Matriptase-2 deficiency protects from obesity by modulating iron homeostasis.

ABSTRACT: Alterations in iron status have frequently been associated with obesity and other metabolic disorders. The hormone hepcidin stands out as a key regulator in the maintenance of iron homeostasis by controlling the main iron exporter, ferroportin. Here we demonstrate that the deficiency in the hepcidin repressor matriptase-2 (Tmprss6) protects from high-fat diet-induced obesity. Tmprss6 ^-/- mice show a significant decrease in body fat, improved glucose tolerance and insulin sensitivity, and are protected against hepatic steatosis. Moreover, these mice exhibit a significant increase in fat lipolysis, consistent with their dramatic reduction in adiposity. Rescue experiments that block hepcidin up-regulation and restore iron levels in Tmprss6^-/- mice via anti-hemojuvelin (H

SUBMITTER: Folgueras AR 

PROVIDER: S-EPMC5893555 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature