ECTS2016 Poster Presentations Genetics and Epigenetics (25 abstracts)
Mitochondrial DNA point mutation is associated with lower bone turnover markers
Jakob H. Langdahl 1, , Stinus J. Hansen 4, , Per H. Andersen 2 , Knud B. Yderstræde 4, , John Vissing 5 , Morten Dunø 6 , Anja L. Frederiksen 1, & Morten Frost Nielsen 4,
1Clinical Genetic Research Unit/Clinical Institute University of Southern Denmark, Odense, Denmark; 2Department of Endocrinology/Hospital of Southwest Jutland, Esbjerg, Denmark; 3Department of Clinical Genetics/Odense University Hospital, Odense, Denmark; 4Department of Endocrinology/Odense University Hospital, Odense, Denmark; 5Department of Neurology/Rigshospitalet, Copenhagen, Denmark; 6Department of Clinical Genetics/Rigshospitalet, Copenhagen, Denmark; 7Endocrine Research Unit/Clinical Institute University of Southern Denmark, Odense, Denmark.
Introduction: Mitochondrial dysfunction is associated with several clinical outcomes including diabetes and myopathy and is implicated in the human aging process. We previously showed that the mitochondrial DNA point mutation mtDNA3243A>G is associated with lower BMD and altered bone structure. The aim of this study was to assess bone turnover markers in individuals with the mutation and controls.
Methods: We recruited 45 patients (29 female, 16 male) with the mtDNA3243A>G mutation aged 47,6±15,2 years. Cases were matched with respect to sex, age, height and menopausal status with healthy controls. All participants gave blood for analysis of general biochemistry and bone markers.
Results: Cases and controls were matched with regard to age, sex and height, but cases had a significantly lower body weight (63.6 vs 74.6 kg, P=0.001) and 24 of 45 patients had manifest diabetes mellitus (DM). Fasting s-CTX was measured in 36 patients and was significantly lower than in the controls (0.41 vs 0.55 μg/l, P=0.024). S-P1NP was measured in 39 patients and was significant lower than in the controls (45.1 vs 57.8 μg/l, P=0.007). The difference in P1NP but not CTX remained significant after adjusting for weight and sex. Stratifying according to DM-status, s-CTX and s-P1NP was significantly lower in cases with DM compared to their controls, whereas levels of bone turnover markers were the same in non-DM cases and controls.
Conclusion: Mitochondrial dysfunction is associated with lower bone turnover, in part possibly explained by lower body mass and diabetes. Further studies are needed to describe the effects of mitochondrial dysfunction on bone remodelling.
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