is no evidence of systemic inflammatory and OS-related changes.

Funding

The work was supported by the State Agency of Science, Innovations and Informatisation of Ukraine contracts #M512–2011, #M473–2012, OEAD Project UA 03/2011, and by COST Actions B35 “LPO – Lipid Peroxidation associated Disorders,” CM1001“Chemistry of non-enzymatic protein modification – modulation of protein structure and function” and CA16112 “Personalised Nutrition in aging society: redox control of major age-related diseases”, A.C. was supported by the Georg Forster (HERMES) Scholarship from Alexander von Humboldt Foundation (Bonn, Germany).

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