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Vitamin D-Spiegel und Risiko für Typ-2-Diabetes

Kein Nachweis für einen ursächlichen Zusammenhang

Aktuelle Studien vorgestellt von Prof. Helmut Schatz

In Blogbeiträgen und in Pressemitteilungen der letzten Jahre stand die DGE einem vielfach postulierten, kausalen Zusammenhang zwischen Vitamin D und einer Vielzahl von extra-muskuloskelettalen Erkrankungen abwartend bis distanziert gegenüber. Gleiches galt für eine breite prophylaktische oder therapeutische Vitamin-D-Gabe bei diesen Erkrankungen, was häufig und zum Teil vehement gefordert wurde. Heute (2. Oktober 2014) erscheint in "The Lancet Diabetes & Endocrinology" online eine sorgfältig geplante und durchgeführte Studie mit der Methode der Mendelschen Randomisierung zu diesem Thema. Diese Publikation liegt auf der Linie, welche die DGE stets eingenommen hat. Unten kann die Zusammenfassung nachgelesen werden.

Zheng Ye et al.: Association between circulating 25-hydroxyvitamin D and incident type 2 diabetes: a mendelian randomisation study

Summary

Background: Low circulating concentrations of 25-hydroxyvitamin D (25[OH]D), a marker of vitamin D status, are associated with an increased risk of type 2 diabetes, but whether this association is causal remains unclear. We aimed to estimate the unconfounded, causal association between 25(OH)D concentration and risk of type 2 diabetes using a mendelian randomisation approach.

Methods: Using several data sources from populations of European descent, including type 2 diabetes cases and non-cases, we did a mendelian randomisation analysis using single nucleotide polymorphisms (SNPs) within or near four genes related to 25(OH)D synthesis and metabolism: DHCR7 (related to vitamin D synthesis), CYP2R1 (hepatic 25-hydroxylation), DBP (also known as GC; transport), and CYP24A1 (catabolism). We assessed each SNP for an association with circulating 25(OH)D concentration (5.449 non-cases; two studies), risk of type 2 diabetes (28.144 cases, 76.344 non-cases; five studies), and glycaemic traits (concentrations of fasting glucose, 2-h glucose, fasting insulin, and HbA1c; 46.368 non-cases; study consortium). We combined these associations in a likelihood-based mendelian randomisation analysis to estimate the causal association of 25(OH)D concentration with type 2 diabetes and the glycaemic traits, and compared them with that from a meta-analysis of data from observational studies (8.492 cases, 89.698 non-cases; 22 studies) that assessed the association between 25(OH)D concentration and type 2 diabetes.

Findings: All four SNPs were associated with 25(OH)D concentrations (p<10-6). The mendelian randomisation-derived unconfounded odds ratio for type 2 diabetes was 0?93 (95 % CI 0?77-1?13; p=0?46) per 25?0 nmol/L (1 SD) lower 25(OH)D concentration. The corresponding (potentially confounded) relative risk from the meta-analysis of data from observational studies was 1?22 (1?16-1?29; p=3?5 x& bsp;10-14). The mendelian randomisation-derived estimates for glycaemic traits were not significant (p>0?25).

Interpretation: The association between 25(OH)D concentration and type 2 diabetes is unlikely to be causal. Efforts to increase 25(OH)D concentrations might not reduce the risk of type 2 diabetes as would be expected on the basis of observational evidence. These findings warrant further investigations to identify causal factors that might increase 25(OH)D concentration and also reduce the risk of type 2 diabetes.

Quelle

  • Zheng Ye et al.: Association between circulating 25-hydroxyvitamin D and incident type 2 diabetes: a mendelian randomisation study. The Lancet Diabetes & Endocrinology, Early Online Publication, 1 October 2014 doi:10.1016/S2213-8587(14)70184-6

zuletzt bearbeitet: 18.10.2014 nach oben

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