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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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The adipocyte IKK/NFkappaB pathway: a therapeutic target for insulin resistance

Hong Ruan1, Henry J Pownall

  • 1University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Department of Physiology and Biophysics, 683 Hoes Lane West, Piscataway, NJ 08854, USA. ruanho@umdnj.edu

Current Opinion in Investigational Drugs (London, England : 2000)
|April 2, 2009
PubMed

Insights

Insulin resistance, a key factor in type 2 diabetes (T2D), is linked to obesity. The inhibitor of kappaB kinase (IKK)/NFkappaB pathway in adipose tissue plays a role in this insulin resistance, offering a potential therapeutic target.

Area of Science:

  • Metabolic diseases
  • Endocrinology
  • Molecular biology

Background:

  • Insulin resistance is a fundamental defect in type 2 diabetes (T2D), particularly when associated with obesity.
  • Adipose tissue, beyond energy storage, secretes factors influencing energy metabolism and insulin sensitivity.
  • Obese adipose tissue exhibits altered secretory profiles, impacting adipocyte function and systemic insulin sensitivity.

Purpose of the Study:

  • To review recent data on pathways contributing to insulin resistance in obesity.
  • To evaluate the role of the inhibitor of kappaB kinase (IKK)/NFkappaB pathway in insulin sensitivity.
  • To assess the therapeutic potential of targeting the IKK/NFkappaB pathway in T2D.

Main Methods:

  • Review of in vitro and in vivo studies.
  • Analysis of signaling pathways and transcriptional regulators.
  • Examination of cross-talk between adipose and non-adipose tissues.

Main Results:

  • The IKK/NFkappaB pathway is implicated in regulating insulin sensitivity.
  • This pathway is involved in both fatty acid and inflammatory cytokine signaling cascades.
  • Obesity-associated insulin resistance involves complex signaling in adipose tissue.

Conclusions:

  • The IKK/NFkappaB pathway is a significant factor in obesity-linked insulin resistance.
  • Targeting the IKK/NFkappaB pathway presents a potential therapeutic strategy for T2D.
  • Understanding adipose-derived factors and their signaling is crucial for T2D research.

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