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CXCL14 and insulin action

Takahiko Hara1, Yuki Nakayama

  • 1The Tokyo Metropolitan Institute of Medical Science, Tokyo Metropolitan Organization for Medical Research, Bunkyo-ku, Tokyo 113-8613, Japan.

Vitamins and Hormones
|March 3, 2009
PubMed

Insights

Chemokine CXCL14 (C-X-C motif chemokine ligand 14) deficiency protects female mice from obesity and insulin resistance by reducing inflammation in white adipose tissue. CXCL14 regulates glucose metabolism and insulin signaling.

Area of Science:

  • Immunology
  • Metabolic research
  • Endocrinology

Background:

  • The physiological roles of CXCL14 (C-X-C motif chemokine ligand 14) are largely unknown.
  • CXCL14 exhibits chemoattractant activity for monocytes and dendritic precursor cells, suggesting a potential tumor suppressive function.
  • Previous studies indicated CXCL14 is dispensable for immune cell development in mice.

Purpose of the Study:

  • To investigate the physiological roles of CXCL14 in vivo, particularly concerning metabolism and inflammation.
  • To elucidate the function of CXCL14 in obesity-induced insulin resistance.

Main Methods:

  • Analysis of CXCL14-deficient (CXCL14(-/-)) mice fed a high-fat diet (HFD).
  • Assessment of metabolic parameters including body weight, glucose levels, insulin sensitivity, and adipose tissue macrophage infiltration.
  • Investigation of CXCL14's effect on glucose uptake in cultured myocytes and insulin signaling pathways.

Main Results:

  • CXCL14(-/-) female mice are protected from obesity and associated metabolic dysfunction (hyperglycemia, hyperinsulinemia, insulin resistance) compared to wild-type mice.
  • CXCL14 expression is elevated in white adipose tissue (WAT) of obese mice.
  • CXCL14 promotes macrophage recruitment into WAT, contributing to chronic inflammation and insulin resistance; it also attenuates insulin-stimulated glucose uptake in myocytes.

Conclusions:

  • CXCL14 is a novel regulator of glucose metabolism and insulin resistance.
  • CXCL14 mediates its effects by influencing macrophage infiltration into WAT and interacting with insulin signaling in skeletal muscle.
  • Targeting CXCL14 may offer a therapeutic strategy for metabolic disorders like insulin resistance.

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