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Evaluation of Apolipoprotein M Serum Concentration as a Biomarker of HNF-1alpha MODY
Author(s) -
Jan Skupień,
Grzegorz Kepka,
Sylwia Górczyńska-Kosiorz,
Anna Gębska,
Tomasz Klupa,
Krzysztof Wanic,
Natalia Nowak,
Maciej Borowiec,
Jacek Sieradzki,
Maciej T. Małecki
Publication year - 2007
Publication title -
the review of diabetic studies
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 41
eISSN - 1614-0575
pISSN - 1613-6071
DOI - 10.1900/rds.2007.4.231
Subject(s) - diabetology , medicine , endocrinology , apolipoprotein b , biomarker , diabetes mellitus , cholesterol , biology , genetics
Apolipoprotein M (apoM) is a 26-kDa protein expressed mainly in the liver and kidneys. It is present predominantly in high-density lipoproteins (HDL). ApoM expression is influenced by the hepatocyte nuclear factor-1alpha (HNF-1alpha), which is a transcription factor associated with the pathogenesis of MODY. Some earlier data suggested that apoM levels were lower in the serum of HNF-1alpha MODY subjects, than in that of other diabetics and healthy controls. The aim of this study was to evaluate apoM as a biomarker for HNF-1alpha MODY. We included in this study 48 HNF-1alpha mutation carriers (40 diabetic patients and 8 subjects with normal glucose levels in the fasted state) from the Polish Nationwide Registry of MODY. In addition, we examined 55 T2DM patients and 55 apparently healthy volunteers who had normal fasting glucose levels. ApoM was measured by the sandwich dot-blot technique with recombinant apoM (Abnova) as a protein standard, mouse anti-human apoM monoclonal primary antibody and rat anti-mouse HRP-conjugated secondary antibody (BD Biosciences). Mean apoM level in the MODY group was 13.6 mug/ml, SD 1.9 (13.5 mug/ml, SD 1.7 in diabetic subjects and 13.9 mug/ml, SD 2.0 in non-diabetic mutation carriers respectively). In the T2DM group, mean apoM level was 13.7 mug/ml, SD 2.1, while it reached 13.8 mug/ml, SD 2.0 in healthy controls. There was no difference between apoM serum concentrations in all the study groups. In summary, our study showed no association between HNF-1alpha mutations resulting in MODY phenotype and apoM levels. Thus, we cannot confirm the clinical usefulness of apoM as a biomarker of HNF-1alpha MODY.

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