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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

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Published on: February 17, 2023

CD14 modulates inflammation-driven insulin resistance.

José Manuel Fernández-Real1, Sofia Pérez del Pulgar, Elodie Luche

  • 1Section of Diabetes, Endocrinology and Nutrition, University Hospital of Girona, Biomedical Research Institute Dr Josep Trueta and CIBERobn Fisiopatología de la Obesidad y Nutrición, Girona, Spain. jmfernandezreal.girona.ics@gencat.cat

Diabetes
|June 25, 2011
PubMed
Summary
This summary is machine-generated.

The macrophage molecule CD14 influences insulin resistance by modulating adipose tissue inflammation. CD14 knockout mice showed resistance to insulin resistance, highlighting its role in metabolic health.

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Area of Science:

  • Metabolic disease research
  • Immunology
  • Molecular biology

Background:

  • Insulin resistance is a key factor in type 2 diabetes and metabolic syndrome.
  • Macrophages play a role in adipose tissue inflammation, contributing to insulin resistance.
  • The specific role of the macrophage molecule CD14 in insulin resistance requires further elucidation.

Purpose of the Study:

  • To investigate the role of the macrophage molecule CD14 in the development of insulin resistance.
  • To assess the impact of CD14 on insulin sensitivity and adipose tissue gene expression.
  • To explore the therapeutic potential of targeting CD14 in metabolic disorders.

Main Methods:

  • Evaluation of recombinant human soluble CD14 (rh-sCD14) effects on insulin sensitivity using clamp procedures in various mouse models (WT, high fat-fed, ob/ob, CD14 KO).
  • Analysis of adipose tissue gene expression changes in response to rh-sCD14.
  • Bone marrow transplantation studies using WT and CD14 KO mice to assess the contribution of bone marrow-derived cells to insulin resistance.
  • Examination of CD14 expression in human adipose tissue and differentiating preadipocytes.

Main Results:

  • rh-sCD14 administration improved insulin action in WT, high-fat-fed, and ob/ob mice, but not in CD14 KO mice.
  • Significant alterations in adipose tissue gene expression, particularly in lipid metabolism pathways, were observed.
  • Mice receiving bone marrow from CD14 KO donors exhibited resistance to high-fat diet-induced insulin resistance.
  • CD14 gene expression was elevated in adipose tissue of obese humans and further induced by tumor necrosis factor-α.

Conclusions:

  • CD14 plays a significant role in modulating adipose tissue inflammatory activity.
  • CD14 is a key regulator of insulin resistance.
  • Targeting CD14 may offer a novel therapeutic strategy for managing insulin resistance and related metabolic conditions.