Variants in STAT5B associate with serum TC and LDL-C levels

J Clin Endocrinol Metab. 2011 Sep;96(9):E1496-501. doi: 10.1210/jc.2011-0322. Epub 2011 Jul 13.

Abstract

Context: Known genetic variants influencing serum lipid levels do not adequately account for the observed population variability of these phenotypes. The GH/signal transducers and activators of transcription (STAT) signaling pathway is an evolutionary conserved system that exerts strong effects on metabolism, including that of lipids.

Research design and methods: We analyzed the association of 11 single-nucleotide polymorphisms (SNP) spanning the STAT5B/STAT5A/STAT3 locus with serum lipid levels in six European populations (n = 5162 nondiabetic individuals).

Results: After adjustment for age, sex, alcohol use, smoking, and body mass index, we identified STAT5B variants (rs8082391 and rs8064638) in novel association with total cholesterol (TC; P = 0.001 and P = 0.002) and low-density lipoprotein cholesterol (P = 0.002 and P = 0.004) levels. The minor alleles of these single-nucleotide polymorphisms were significantly enriched in hyperlipidemic individuals across the six discovery populations (P = 0.004 and P = 0.006). In transgenic mice deficient for hepatic STAT5A and STAT5B, reduced serum TC levels coincided with reduced hepatic cholesterol biosynthesis as demonstrated using gene expression profiling and pathway enrichment analysis.

Conclusions: Genetic variants in STAT5B are associated with TC and low-density lipoprotein cholesterol levels among six populations. Mechanistically, STAT5B transcriptionally regulates hepatic cholesterol homeostasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cholesterol / blood
  • Cholesterol / genetics*
  • Cholesterol, LDL / blood
  • Cholesterol, LDL / genetics*
  • Female
  • Genetic Association Studies
  • Genetic Variation
  • Genotype
  • Humans
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Transgenic
  • Polymorphism, Single Nucleotide
  • STAT5 Transcription Factor / genetics*
  • STAT5 Transcription Factor / metabolism
  • White People / genetics

Substances

  • Cholesterol, LDL
  • STAT5 Transcription Factor
  • Cholesterol