Adipocytes recognize and degrade oxidized low density lipoprotein through CD36

Kuniyasu, Akihiko; Hayashi, Shigeki; Nakayama, Hitoshi

doi:10.1016/s0006-291x(02)00666-6

Cited by 60 publications

(50 citation statements)

References 34 publications

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“…Plasma levels of SPARC also correlate with coronary artery disease [52], and its expression was highly increased after myocardial infarction [34]. A correlation with cardiovascular disease also exists for Annexin A5, a structural cytosolic plasma membrane protein, which is an indirect inhibitor of thromboplastin specific complex [22] and for CD36, a fatty acid translocase with a role in fatty acid transport [37] which also functions as a thrombospondin receptor [3].…”

Section: Discussionmentioning

confidence: 98%

Intra- and interindividual variation in gene expression in human adipose tissue

Beek¹,

Bakker

Kruyt

et al. 2006

Pflugers Arch - Eur J Physiol

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show abstract

Section: Discussionmentioning

confidence: 98%

Intra- and interindividual variation in gene expression in human adipose tissue

Beek¹,

Bakker

Kruyt

et al. 2006

Pflugers Arch - Eur J Physiol

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“…[54][55][56] This receptor interacts with fatty acids as well as oxidized lipids to drive their endocytosis and their degradation by lysosomes during differentiation in 3T3L1 adipocytes. 57 Therefore we have focused our attention on this fatty acid receptor and study its function in adipogenesis both in mouse 3T3L1 cell line and in human adipose stem cells by comparison to insulin and oleic acid, a long-fatty acid chain.…”

Section: Discussionmentioning

confidence: 99%

“…59 It is strictly located in adipocyte lipid rafts and is translocated to the membrane by insulin, 60 where it mediates long fatty acid chain uptake, including oleic acid 61 and 65% of oxidized lipids uptake and degradation. 57 Activation of FAT/CD36 stimulates the proinflammatory response of adipocytes, possibly through activation of mitochondrial fatty-acid oxidation which increases during differentiation, 62,63 induction of endoplasmic stress 53 and in turn activates JNK to impair insulin signaling in adipocytes. 64 In our experiments, we found that inhibition of both FAT/CD36 and JNK improved cell survival.…”

Section: Discussionmentioning

confidence: 99%

Pathways commonly dysregulated in mouse and human obese adipose tissue: FAT/CD36 modulates differentiation and lipogenesis

et al. 2015

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Obesity is linked to adipose tissue hypertrophy (increased adipocyte cell size) and hyperplasia (increased cell number). Comparative analyses of gene datasets allowed us to identify 1426 genes which may represent common adipose phenotype in humans and mice. Among them we identified several adipocyte-specific genes dysregulated in obese adipose tissue, involved in either fatty acid storage (acyl CoA synthase ACSL1, hormone-sensitive lipase LIPE, aquaporin 7 AQP7, perilipin PLIN) or cell adhesion (fibronectin FN1, collagens COL1A1, COL1A3, metalloprotein MMP9, or both (scavenger receptor FAT/CD36). Using real-time analysis of cell surface occupancy on xCELLigence system we developed a new method to study lipid uptake and differentiation of mouse 3T3L1 fibroblasts and human adipose stem cells. Both processes are regulated by insulin and fatty acids such as oleic acid. We showed that fatty acid addition to culture media increased the differentiation rate and was required for full differentiation into unilocular adipocytes. Significant activation of lipogenesis, i.e. lipid accumulation, by either insulin or oleic acid was monitored in times ranging from 1 to 24 h, depending on differentiation state, whereas significant effects on adipogenesis, i.e., surperimposed lipid accumulation and gene transcriptional regulations were measured after 3 to 4 d. Combination of selected times for analysis of lipid contents, cell counts, size fractionations, and gene transcriptional regulations showed that FAT/CD36 specific inhibitor AP5258 significantly increased cell survival of oleic acid-treated mouse and human adipocytes, and partially restored the transcriptional response to oleic acid in the presence of insulin through JNK pathway. Taken together, these data open new perspectives to study the molecular mechanisms commonly dysregulated in mouse and human obesity at the level of lipogenesis linked to hypertrophy and adipogenesis linked to hyperplasia

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“…Furthermore, CD36 has been previously demonstrated to internalize oxLDL in adipocytes, suggesting that they can function as phagocytes, like macrophages, and that might participate in the clearance of circulating oxLDL [10].…”

Section: Discussionmentioning

confidence: 99%

Oxidised LDL up‐regulate CD36 expression by the Nrf2 pathway in 3T3‐L1 preadipocytes

et al. 2008

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The effect of oxLDL on CD36 expression has been assessed in preadipocytes induced to differentiate. Novel evidence is provided that oxLDL induce a peroxisome proliferator-activated receptor c-independent CD36 overexpression, by up-regulating nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2). The nuclear translocation of Nrf2 appeared to depend on PKC pathway activation. In adipocytes, the CD36 up-regulation may indicate a compensation mechanism to meet the demand of excess oxLDL and oxidised lipids in blood, reducing the risk of atherogenesis. Besides strengthening the hypothesis that oxLDL can contribute to the onset of insulin-resistance, data herein presented highlight the significance of oxLDL-induced CD36 overexpression within the cellular defence response.

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Adipocytes recognize and degrade oxidized low density lipoprotein through CD36

Cited by 60 publications

References 34 publications

Intra- and interindividual variation in gene expression in human adipose tissue

Intra- and interindividual variation in gene expression in human adipose tissue

Pathways commonly dysregulated in mouse and human obese adipose tissue: FAT/CD36 modulates differentiation and lipogenesis

Oxidised LDL up‐regulate CD36 expression by the Nrf2 pathway in 3T3‐L1 preadipocytes

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