title: Prolactin regulatory element-binding protein is involved in suppression of the adiponectin gene in vivo.
abstract: OBJECTIVE
  Prolactin regulatory element-binding protein (PREB), a member of the WD-repeat protein family, has been recognized as a transcriptional factor that regulates prolactin promoter activity in the anterior pituitary of rats. PREB is expressed not only in the pituitary but also in various other tissues, including the adipose tissue. Previous studies have shown that PREB acts as a transcriptional regulator and suppresses the expression of the adiponectin gene in cultured 3T3L1 preadipocytes. The aim of this study was to further examine the potential role of PREB in adipose tissue in vivo.
  
  
  METHODS
  Transgenic mice that overexpressing PREB (PREB transgenic mice) were generated. Insulin resistance was evaluated in PREB transgenic mice using glucose and insulin tolerance tests. Adiponectin expression in the adipose tissue was examined by western blot analysis and quantitative polymerase chain reaction (qPCR). The expression levels of stearoyl-CoA desaturase (Scd) and adiponectin receptor 2(ADIPOR2) were quantified by qPCR.
  
  
  RESULTS
  Glucose and insulin tolerance tests revealed insulin resistance in PREB transgenic mice. Serum adiponectin and leptin concentrations were decreased. Adiponectin gene expression was decreased in the adipose tissue, which was confirmed by the downregulation of the adiponectin-dependent hepatic Scd gene and upregulation of the ADIPOR2 gene in the liver of PREB transgenic mice. We also found that pioglitazone, an agonist for the peroxisome proliferator-activated receptor-r, improved the insulin resistance in the PREB transgenic mice after a 10-day feeding period.
  
  
  CONCLUSIONS
  These results demonstrated that PREB might contribute to the regulation of adiponectin gene expression in vivo.
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan. xiaozhou@med.kagawa-u.ac.jp.
authors.forename: X Z
authors.initials: XZ
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Imachi
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: J Y
authors.initials: JY
authors.lastname: Lyu
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Fukunaga
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ibata
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshimoto
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Kikuchi
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Dong
authors.affiliation: Department of Endocrinology and Metabolism, Faculty of Medicine, Kagawa University, 1750-1, ikenobe, Miki-CHO, 761-0793, Kagawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Murao
mesh_terms: D052242:Adiponectin / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D000818:Animals; D004268:DNA-Binding Proteins / Q000502:physiology*; D005786:Gene Expression Regulation; D020662:Guanine Nucleotide Exchange Factors / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D014157:Transcription Factors / Q000502:physiology*
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; D004268:DNA-Binding Proteins; D020662:Guanine Nucleotide Exchange Factors; D020738:Leptin; C485591:Preb protein, mouse; D014157:Transcription Factors
keywords: Adiponectin; Adipose tissue; Diabetes; Insulin resistance; PREB