Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency.

Journal Article (Journal Article)

Obesity typically is linked to caloric imbalance as a result of overnutrition. Here we propose a cell-autonomous mechanism for adiposity as a result of persistent cell surface glucose transporter type 4 (GLUT4) in adipocytes resulting from impaired function of ankyrin-B (AnkB) in coupling GLUT4 to clathrin-mediated endocytosis. Adipose tissue-specific AnkB-KO mice develop obesity and progressive pancreatic islet dysfunction with age or high-fat diet (HFD). AnkB-deficient adipocytes exhibit increased lipid accumulation associated with increased glucose uptake and impaired endocytosis of GLUT4. AnkB binds directly to GLUT4 and clathrin and promotes their association in adipocytes. AnkB variants that fail to restore normal lipid accumulation and GLUT4 localization in adipocytes are present in 1.3% of European Americans and 8.4% of African Americans, and are candidates to contribute to obesity susceptibility in humans.

Full Text

Duke Authors

Cited Authors

  • Lorenzo, DN; Bennett, V

Published Date

  • November 28, 2017

Published In

Volume / Issue

  • 114 / 48

Start / End Page

  • 12743 - 12748

PubMed ID

  • 29133412

Pubmed Central ID

  • PMC5715754

Electronic International Standard Serial Number (EISSN)

  • 1091-6490

Digital Object Identifier (DOI)

  • 10.1073/pnas.1708865114


  • eng

Conference Location

  • United States