Adipokines in inflammation, insulin resistance and cardiovascular disease

Li, Zhi-Yong; Wang, Pei; Miao, Chao‐Yu

doi:10.1111/j.1440-1681.2011.05602.x

Cited by 64 publications

(61 citation statements)

References 91 publications

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“…From previous studies, it is well established that when there is an expansion of adipose tissue, there is a sustained inflammatory response accompanied by adipokine dysregulation, which leads to chronic subclinical inflammation as well as insulin resistance [15]. But the impact of insulin resistance on the effects of adipokines are unclear.…”

Section: Discussionmentioning

confidence: 99%

CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes

Jiang

Yang

et al. 2014

Endocr J

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Section: Discussionmentioning

confidence: 99%

CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes

Jiang

Yang

et al. 2014

Endocr J

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“…LDH release was determined by a lactate dehydrogenase (LDH) release assay using Promega CytoTox-ONE™ kit (Promega) [17]. In brief, 10 4 cells were seeded in 96-well plates.…”

Section: Methodsmentioning

confidence: 99%

Activation of a7 Nicotinic Acetylcholine Receptor Protects Against Oxidant Stress Damage Through Reducing Vascular Peroxidase-1 in a JNK Signaling-Dependent Manner in Endothelial Cells

Zhao

Xin

et al. 2014

Cell Physiol Biochem

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Aim: Alpha7 nicotinic acetylcholine receptor (α7nAChR), a subtype of nAChR regulating neurotransmission in central nervous system, is an essential regulator of cholinergic anti-inflammatory pathway in periphery. The present study was to determine the effects of activation of α7nAChR on oxidant stress-induced injury in endothelial cells. Methods: Cultured human umbilical vein endothelial cells were treated with H₂O₂ (400 µM) or H₂O₂ plus PNU-282987 (10 µM). Cell viability and membrane integrity were measured. Annexin V + PI assay, immunoblotting of bcl-2, bax and cleaved capase-3, and immunofluorescence of apoptosis inducing factor (AIF) were performed to evaluate apoptosis. Protein expression of vascular peroxidase-1 (VPO-1) and phosphor-JNK were measured by immunoblotting. Results: Activation of α7nAChR by a selective agonist PNU-282987 prevented H₂O₂-indced decrease of cell viability and increase of lactate dehydrogenase release. Activation of α7nAChR markedly reduced cell apoptosis and intracellular oxidative stress level. Moreover, activation of α7nAChR reduced H₂O₂-induced VPO-1 protein upregulation and JNK1/2 phosphorylation. The inhibitory effect of α7nAChR activation on VPO-1 was blocked by JNK inhibitor SP600125. In addition, pretreatment of α7nAChR antagonist methyllycaconitine blocked the cytoprotective effect of PNU-282987. Conclusion: These results provide the first evidence that activation of α7nAChR protects against oxidant stress-induced damage by suppressing VPO-1 in a JNK signaling pathway-dependent manner in endothelial cells.

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“…Furthermore, several studies demonstrated the important role of adiponectin in the regulation of others physiological processes, including lipid metabolism, endothelial function, inflammatory response and cytokine signalling 28 . Dyslipidemia is known as a major risk factor of insulin resistance and MS.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2017

IJPSR

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Adiponectin has been schown to protect from insulin resistance, demonstrate anti-inflammatory and anti-atherosclerotic effects and be involved in the pathogenesis of metabolic syndrome (MS). We aimed to assess the association between serum adiponectin concentration, insulin resistance and various risk factors of MS and to investigate the relationship between the single nucleotide polymorphism (SNP) +45 T>G ( rs 2241766) in the adiponectin (ADIPOQ) gene and the risk of MS. 200 patients with MS and 250 healthy controls were enrolled in this study. The level of fasting serum insulin, glucose, and lipid levels were measured. Insulin resistance was estimated using homeostasis model of assessment for insulin resistance (HOMA-IR). Serum adiponectin levels were measured by enzyme-linked immunosorbent assay and the SNP +45 T>G in the ADIPOQ gene was performed by the polymerase chain reaction-restriction fragment length polymorphism method. MS patients had a significantly higher levels of HOMA-IR (p<0.001) and lower serum adiponectin concentrations (p<0.001) compared to controls. Multiple regression analysis showed that serum adiponectin levels was associated negatively with HOMA-IR (r=-0.307; p=0.001) and positively with high-density lipoprotein cholesterol (HDL-C) (r=0.369; p=0.000) in MS patients. In addition, there was no significant association between genotypes of rs 2241766 and the risk of MS. In conclusion, adiponectin is known to play key regulator of insulin sensitivity, endothelial function and lipid metabolism. Our findings confirm the associations of hypoadiponectinemia with MS and gave evidence that the SNP+45 T>G polymorphism in the gene of ADIPOQ is not associated with MS.

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Adipokines in inflammation, insulin resistance and cardiovascular disease

Cited by 64 publications

References 91 publications

CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes

CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes

Activation of a7 Nicotinic Acetylcholine Receptor Protects Against Oxidant Stress Damage Through Reducing Vascular Peroxidase-1 in a JNK Signaling-Dependent Manner in Endothelial Cells

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