Scholarlink

<p>Individuals of African ancestry remain largely underrepresented in genetic and proteomic studies. Here we measure the levels of 2,873 proteins in plasma samples from 163 individuals with type 2 diabetes (T2D) or prediabetes and 362 normoglycemic controls from the Ugandan population. We identify 88 differentially expressed proteins between the two groups. We link genome-wide data to protein expression levels and construct a protein quantitative trait locus (pQTL) map for this population. We identify 399 independent associations with 346 (86.7%) <i>cis</i>-pQTLs and 53 (13.3%) <i>trans</i>-pQTLs; 16.7% of the <i>cis</i>-pQTLs and all of the <i>trans</i>-pQTLs have not been previously reported in individuals of African ancestry. Of these, 37 pQTLs have not been previously reported in any population. We find evidence for colocalization between a pQTL and T2D genetic risk. Our findings reveal proteins causally implicated in the pathogenesis of T2D, which may be leveraged for personalized medicine tailored to individuals of African ancestry.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Linking the plasma proteome to genetics in individuals from continental Africa provides insights into type 2 diabetes pathogenesis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月8日

查看全文
  • Opeyemi Soremekun,
  • Young-Chan Park,
  • Mauro Tutino,
  • Ana Luiza Arruda,
  • Allan Kalungi,
  • N. William Rayner,
  • Moffat Nyirenda,
  • Segun Fatumo,
  • Eleftheria Zeggini

摘要

Individuals of African ancestry remain largely underrepresented in genetic and proteomic studies. Here we measure the levels of 2,873 proteins in plasma samples from 163 individuals with type 2 diabetes (T2D) or prediabetes and 362 normoglycemic controls from the Ugandan population. We identify 88 differentially expressed proteins between the two groups. We link genome-wide data to protein expression levels and construct a protein quantitative trait locus (pQTL) map for this population. We identify 399 independent associations with 346 (86.7%) cis-pQTLs and 53 (13.3%) trans-pQTLs; 16.7% of the cis-pQTLs and all of the trans-pQTLs have not been previously reported in individuals of African ancestry. Of these, 37 pQTLs have not been previously reported in any population. We find evidence for colocalization between a pQTL and T2D genetic risk. Our findings reveal proteins causally implicated in the pathogenesis of T2D, which may be leveraged for personalized medicine tailored to individuals of African ancestry.