Gene expression profile in the fat tissue of Fsp27 deficient mice

نویسندگان

  • Li Xu
  • Xiayu Xia
  • Muhammad Arshad
  • Linkang Zhou
چکیده

Fsp27 is a lipid droplet-associated protein almost exclusively expressed in adipocytes where it facilitates unilocular lipid droplet formation. In mice, Fsp27 deficiency is associated with increased basal lipolysis, browning of white fat and a healthy metabolic profile, whereas energetically challenged Fsp27 deficient mice (ob/ob/Fsp27 (-/-)) show dramatically reduced fat mass, hepatic steatosis and insulin resistance which represents a typical lipodystrophy phenotype. Here, we investigate the effect of Fsp27 depletion on the gene expression of gonadal white adipose tissue (GWAT) under normal or energetically challenged condition (Fsp27 (-/-) vs Wild type; ob/ob/Fsp27 (-/-) vs ob/ob). We systematically analyzed the change in signaling pathway in Fsp27 deficient mice. The raw data have been deposited into Gene Expression Omnibus (GEO): GSE59807 and GSE22693.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Expression of hepatic fat-specific protein 27 depends on the specific etiology of fatty liver.

Fat-specific protein 27 gene (FSP27), isolated by screening for genes specifically expressed in fully differentiated mouse adipocytes, belongs to the cell death-inducing DNA fragmentation factor, alpha subunit-like effector family. FSP27 is induced in not only adipose tissue but also the liver of ob/ob mice, and it promotes the development of fatty liver. The FSP27 gene is expressed in a fatty ...

متن کامل

Up-Regulation of Mitochondrial Activity and Acquirement of Brown Adipose Tissue-Like Property in the White Adipose Tissue of Fsp27 Deficient Mice

Fsp27, a member of the Cide family proteins, was shown to localize to lipid droplet and promote lipid storage in adipocytes. We aimed to understand the biological role of Fsp27 in regulating adipose tissue differentiation, insulin sensitivity and energy balance. Fsp27(-/-) mice and Fsp27/lep double deficient mice were generated and we examined the adiposity, whole body metabolism, BAT and WAT m...

متن کامل

Effects of Endurance Training on the Expression of Cathepsin B (CTSB) and Cathepsin L (CTSL) genes in the Adipose Tissue of Mice with a High-Fat Diet

Introduction: In high-fat diet-induced obesity, the levels of cathepsin L (CTSL) and cathepsin B (CTSB) increase in adipocytes, resulting in insulin resistance in the adipose tissue. In this study, the preventive effect of endurance training on the gene expression of CTSL and CTSB was investigated in the adipose tissue of mice with a high-fat diet. Materials and Methods: Twenty-one male mice (a...

متن کامل

Insulin resistance and white adipose tissue inflammation are uncoupled in energetically challenged Fsp27-deficient mice

Fsp27 is a lipid droplet-associated protein almost exclusively expressed in adipocytes where it facilitates unilocular lipid droplet formation. In mice, Fsp27 deficiency is associated with increased basal lipolysis, 'browning' of white fat and a healthy metabolic profile, whereas a patient with congenital CIDEC deficiency manifested an adverse lipodystrophic phenotype. Here we reconcile these d...

متن کامل

Assessment of fat-specific protein 27 in the adipocyte lineage suggests a dual role for FSP27 in adipocyte metabolism and cell death.

Fat-specific protein 27 (FSP27)/CIDEC was initially identified by its upregulation in TA1 adipogenesis and is one of three cell death-inducing DFF45-like effector (CIDE) family proapoptotic proteins. Ectopic expression of CIDEs promotes apoptosis of mammalian cells. On the other hand, FSP27 has very recently been illustrated to regulate lipid droplet size and promote lipid storage in adipocytes...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2015