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ABSTRACT: Objective
Ectopic lipid accumulation in the liver and kidneys is a hallmark of metabolic diseases leading to non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). Moreover, recent data have highlighted a strong correlation between NAFLD and CKD incidences. In this study, we use two mouse models of hepatic steatosis or CKD, each initiated independently of the other upon the suppression of glucose production specifically in the liver or kidneys, to elucidate the mechanisms underlying the development of CKD in the context of NAFLD-like pathology.Methods
Mice with a deletion of G6pc, encoding glucose-6 phosphatase catalytic subunit, specifically in the liver (L.G6pc-/- mice) or the kidneys (K.G6pc-/- mice), were fed with either a stan
SUBMITTER: Monteillet L
PROVIDER: S-EPMC6157648 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature