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Mice lacking global Stap1 expression do not manifest hypercholesterolemia.

Babunageswararao Kanuri1, Vincent Fong1, April Haller2

  • 1Division of Endocrinology, Diabetes and Metabolism, University of Cincinnati, Cincinnati, OH, USA.

BMC Medical Genetics
|November 24, 2020
PubMed
Summary
This summary is machine-generated.

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Mice lacking signal transducing adaptor family member protein 1 (STAP1) expression did not develop hypercholesterolemia, even on a western diet. These findings suggest STAP1 is not causative for autosomal dominant familial hypercholesterolemia.

Area of Science:

  • Genetics and Molecular Biology
  • Metabolic Disorders
  • Cardiovascular Research

Background:

  • Autosomal dominant familial hypercholesterolemia (ADH) is a common monogenic disorder causing high LDL cholesterol.
  • Previous studies suggested a link between ADH and variants in the signal transducing adaptor family member protein 1 (STAP1) gene, but findings were contradictory.

Purpose of the Study:

  • To investigate the role of STAP1 in lipid metabolism and hypercholesterolemia.
  • To determine if STAP1 deficiency exacerbates metabolic dysfunction, particularly under a high-fat diet.

Main Methods:

  • Generated global Stap1 knockout mice (Stap1-/-).
  • Assessed metabolic parameters including growth, body fat, circulatory lipids, and glucose homeostasis in Stap1-/- mice fed standard chow and a western diet (WD) for 16 weeks.
Keywords:
Autosomal dominant familial hypercholesterolemiaB-cellsFamilial hypercholesterolemia 4Fast performance liquid chromatographySTAP1Western diet

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  • Analyzed liver architecture and cholesterol content in lipoprotein fractions.

    • Main Results:

    • Stap1-/- mice showed no significant differences in metabolic parameters compared to wild-type (Stap1+/+) mice, even after a 16-week WD.
    • Hepatic architecture and cholesterol levels in isolated lipoprotein fractions remained comparable between knockout and wild-type mice.
    • No exacerbation of lipid disorders or metabolic dysfunction was observed in Stap1-deficient mice.

    Conclusions:

    • STAP1 does not appear to significantly alter lipid levels or contribute to hyperlipidemia.
    • A western diet does not exacerbate lipid disorders in the absence of STAP1.
    • The findings question the role of STAP1 in the pathogenesis of human hypercholesterolemia, aligning with other studies.