29 research outputs found

    CETP expression increases mRNA for muscle PGC-1α.

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    <p>Gene expression in muscle tissue collected immediately following exercise. Data represent mean ± SEM. n = 4 mice per group. * indicates p<0.05 by unpaired t-test.</p

    CETP expression does not alter weight or adiposity gain on HFD.

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    <p>(A) Body weight over the course of HFD-feeding. (B) Body composition at baseline and 4-weeks post HFD. n = 5–8 mice per group.</p

    CETP expression does not alter VO<sub>2</sub>Max.

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    <p>(A) VO<sub>2</sub>Max in WT and CETP mice throughout the course of HFD. (B) Oxygen consumption in chow-fed mice during the initial exercise study. Solid line indicates beginning of exercise trial. Dashed line indicates median exercise time for both WT and CETP mice. (C) Oxygen consumption in HFD-fed mice during the exercise trial following 4 weeks of HFD. Solid line indicates beginning of exercise trial. Dotted line indicates median exercise time for WT mice. Dashed line indicates median exercise time for CETP mice. Error bars represent mean ± SEM. n = 5–8 mice per group.</p

    CETP expression increases mitochondrial oxidation in female mice.

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    <p>(A) Oxygen consumption in isolated muscle fibers treated with glutamate/malate mixture to measure total substrate oxidation. (B) Oxygen consumption in isolated muscle fibers treated with palmitoylcarnitine to measure fatty acid oxidation. Data represent mean ± SEM. n = 8–14 muscle fibers per group. * indicates p<0.05 by unpaired t-test.</p

    Basal characteristics of wild-type (WT) and littermate mice with over-expression of glucose transporter 4 (G4Tg).

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    <p>Measurements were taken in 5h fasted mice prior to phloridzin-glucose clamps and represent combined data from control and experimental animals. * indicates p<0.05 compared to WT littermates.</p

    Hepatic glycogen and related enzyme activities in response to acutely normalizing blood glucose in glucose transporter 4 over-expressing mice (G4Tg) and wild-type (WT) littermates.

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    <p>Hepatic glycogen content (A), hepatic glycogen breakdown (B), and activities or activity ratios of glucokinase (GK; C), glucose-6-phosphatase (G6Pase; D), glycogen phosphorylase (GP; E), and glycogen synthase (GS; F)] are shown before and after normalizing blood glucose in 5 h-fasted mice that over-express glucose transporter 4 (Glut4) in skeletal muscle, heart, and adipose tissue and wild-type (WT) littermates using a 90 min phloridzin (80 μg·kg<sup>−1</sup>·min<sup>−1</sup>)-glucose (115 mg·dL<sup>−1</sup>) clamp. Separate cohorts of mice were used to obtain basal and clamp data. Dashed lines in panel B denote changes in endogenous appearance of glucose (endoR<sub>a</sub>; shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052355#pone-0052355-g001" target="_blank">Figure 1C</a>). Data are presented as means ± SEM and * and ϕ indicate p<0.05 compared to WT littermates or to basal values within a genotype, respectively. n = 7–8 mice in each group.</p

    Arterial plasma insulin levels after a hyperinsulinemic-euglycemic clamp following vehicle or LPS treatment.

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    <p>Arterial plasma insulin levels in response to vehicle, low- (1 µg/gBW), or high- (10 µg/gBW) dose LPS in chronically catheterized conscious mice during the basal period (0 min) and 125 min after initiation of a hyperinsulinemic-euglycemic clamp. Data are expressed as mean±SEM.</p

    Effect of vehicle and LPS treatment on insulin signaling.

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    <p>Akt phosphorylation (Ser<sup>473</sup>; Panel A) and GSK phosphorylation (Panel B) in the gastrocnemius muscle of C57/BL6j mice that received vehicle (VEH) or high-dose LPS (HD LPS; 10 µg/gBW) after a hyperinsulinemic-euglycemic clamp. Akt phosphorylation (Ser<sup>473</sup>; Panel C) and phosphorylation of IRS-1 (Tyr<sup>895</sup> and Ser<sup>307</sup>; Panel D) in the gastrocnemius muscle of C57/BL6j mice after an acute bolus of saline or insulin. Data are expressed as mean±SEM. *p<0.05.</p

    Protocol used during the hyperinsulinemic-euglycemic clamp.

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    <p>On the day of the <i>in vivo</i> metabolic experiments, chronically catheterized conscious mice were placed on a 5 h fast (t = −300 min). A bolus of VEH, low- or high-dose LPS was injected at t = −240 min. At t = −120 a primed continuous tracer infusion was begun. At t = 0 an infusion of insulin and glucose or vehicle (i.e. saline) was initiated. After 100 min, 2-deoxy glucose was injected and mice were sacrificed after 25 min.</p

    Renal and tissue blood flow following vehicle or LPS treatment.

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    <p>Renal and muscle (soleus, gastrocnemius, superficial vastus lateralis, and heart) blood flow were compared in mice that received either vehicle (VEH) or high-(10 µg/gBW) dose LPS. Data are expressed as mean±SEM.</p><p>*p<0.05.</p
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