Leveraging Genetics to Address the Role of GALNT2 on Atherogenic Dyslipidemia

Adv Biol (Weinh). 2023 Sep;7(9):e2200319. doi: 10.1002/adbi.202200319. Epub 2023 Mar 2.

Abstract

Several studies have shown that downregulation of GALNT2 (Polypeptide N-Acetylgalactosaminyltransferase 2), encoding polypeptide N-acetylgalactosaminyltransferase 2, decreases high-density lipoprotein cholesterol (HDL-C) and increases triglycerides levels by glycosylating key enzymes of lipid metabolism, such as angiopoietin like 3, apolipoprotein C-III, and phospholipid transfer protein. GALNT2 is also a positive modulator of insulin signaling and action, associated with in vivo insulin sensitivity and during adipogenesis strongly upregulates adiponectin. Thus, the hypothesis that GALNT2 affects HDL-C and triglycerides levels also through insulin sensitivity and/or circulating adiponectin, is tested. In 881 normoglycemic individuals the G allele of rs4846914 SNP at the GALNT2 locus, known to associate with GALNT2 downregulation, is associated with low HDL-C and high values of triglycerides, triglycerides/HDL-C ratio, and theHomeostatic Model Assessment of insulin resistance HOMAIR (p-values = 0.01, 0.027, 0.002, and 0.016, respectively). Conversely, no association is observed with serum adiponectin levels (p = 0.091). Importantly, HOMAIR significantly mediates a proportion of the genetic association with HDL-C (21%, 95% CI: 7-35%, p = 0.004) and triglyceride levels (32%, 95% CI: 4-59%, p = 0.023). The results are compatible with the hypothesis that, besides the effect on key lipid metabolism enzymes, GALNT2 alters HDL-C and triglyceride levels also indirectly through a positive effect on insulin sensitivity.

Keywords: GALNT2 genetic variability; adiponectin; dyslipidemia; insulin sensitivity; rs4846914.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin
  • Atherosclerosis* / complications
  • Atherosclerosis* / genetics
  • Cholesterol, HDL / genetics
  • Dyslipidemias* / complications
  • Dyslipidemias* / genetics
  • Humans
  • Insulin Resistance* / genetics
  • Polypeptide N-acetylgalactosaminyltransferase
  • Triglycerides

Substances

  • Adiponectin
  • Cholesterol, HDL
  • Triglycerides