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Role of Receptor-Interacting Protein 140 in human fat cells

Niklas Mejhert1, Jurga Laurencikiene, Amanda T Pettersson

  • 1Department of Medicine, Huddinge, Lipid Laboratory, NVS, Karolinska Institutet, SE- 141 86 Stockholm, Sweden. niklas.mejhert@ki.se.

BMC Endocrine Disorders
|March 9, 2010
PubMed
Abstract

Insights

Human Receptor-interacting protein 140 (RIP140) inhibits glucose uptake and energy expenditure genes. Lower RIP140 in obese individuals suggests it doesn't drive human obesity but may conserve energy in lean subjects.

Area of Science:

  • Metabolism and Endocrinology
  • Adipose Tissue Biology

Background:

  • Receptor-interacting protein 140 (RIP140) deficiency in mice reduces body fat via enhanced adipose tissue metabolism.
  • Human RIP140 expression is lower in visceral white adipose tissue (WAT) of obese individuals compared to lean ones.
  • This study focuses on RIP140's role in human subcutaneous WAT, the body's primary fat depot.

Purpose of the Study:

  • To investigate the role of RIP140 in human subcutaneous white adipose tissue (WAT).
  • To determine RIP140's impact on glucose transport and energy expenditure gene expression in human adipocytes.

Main Methods:

  • Quantified RIP140 mRNA levels in subcutaneous WAT from women across a range of BMIs.
  • Utilized siRNA to knock down RIP140 in in vitro differentiated adipocytes.
  • Assessed the effects of RIP140 knockdown on glucose transport and target gene expression.

Main Results:

  • RIP140 mRNA levels were lower in subcutaneous WAT of obese women and increased with weight loss.
  • RIP140 expression increased during in vitro adipocyte differentiation and was higher in isolated adipocytes.
  • RIP140 knockdown enhanced basal glucose transport and increased mRNA levels of glucose transporter 4 and uncoupling protein-1.

Conclusions:

  • Human RIP140 inhibits glucose uptake and energy expenditure gene expression, similar to its mouse counterpart.
  • Elevated RIP140 in lean subcutaneous WAT may promote energy conservation.
  • RIP140's expression pattern and function do not support its role in regulating human obesity.

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