Effects of Statins on Adipose Tissue Inflammation

Abe, Manabu; Matsuda, Morihiro; Kobayashi, Hironori; Miyata, Yugo; Nakayama, Yuki; Komuro, Ryutaro; Fukuhara, Atsunori; Shimomura, Iichiro

doi:10.1161/atvbaha.107.160663

Cited by 95 publications

(43 citation statements)

References 41 publications

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“…Adiponectin promotes HDL production via ApoA-I production and increased ABCA1 expression in the liver 77,78) , and also in macrophages to activate RCT 79) . Pitavastatin and pravastatin elevate adiponectin expression in adipocytes 80) . Clinically, the adiponectin-elevating effects differ among statins [81][82][83][84] , and pitavastatin reportedly increases adiponectin levels in hyperlipidemic patients with diabetes mellitus.…”

Section: Other Factors Involved In Rct 1) Adiponectinmentioning

confidence: 99%

Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Yamashita

Tsubakio-Yamamoto

Ohama

et al. 2010

JAT

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Section: Other Factors Involved In Rct 1) Adiponectinmentioning

confidence: 99%

Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Yamashita

Tsubakio-Yamamoto

Ohama

et al. 2010

JAT

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“…0 primer-GACTGTACAAATCACGTTGGGA), and GAPDH (5 0 primer-TTGTCTCCTGCGACTTCA, 3 0 primer-CACCACC-CTGTTGCTGTA) were employed (28)(29)(30)(31). To assess the specificity of each primer set, amplicons generated from the PCR reaction were analyzed for melting curves and also by electrophoresis in 2% agarose gels.…”

Section: Real-time Pcr Analysismentioning

confidence: 99%

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Teraoka

Mutoh

Takasu

et al. 2011

Cancer Prevention Research

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It has been suggested that hyperlipidemia is positively associated with colon carcinogenesis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors, reduce serum lipid levels. In this study, we clarified the effects of a novel chemically synthesized statin, pitavastatin, on intestinal polyp formation in Min mice, and further examined serum lipid and adipocytokine levels, and proinflammatory and adipocytokine gene levels in intestinal mucosa of Min mice. Treatment with pitavastatin at doses of 20 and 40 ppm decreased the total number of polyps dose-dependently to 85.2% and 65.8% (P < 0.05) of the untreated value, respectively. Serum levels of total cholesterol and triglyceride were slightly reduced and those of IL-6, leptin, and MCP-1 were decreased by 40-ppm pitavastatin treatment. mRNA expression levels of cyclooxygenase-2, IL-6, inducible nitric oxide (iNOS), MCP-1, and Pai-1 were significantly reduced in intestinal nonpolyp parts by pitavastatin treatment. Among them, iNOS mRNA levels were also reduced in the intestinal polyps. Moreover, oxidative stress represented by 8-nitroguanosine in the small intestinal epithelial cells was reduced by pitavastatin treatment. Related to these proinflammatory genes, PPARg activity was activated in the intestinal nonpolyp parts and in the liver of Min mice with pitavastatin treatment. These results indicated that pitavastatin has potential benefit for the suppression of intestinal polyp development. Cancer Prev Res; 4(3); 445-53. Ó2011 AACR.

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“…Abe et al (17) demonstrated that pravastatin did not increase plasma adiponectin levels although normal mice treated with pravastin did show such an increase. Adiponectin is an insulin sensitizing factor derived from adipocytes.…”

Section: Discussionmentioning

confidence: 99%

Effect of simvastatin on burn-induced alterations in tissue specific glucose metabolism: implications for burn associated insulin resistance

Bonab

Carter²,

Paul³

et al. 2010

Int J Mol Med

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Abstract. In addition to their primary role in lowering plasma cholesterol, statins have a variety of other actions. We studied the effect of simvastatin treatment on burn injuryinduced changes in regional glucose metabolism. Groups of six CD-1 mice (male, ~25 g) were subjected to full thickness 30% total body surface area (TBSA) burn injury. The animals were treated with simvastatin at various doses (0.02, 0.2 and 2.0 μg/kg, i.p.) for seven days. The following morning, mice were injected with 18 F labeled 2-fluoro-2-deoxy-Dglucose ( 18 FDG) (50 μCi) via the tail vein. Approximately 60 min after tracer injection, the animals were sacrificed and biodistribution was measured. A sub-set of burned mice with and without statin treatment and sham controls was injected with ~1.0 mCi of FDG and tracer distribution was evaluated by μPET. In addition, oral glucose tolerance tests (OGTT) were performed in other groups of burned mice with and without statin treatment and sham controls. In the heart and brown adipose tissue (BAT), burn injury produced a highly significant increase in 18 FDG accumulation (p<0.01), whereas tracer accumulation in brain was markedly reduced (p<0.01). In the heart and BAT, simvastatin treatment produced dosedependent reductions in 18 FDG accumulation. In contrast, simvastatin did not affect 18 FDG accumulation in the brain. There was no effect of simvastatin treatment on 18 FDG accumulation in the heart, BAT or brain of sham-treated mice. Less pronounced effects were detected in other tissues that were studied. All animals had normal plasma glucose levels (~90 mg/dl). The OGTTs demonstrated insulin resistance in burn injured mice which was reversed by statin treatment. Our results indicate that simvastatin reverses burn-induced increases in 18 FDG accumulation by the heart and BAT in a dose-dependent manner but does not affect burn-induced reductions of 18 FDG accumulation by the brain. These findings suggest that statins exert some of their effects by tissue specific modulation of glucose metabolism.

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Effects of Statins on Adipose Tissue Inflammation

Cited by 95 publications

References 41 publications

Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Effect of simvastatin on burn-induced alterations in tissue specific glucose metabolism: implications for burn associated insulin resistance

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