Parental diabetes status reveals association of mitochondrial DNA haplogroup J1 with type 2 diabetes

doi:10.1186/1471-2350-10-60

BMC Medical Genetics

Volume 10

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Feder J
Ovadia O
Blech I
Cohen J
Wainstein J
Harman-Boehm I
Glaser B
Mishmar D

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Ovadia O
Blech I
Cohen J
Wainstein J
Harman-Boehm I
Glaser B
Mishmar D
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Research article

Parental diabetes status reveals association of mitochondrial DNA haplogroup J1 with type 2 diabetes

Jeanette Feder¹^,2 , Ofer Ovadia¹ , Ilana Blech³ , Josef Cohen⁴^,7 , Julio Wainstein⁵^,7 , Ilana Harman-Boehm⁶^,7 , Benjamin Glaser³^,7 and Dan Mishmar¹^,2

¹Department of Life Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel

²The National Institute of Biotechnology (NIBN), Ben-Gurion University of the Negev, Beer-Sheva, Israel

³Endocrinology and Metabolism Service, Hadassah-Hebrew University Medical School, Jerusalem, Israel

⁴Maccabi Health Services, Diabetes Clinic, Rishon LeZion, Israel

⁵Wolfson Medical Center, Holon, Israel

⁶Soroka Hospital, Ben-Gurion University of the Negev, Beer-Sheva, Israel

⁷Israel Diabetes Research Group (IDRG), Israel

author email corresponding author email

BMC Medical Genetics 2009, 10:60doi:10.1186/1471-2350-10-60


Published:	18 June 2009

Abstract

Background

Although mitochondrial dysfunction is consistently manifested in patients with Type 2 Diabetes mellitus (T2DM), the association of mitochondrial DNA (mtDNA) sequence variants with T2DM varies among populations. These differences might stem from differing environmental influences among populations. However, other potentially important considerations emanate from the very nature of mitochondrial genetics, namely the notable high degree of partitioning in the distribution of human mtDNA variants among populations, as well as the interaction of mtDNA and nuclear DNA-encoded factors working in concert to govern mitochondrial function. We hypothesized that association of mtDNA genetic variants with T2DM could be revealed while controlling for the effect of additional inherited factors, reflected in family history information.

Methods

To test this hypothesis we set out to investigate whether mtDNA genetic variants will be differentially associated with T2DM depending on the diabetes status of the parents. To this end, association of mtDNA genetic backgrounds (haplogroups) with T2DM was assessed in 1055 Jewish patients with and without T2DM parents ('DP' and 'HP', respectively).

Results

Haplogroup J1 was found to be 2.4 fold under-represented in the 'HP' patients (p = 0.0035). These results are consistent with a previous observation made in Finnish T2DM patients. Moreover, assessing the haplogroup distribution in 'DP' versus 'HP' patients having diabetic siblings revealed that haplogroup J1 was virtually absent in the 'HP' group.

Conclusion

These results imply the involvement of inherited factors, which modulate the susceptibility of haplogroup J1 to T2DM.