Mutations in HNF1A Result in Marked Alterations of Plasma Glycan Profile

نویسندگان

  • Gaya Thanabalasingham
  • Jennifer E. Huffman
  • Jayesh J. Kattla
  • Mislav Novokmet
  • Igor Rudan
  • Anna L. Gloyn
  • Caroline Hayward
  • Barbara Adamczyk
  • Rebecca M. Reynolds
  • Ana Muzinic
  • Neelam Hassanali
  • Maja Pucic
  • Amanda J. Bennett
  • Abdelkader Essafi
  • Ozren Polasek
  • Saima A. Mughal
  • Irma Redzic
  • Dragan Primorac
  • Lina Zgaga
  • Ivana Kolcic
  • Torben Hansen
  • Daniela Gasperikova
  • Erling Tjora
  • Mark W.J. Strachan
  • Trine Nielsen
  • Juraj Stanik
  • Iwar Klimes
  • Oluf B. Pedersen
  • Pål R. Njølstad
  • Sarah H. Wild
  • Ulf Gyllensten
  • Olga Gornik
  • James F. Wilson
  • Nicholas D. Hastie
  • Harry Campbell
  • Mark I. McCarthy
  • Pauline M. Rudd
  • Katharine R. Owen
  • Gordan Lauc
  • Alan F. Wright
چکیده

A recent genome-wide association study identified hepatocyte nuclear factor 1-α (HNF1A) as a key regulator of fucosylation. We hypothesized that loss-of-function HNF1A mutations causal for maturity-onset diabetes of the young (MODY) would display altered fucosylation of N-linked glycans on plasma proteins and that glycan biomarkers could improve the efficiency of a diagnosis of HNF1A-MODY. In a pilot comparison of 33 subjects with HNF1A-MODY and 41 subjects with type 2 diabetes, 15 of 29 glycan measurements differed between the two groups. The DG9-glycan index, which is the ratio of fucosylated to nonfucosylated triantennary glycans, provided optimum discrimination in the pilot study and was examined further among additional subjects with HNF1A-MODY (n = 188), glucokinase (GCK)-MODY (n = 118), hepatocyte nuclear factor 4-α (HNF4A)-MODY (n = 40), type 1 diabetes (n = 98), type 2 diabetes (n = 167), and nondiabetic controls (n = 98). The DG9-glycan index was markedly lower in HNF1A-MODY than in controls or other diabetes subtypes, offered good discrimination between HNF1A-MODY and both type 1 and type 2 diabetes (C statistic ≥ 0.90), and enabled us to detect three previously undetected HNF1A mutations in patients with diabetes. In conclusion, glycan profiles are altered substantially in HNF1A-MODY, and the DG9-glycan index has potential clinical value as a diagnostic biomarker of HNF1A dysfunction.

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عنوان ژورنال:

دوره 62  شماره 

صفحات  -

تاریخ انتشار 2013