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Accelerated epigenetic aging and DNA methylation alterations in Berardinelli-Seip congenital lipodystrophy. | LitMetric

AI Article Synopsis

  • Berardinelli-Seip congenital lipodystrophy type 2 (CGL2) is a rare genetic disorder linked to aging and characterized by diabetes, insulin resistance, and fatty liver.
  • A study of CGL2 patients showed significant DNA methylation changes and accelerated biological aging compared to controls, using advanced epigenetic clocks.
  • Additionally, research on a worm model revealed that disrupting the BSCL2 gene's homolog can shorten lifespan, highlighting important molecular pathways that may be affected in CGL2.

Article Abstract

Berardinelli-Seip congenital lipodystrophy type 2 (CGL2) is a very rare human genetic disorder with potential significance to the understanding of the pathobiology of aging. CGL2 patients display characteristic progeroid features and suffer from type 2 diabetes, insulin resistance and fatty liver. In this study, we profiled genome-wide DNA methylation levels in CGL2 patients with BSCL2 mutations to study epigenetic age acceleration and DNA methylation alterations. This analysis revealed significant age acceleration in blood DNA of CGL2 patients using both first- and second-generation epigenetic clocks. We also observed a shortened lifespan of Caenorhabditis elegans following knockdown of the BSCL2 homolog seip-1 on a daf-16/forkhead box, class O mutant background. DNA methylation analysis revealed significant differentially methylated sites enriched for lyase activity, kinase regulator activity, protein kinase regulator activity and kinase activator activity. We could also observe significant hypomethylation in the promoter of the dual specificity phosphatase 22 gene when comparing CGL2 patients versus controls. We conclude that in line with the observed progeroid features, CGL2 patients exhibit significant epigenetic age acceleration and DNA methylation alterations that might affect pathways/genes of potential relevance to the disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10196674PMC
http://dx.doi.org/10.1093/hmg/ddad016DOI Listing

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