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Regulation of cytosolic phosphoenolpyruvate carboxykinase gene expression in adipocytes

Elmus G Beale1, Claude Forest, Robert E Hammer

  • 1Department of Cell Biology and Biochemistry, School of Medicine, Stop 6540, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, USA. elmus.beale@ttuhsc.edu

Biochimie
|January 24, 2004
PubMed

Insights

Researchers identified two DNA elements, gAF1/PCK1 and PCK2, controlling adipocyte glyceroneogenesis. PCK2 acts as an enhancer during adipogenesis, while gAF1/PCK1 mediates tissue-specific glucocorticoid effects on the PEPCK-C gene.

Area of Science:

  • Molecular Biology
  • Metabolic Regulation
  • Gene Transcription

Background:

  • Cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C) is key to adipocyte glyceroneogenesis.
  • Hormones and nutrients regulate PEPCK-C transcription, but the underlying cis-acting elements are not fully understood.

Purpose of the Study:

  • To identify and characterize cis-acting DNA elements controlling adipocyte-specific transcription of the PEPCK-C gene (Pck1).
  • To elucidate the mechanisms regulating adipocyte glyceroneogenesis.

Main Methods:

  • Identification and characterization of cis-acting DNA elements (gAF1/PCK1 and PCK2) upstream of the Pck1 gene.
  • Analysis of their roles in adipocyte-specific gene expression and response to various factors.

Main Results:

  • Two direct repeat hexanucleotide elements (DR1), gAF1/PCK1 and PCK2, were identified.
  • PCK2 functions as an adipocyte-specific enhancer and a peroxisome proliferator-activated receptor gamma (PPARγ) and thiazolidinedione response element, crucial for adipogenesis.
  • gAF1/PCK1 is a pleiotropic element mediating tissue-specific glucocorticoid effects and interacting with multiple transcription factors.

Conclusions:

  • The identified elements, PCK2 and gAF1/PCK1, are critical regulators of PEPCK-C gene transcription in adipocytes.
  • This work provides insights into the complex mechanisms controlling adipocyte glyceroneogenesis and its regulation by hormones and nuclear receptors.

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