Therapeutic silencing of fat-specific protein 27 improves glycemic control in mouse models of obesity and insulin resistance.

ABSTRACT: Obesity is a component of the metabolic syndrome, mechanistically linked to diabetes, fatty liver disease, and cardiovascular disease. Proteins that regulate the metabolic fate of intracellular lipid droplets are potential therapeutic candidates to treat obesity and its related consequences. CIDEC (cell death-inducing DFFA-like effector C), also known in mice as Fsp27 (fat-specific protein 27), is a lipid droplet-associated protein that prevents lipid mobilization and promotes intracellular lipid storage. The consequences of complete loss of FSP27 on hepatic metabolism and on insulin resistance are controversial, as both healthy and deleterious lipodystrophic phenotypes have been reported in Fsp27^-/- mice. To test whether therapeutic silencing of Fsp27 might be useful to improve

SUBMITTER: Langhi C 

PROVIDER: S-EPMC5234712 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature