Mest/Peg1 imprinted gene enlarges adipocytes and is a marker of adipocyte size

Am J Physiol Endocrinol Metab. 2005 Jan;288(1):E117-24. doi: 10.1152/ajpendo.00244.2004. Epub 2004 Sep 7.


Obesity is a common and serious metabolic disorder in the developed world that is occasionally accompanied by type II diabetes, atherosclerosis, hypertension, and hyperlipidemia. We have found that mesoderm-specific transcript (Mest)/paternally expressed gene 1 (Peg1) gene expression was markedly enhanced in white adipose tissue of mice with diet-induced and genetically caused obesity/diabetes but not with streptozotocin-induced diabetes, which does not cause obesity. Administration of pioglitazone, a drug for type II diabetes and activator of peroxisome proliferator-activated receptor (PPAR)gamma, in obese db/db mice reduced the enhanced expression of Mest mRNA in adipose tissue, concomitant with an increase in body weight and a decrease in the size of adipose cells. Ectopic expression of Mest in 3T3-L1 cells caused increased gene expression of adipose markers such as PPARgamma, CCAAT/enhancer binding protein (C/EBP)alpha, and adipocyte fatty acid binding protein (aP)2. In transgenic mice overexpressing Mest in adipose tissue, enhanced expression of the adipose genes was observed. Moreover, adipocytes were markedly enlarged in the transgenic mice. Thus Mest appears to enlarge adipocytes and could be a novel marker of the size of adipocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / cytology*
  • Adipocytes / physiology*
  • Adipose Tissue / cytology
  • Adipose Tissue / physiology
  • Animals
  • Biomarkers
  • Cell Size
  • Diabetes Mellitus, Experimental / drug therapy
  • Diabetes Mellitus, Experimental / physiopathology
  • Dietary Fats / pharmacology
  • Down-Regulation / drug effects
  • Down-Regulation / physiology
  • Gene Expression / drug effects
  • Gene Expression / physiology
  • Genomic Imprinting
  • Hypoglycemic Agents / pharmacology
  • In Vitro Techniques
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Mice, Transgenic
  • Obesity / physiopathology
  • Pioglitazone
  • Proteins / genetics*
  • Proteins / metabolism*
  • RNA, Messenger / analysis
  • Thiazolidinediones / pharmacology


  • Biomarkers
  • Dietary Fats
  • Hypoglycemic Agents
  • Proteins
  • RNA, Messenger
  • Thiazolidinediones
  • mesoderm specific transcript protein
  • Pioglitazone