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Rev Diabet Stud, 2007, 4(4):231-235 DOI 10.1900/RDS.2007.4.231

Evaluation of Apolipoprotein M Serum Concentration as a Biomarker of HNF-1alpha MODY

Jan Skupien1, Grzegorz Kepka1, Sylwia Gorczynska-Kosiorz2, Anna Gebska3, Tomasz Klupa1, Krzysztof Wanic1, Natalia Nowak1, Maciej Borowiec4, Jacek Sieradzki1, Maciej T. Malecki1

1Department and Chair of Metabolic Diseases, Jagiellonian University Medical College, Krakow, Poland
2Department of Internal Medicine, Diabetology and Nephrology, Medical University of Silesia, Zabrze, Poland
3Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland
4Department of Pediatrics, Medical University of Lodz, Lodz, Poland
Address correspondence to: Maciej T. Malecki, e-mail: mmalecki@cm-uj.krakow.pl

Manuscript submitted January 22, 2008; resubmitted February 19, 2008; accepted February 22, 2008.

Keywords: maturity onset diabetes of the young, MODY, apolipoprotein M, HNF-1alpha

Abstract

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-1α (HNF-1α), 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-1α 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-1α MODY. We included in this study 48 HNF-1α 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 μg/ml, SD 1.9 (13.5 μg/ml, SD 1.7 in diabetic subjects and 13.9 μg/ml, SD 2.0 in non-diabetic mutation carriers respectively). In the T2DM group, mean apoM level was 13.7 μg/ml, SD 2.1, while it reached 13.8 μg/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-1α mutations resulting in MODY phenotype and apoM levels. Thus, we cannot confirm the clinical usefulness of apoM as a biomarker of HNF-1α MODY.

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