26 research outputs found

    Rosiglitazone and not fenofibrate treatment decreases atherogenesis in obese, insulin resistant mice.

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    <p>(<b>A</b>) Representative Mac-3 staining of aortic sinus plaques of placebo-, fenofibrate- and rosiglitazone-treated DKO mice at 24 weeks. (<b>B</b>) Gene expression in the aorta was analyzed by measuring relative <i>RNA</i> levels using qRT-PCR for <i>Tnfα</i>, <i>IL6</i>, <i>Mcp1</i> and <i>Irak3</i>. Data are means ± SEM. Scale bar = 500 µm. *<i>P</i><0.05, **<i>P</i><0.01 and ***<i>P</i><0.001 DKO compared with C57BL/6 J mice; <sup></sup><i>P</i><0.01and<sup></sup><i>P</i><0.01 and <sup>$</sup><i>P</i><0.001 PPAR agonist-treated compared with placebo-treated DKO mice; <sup>£</sup><i>P</i><0.05, <sup>££</sup><i>P</i><0.01 and <sup>£££</sup><i>P</i><0.001 rosiglitazone-treated compared with fenofibrate-treated DKO mice.</p

    Group characteristics and hormone levels in serum in the two subgroups of subfertile men (hypo- and eugonadal) as compared to the 20 controls.

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    <p>All data are presented as means (SD). Univariate regression analysis. <i>P</i> adjusted refers to the factors age, BMI and fertility status. HG, hypogonadal; EG, eugonadal; BMI, body mass index; TT, total testosterone; SHBG, sex hormone binding globuline; cFT, calculated free testosterone; LH, luteinizing hormone; NS, not significant; NA, not applicable;</p>*<p>, <i>P</i><0.05;</p>**<p>, <i>P</i><0.01.</p

    HFD increases atherogenesis in insulin resistant mice.

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    <p>Plaque volume was determined by measuring lipid (oil red O)-stained surfaces in subsequent sections; macrophages were stained with anti-Mac-3 antibody. Gene expression in the aorta was analyzed by measuring relative <i>RNA</i> levels using qRT-PCR for <i>Pparγ</i>, <i>Mcp1, Irak3</i> and <i>Adipoq</i>. Data are means ± SEM. **<i>P</i><0.01 and ***<i>P</i><0.001 HFD-fed compared with SD-fed LDL-receptor deficient mice. Abbreviations: HFD, high fat diet; SD, standard diet.</p

    HFD-induced weight gain is associated with dyslipidemia, insulin resistance and hyperleptinemia in the presence of high blood adiponectin.

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    <p>Data are means ± SEM. **<i>P</i><0.01 and ***<i>P</i><0.001 HFD-fed compared with SD-fed LDL-receptor deficient mice. Abbreviations: HFD, high fat diet; SD, standard diet.</p

    <i>Pparα</i> and <i>Pparγ</i> expressions in visceral adipose and aortic tissues of PPAR agonist-treated DKO mice.

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    <p>Data are means ± SEM.</p>*<p><i>P<</i>0.05 and</p>***<p><i>P<</i>0.001 DKO compared with C57BL/6 J mice;</p><p><i>P</i><0.01and</p><p><i>P</i><0.01 and</p>$<p><i>P</i><0.001 PPAR agonist-treated compared with placebo-treated DKO mice;</p>£<p><i>P</i><0.05 and</p>£££<p><i>P</i><0.001 rosiglitazone-treated compared with fenofibrate-treated DKO mice.</p

    Associations between TT and (A) TNFa, (B) MIP1B, (C) MIP1aand between cFT and (D) TNFa, (E) MIP1B, (F) MIP1a.

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    <p>All inflammatory markers are log values. B represents regression coefficients derived from univariate regression analysis adjusted for age and fertility status. Initial grouping of men indicated in figure as subfertile hypogonadal (n = 20), subfertile eugonadal (n = 20) and controls (n = 20). TT, total testosterone; cFT, calculated free testosterone; TNFa, tumor necrosis factor alpha; MIP1B, macrophage inflammatory protein 1−beta; MIP1a, macrophage inflammatory protein 1-alpha.</p
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