Resistin increases lipid accumulation and CD36 expression in human macrophages

Xu, Weibin; Yu, Li-Fang; Zhou, Wenzhong; Luo, Min

doi:10.1016/j.bbrc.2006.10.051

Cited by 75 publications

(62 citation statements)

References 35 publications

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“…As described above, macrophages which accumulate in atherosclerotic plaques predominantly secrete resistin 4) . The resistin secreted by macrophages subsequently stimulates production of the pro-inflammatory cytokines TNFalpha and IL-12 in macrophages by an NF-kappaBdependent pathway 15) , the accumulation of lipids in macrophages 16) , and the proliferation and migration of human endothelial cells 5,6) .…”

Section: Discussionmentioning

confidence: 79%

“…Resistin is considered to play an important role in the pathogenesis of insulin resistance and atherosclerosis 2,3) . Recent studies have shown that resistin increases lipid accumulation in human macrophages through its upregulation of CD36 cell surface expression 4) . Macrophages infiltrating atherosclerotic aneurysms secrete in vitro study by Saiki et al showed that pitavastatin enhanced the expression of lipoprotein lipase mouse 3T3-L1 preadipocytes more than did other statins (simvastatin and atorvastatin) 12) .…”

Section: Introductionmentioning

confidence: 99%

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Pitavastatin Improves Serum Resistin Levels in Patients with Hypercholesterolemia

Ohbayashi

2008

JAT

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Aim: Resistin in serum is associated with high risk in patients with atherosclerosis. This clinical study aimed to investigate whether pitavastatin can regulate the serum level of resistin, together with levels of other inflammatory cytokines and adipocytokines. Methods: Forty two outpatients (mean age 65.2 12.6 yr, M/F: 21/21) with hypercholesterolemia were administered 2 mg of pitavastatin and serum levels of resistin, together with serum levels of adiponectin, leptin, TNF-alpha and hsCRP, were measured before, and 12 weeks after enrollment. Results: There was no significant gender-related difference in initial serum resistin levels. Pitavastatin significantly decreased LDL-cholesterol after 12 weeks. Initial levels of resistin showed a significant correlation with those of hsCRP (r 0.38, p 0.013), but not TNF-alpha or HOMA-R. Serum resistin, but not adiponectin and leptin, levels were significantly decreased, dropping from 17.1 9.9 ng/ dL to 15.

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Pitavastatin Improves Serum Resistin Levels in Patients with Hypercholesterolemia

Ohbayashi

2008

JAT

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“…Different impacts of resistinon insulin sensitivity have been previously reported. These include: (1) resistin-induced reduction in IRS-1 and IRS-2 resulting in upregulated expression of gluconeogenic enzymes in the liver (Moon et al, 2003); (2) resistin reduces liver, skeletal muscle and adipose tissue AMPK activity, thereby decreasing insulin sensitivity (Rajala et al, 2003); (3) resistin decreased activity of glycogen synthase in the presence and absence of insulin (Ferrer et al, 2003); and (4) resistin up-regulates CD36 in human macrophages and induces lipid accumulation (Xu et al, 2006). BBR supplementation to diabetic rats significantly down-regulated adipose tissue resistin expression.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

2017

J App Pharma Sci

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The current study was designed to investigate the anti-hyperglycemic and antioxidant effects of berberine (BBR) in high fat diet/streptozotocin (HFD/STZ)-induced type 2 diabetic rats, focusing on the role of adipose tissue peroxisome proliferator activated receptor gamma (PPARγ), resistin and inflammatory cytokines. Type 2 diabetes was induced by feeding rats with HFD for 4 weeks followed by a single intraperitoneal injection of 35 mg/kg body weight STZ. Diabetic rats were supplemented with 50 and 100 mg/kg BBR orally for 4 weeks. HFD/STZ-induced diabetic rats showed a significant increase in serum glucose and fructoseamine, and significant decrease in body weight and serum insulin. Serum pro-inflammatory cytokines were significantly increased in serum of the diabetic rats. BBR significantly ameliorated body weight, and serum glucose, insulin and pro-inflammatory cytokines. In addition, diabetic rats exhibited a significant increase in liver lipid peroxidation and nitric oxide levels, and declined antioxidant defenses, an effect that was reversed following treatment with BBR. Adipose tissue PPARγ mRNA was significantly down-regulated while resistin mRNA was markedly up-regulated in diabetic rats. BBR treatment significantly ameliorated both PPARγ and resistin mRNA expression. In conclusion, BBR attenuates hyperglycemia and its associated oxidative stress and inflammation, possibly through potentiation of the antioxidant defenses and up-regulation of PPARγ expression.

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“…Korah et al reported that resistin levels significantly increased especially in ACS patients with type 2 diabetes mellitus and therefore it may be used as a diagnostic marker for diagnosing ACS (38) . Resistin impairs endothelial functions and causes the uptake of oxidized low density lipoprotein cholesterol and the formation of foam cells after being released by macrophages [39][40][41] . Resistin upregulates the release of adhesion molecules, increases the secretion of proinflammatory factors such as tumour necrosis factor-α, interleukin-6, interleukin-12, nitric oxide, endothelin-1 and matrix metalloproteinases and induces angiogenesis by increasing vascular epithelial growth factor (42)(43)(44)(45)(46)(47) .…”

Section: Discussionmentioning

confidence: 99%

High Serum Resistin Levels in Coronary Artery Ectasia

Sayın¹,

Çetiner²,

Tekin³

et al. 2016

Kosuyolu Heart Journal

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Introduction: The etiological and pathogenic factors responsible for coronary artery ectasia (CAE) are unclear. Therefore, we aimed to compare subjects with and without CAE with respect to resistin levels and determine whether resistin plays a role in the aetiology or pathogenesis of CAE. Patients and Methods:This study enrolled a total of 81 subjects, of whom 42 had CAE [15 female (F), mean age 60.4 ± 9.0 years] and 39 had a normal coronary anatomy (22 F, mean age 56.2 ± 10.7 years). Using coronary artery diameters of the control group as reference, subjects having coronary artery dilatation that was at least 1.5 times larger than the normal adjacent segments were considered to have CAE. Resistin levels were measured from blood samples obtained on the day of the coronary angiography. Sonuç: KAE ve aterosklerozis ortak histopatolojik ve klinik özellikler arz etmektedir. Resistin, aterosklerozun gelişiminde ve klinik tablonun oluşumundaki yeri iyi bilinen bir polipeptid olup, aynı zamanda KAE oluşu-munda da rol alıyor olabilir. Resistinin KAE'nin oluşumunda ki yerinin daha iyi anlaşılabilmesi için büyük ölçekli çalışmalara ihtiyaç duyulmaktadır.

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Resistin increases lipid accumulation and CD36 expression in human macrophages

Cited by 75 publications

References 35 publications

Pitavastatin Improves Serum Resistin Levels in Patients with Hypercholesterolemia

Pitavastatin Improves Serum Resistin Levels in Patients with Hypercholesterolemia

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

High Serum Resistin Levels in Coronary Artery Ectasia

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