What question did this study set out to answer?

To identify the molecular and cellular inflammatory pathways in adipose tissue that contribute to the onset of obesity-induced insulin resistance.

December 15, 2003Journal of Clinical Investigation

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

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Authors

HXHaiyan XuTongji University GBGlenn T. BarnesMillennium Engineering and Integration (United States)QYQing YangDalian Medical University

Discussion

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Implication

Animal study demonstrates macrophage infiltration into adipose tissue drives insulin resistance in obese mice, suggesting metabolic dysfunction originates from fat inflammation.

Key Points

To identify the molecular and cellular inflammatory pathways in adipose tissue that contribute to the onset of obesity-induced insulin resistance.
Analyzed gene expression profiles of inflammatory and macrophage markers in white adipose tissue across genetic and diet-induced obesity mouse models.
Conducted histological evaluations of white adipose tissue and measured molecular changes following treatment with the insulin-sensitizing drug rosiglitazone.
Macrophage-specific inflammatory genes were progressively upregulated in white adipose tissue during diet-induced obesity before any marked rise in circulating insulin.
Treatment with rosiglitazone reversed the upregulation of macrophage-derived inflammatory genes in adipose tissue.
Histological analysis revealed marked infiltration of macrophages—accompanying adipocyte lipolysis and multinucleate giant cell formation—without significant recruitment of neutrophils or lymphocytes.

Cite This Study

Xu et al. (2003) studied this question.

synapsesocial.com/papers/69e082d0a4fa27a5614591dc https://doi.org/10.1172/jci200319451

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December 15, 2003Journal of Clinical Investigation

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

View Full Paper

Ask AI

Bookmark

Authors

HXHaiyan XuTongji University GBGlenn T. BarnesMillennium Engineering and Integration (United States)QYQing YangDalian Medical University

Discussion

Member takes

Implication

Animal study demonstrates macrophage infiltration into adipose tissue drives insulin resistance in obese mice, suggesting metabolic dysfunction originates from fat inflammation.

Key Points

To identify the molecular and cellular inflammatory pathways in adipose tissue that contribute to the onset of obesity-induced insulin resistance.
Analyzed gene expression profiles of inflammatory and macrophage markers in white adipose tissue across genetic and diet-induced obesity mouse models.
Conducted histological evaluations of white adipose tissue and measured molecular changes following treatment with the insulin-sensitizing drug rosiglitazone.
Macrophage-specific inflammatory genes were progressively upregulated in white adipose tissue during diet-induced obesity before any marked rise in circulating insulin.
Treatment with rosiglitazone reversed the upregulation of macrophage-derived inflammatory genes in adipose tissue.
Histological analysis revealed marked infiltration of macrophages—accompanying adipocyte lipolysis and multinucleate giant cell formation—without significant recruitment of neutrophils or lymphocytes.

Cite This Study

Xu et al. (2003) studied this question.

synapsesocial.com/papers/69e082d0a4fa27a5614591dc https://doi.org/10.1172/jci200319451

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