Inheritance of rare functional GCKR variants and their contribution to triglyceride levels in families

Hum Mol Genet. 2014 Oct 15;23(20):5570-8. doi: 10.1093/hmg/ddu269. Epub 2014 May 30.

Abstract

Significant resources have been invested in sequencing studies to investigate the role of rare variants in complex disease etiology. However, the diagnostic interpretation of individual rare variants remains a major challenge, and may require accurate variant functional classification and the collection of large numbers of variant carriers. Utilizing sequence data from 458 individuals with hypertriglyceridemia and 333 controls with normal plasma triglyceride levels, we investigated these issues using GCKR, encoding glucokinase regulatory protein. Eighteen rare non-synonymous GCKR variants identified in these 791 individuals were comprehensively characterized by a range of biochemical and cell biological assays, including a novel high-throughput-screening-based approach capable of measuring all variant proteins simultaneously. Functionally deleterious variants were collectively associated with hypertriglyceridemia, but a range of in silico prediction algorithms showed little consistency between algorithms and poor agreement with functional data. We extended our study by obtaining sequence data on family members; however, functional variants did not co-segregate with triglyceride levels. Therefore, despite evidence for their collective functional and clinical relevance, our results emphasize the low predictive value of rare GCKR variants in individuals and the complex heritability of lipid traits.

Publication types

  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / chemistry
  • Adaptor Proteins, Signal Transducing / genetics*
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Algorithms
  • Animals
  • COS Cells
  • Case-Control Studies
  • Chlorocebus aethiops
  • Genetic Variation
  • HeLa Cells
  • Humans
  • Hyperlipoproteinemia Type IV / blood
  • Hyperlipoproteinemia Type IV / genetics*
  • Mice
  • Models, Molecular
  • Polymorphism, Single Nucleotide*
  • Protein Structure, Tertiary
  • Sequence Analysis, DNA
  • Triglycerides / blood*

Substances

  • Adaptor Proteins, Signal Transducing
  • GCKR protein, human
  • Triglycerides