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Published on: May 22, 2013
CD36/ANXA1/TLR4/NF-κB axis orchestrates lipid metabolism, chronic inflammation, and insulin resistance in obese
Yiqing Yao1, Weiming Yang1, Feng Cheng1
1Department of Pediatrics, First Hospital of Jiaxing, No. 1882, Zhonghuan South Road, Chengnan Street, Nanhu District, Jiaxing, Zhejiang 314000, China.
Insights
Childhood obesity involves inflammation and insulin resistance (IR). Targeting the CD36/ANXA1/TLR4/NF-κB pathway in adipocytes may improve lipid metabolism and reduce IR in obese children.
Area of Science:
- Metabolic Research
- Molecular Biology
- Pediatric Endocrinology
Background:
- Childhood obesity is linked to dyslipidemia, inflammation, and insulin resistance (IR).
- The role of CD36 in pediatric metabolic disease requires further elucidation.
- This study investigates the CD36/ANXA1/TLR4/NF-κB axis as a therapeutic target.
Purpose of the Study:
- To investigate the CD36/ANXA1/TLR4/NF-κB axis in childhood obesity.
- To understand the role of CD36 in adipogenesis, insulin signaling, and inflammation.
- To explore therapeutic potential for lipid metabolism and IR.
Main Methods:
- Case-control study of 50 obese and 50 healthy children.
- In vitro analysis using primary adipocytes with CD36 knockdown/overexpression.
- Assays for adipogenesis, insulin signaling, and inflammatory pathways.
Main Results:
- Obese children had elevated BMI, glucose/insulin, TAG, TC, and soluble CD36 (sCD36).
- CD36 overexpression enhanced adipogenesis and inflammation; knockdown suppressed these.
- CD36 silencing improved insulin signaling via PI3K/AKT and reduced inflammation by interacting with ANXA1/TLR4/NF-κB.
Conclusions:
- The CD36/ANXA1/TLR4/NF-κB axis is implicated in childhood obesity's inflammation and lipid dysregulation.
- Targeting this axis may offer a therapeutic strategy to improve insulin resistance and adipogenesis.
Background:
Childhood obesity is tightly linked to dyslipidemia, chronic low-grade inflammation, and insulin resistance (IR). CD36 has been implicated in metabolic disease, yet its pediatric mechanisms remain unclear. This study aims to investigate the CD36/ANXA1/TLR4/NF-κB axis as a potential therapeutic target for lipid metabolism and IR in childhood obesity.
Methods:
A case-control study was conducted involving 50 obese and 50 healthy control children. Clinical data and blood samples were collected to assess metabolic profiles. Primary adipocytes isolated from subcutaneous adipose tissue were used for in vitro experiments. We established CD36 knockdown and overexpression models and performed a range of molecular and cellular assays. These experiments were designed to analyze the effects of CD36 on adipogenesis, insulin signaling, and inflammatory pathways, both with and without the addition of insulin, LPS, or a TLR4-blocking antibody.
Results:
Compared with controls, children with obesity showed higher BMI, fasting glucose/insulin, TAG, and TC. Circulating levels of soluble CD36 (sCD36) were markedly elevated in plasma, and CD36 expression was increased in adipocytes from obese children, accompanied by enhanced pro-inflammatory cytokine production and reduced GLUT4/IRS1 expression. In primary adipocytes, CD36 overexpression enhanced PPARγ and adipogenesis, whereas CD36 knockdown suppressed lipid accumulation. Mechanistically, CD36 silencing increased AKT phosphorylation and restored GLUT4/IRS1, indicating relief of IR via PI3K/AKT activation. Notably, CD36 physically interacted with ANXA1 and potentiated TLR4/NF-κB signaling. Functionally, LPS reversed anti-inflammatory and anti-adipogenic effects of CD36 knockdown, whereas TLR4 blockade countered CD36-driven cytokine production and adipogenesis.
Conclusions:
This study shows the CD36/ANXA1/TLR4/NF-κB axis as a signaling pathway associated with inflammation and lipid metabolism dysregulation in childhood obesity and provides mechanistic evidence that targeting this axis may ameliorate insulin resistance and adipogenesis.
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