13 research outputs found

    Green tea extracts ameliorate high-fat diet-induced muscle atrophy in senescence-accelerated mouse prone-8 mice.

    No full text
    Muscle atrophy (loss of skeletal muscle mass) causes progressive deterioration of skeletal function. Recently, excessive intake of fats was suggested to induce insulin resistance, followed by muscle atrophy. Green tea extracts (GTEs), which contain polyphenols such as epigallocatechin gallate, have beneficial effects on obesity, hyperglycemia, and insulin resistance, but their effects against muscle atrophy are still unclear. Here, we found that GTEs prevented high-fat (HF) diet-induced muscle weight loss in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, an HF diet, or HF with 0.5% GTEs (HFGT) diet for 4 months. The HF diet induced muscle weight loss with aging (measured as quadriceps muscle weight), whereas GTEs prevented this loss. In HF diet-fed mice, blood glucose and plasma insulin concentrations increased in comparison with the control group, and these mice had insulin resistance as determined by homeostasis model assessment of insulin resistance (HOMA-IR). In these mice, serum concentrations of leukocyte cell-derived chemotaxin 2 (LECT2), which is known to induce insulin resistance in skeletal muscle, were elevated, and insulin signaling in muscle, as determined by the phosphorylation levels of Akt and p70 S6 kinases, tended to be decreased. In HFGT diet-fed mice, these signs of insulin resistance and elevation of serum LECT2 were not observed. Although our study did not directly show the effect of serum LECT2 on muscle weight, insulin resistance examined using HOMA-IR indicated an intervention effect of serum LECT2 on muscle weight, as revealed by partial correlation analysis. Accordingly, GTEs might have beneficial effects on age-related and HF diet-induced muscle weight loss, which correlates with insulin resistance and is accompanied by a change in serum LECT2

    Green Tea Extracts Attenuate Brain Dysfunction in High-Fat-Diet-Fed SAMP8 Mice

    No full text
    Unhealthy diet promotes progression of metabolic disorders and brain dysfunction with aging. Green tea extracts (GTEs) have various beneficial effects and alleviate metabolic disorders. GTEs have neuroprotective effects in rodent models, but their effects against brain dysfunction in models of aging fed unhealthy diets are still unclear. Here, we showed that GTEs attenuate high-fat (HF) diet-induced brain dysfunction in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, HF diet, or HF diet with 0.5% GTEs (HFGT) for four months. The HF diet reduced memory retention and induced amyloid β1–42 accumulation, whereas GTEs attenuated these changes. In HF diet-fed mice, lipid oxidative stress, assessed by malondialdehyde levels, was increased. The levels of proteins that promote synaptic plasticity, such as brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95), were reduced. These alterations related to brain dysfunction were not observed in HFGT diet-fed mice. Overall, our data suggest that GTEs intake might attenuate brain dysfunction in HF diet-fed SAMP8 mice by protecting synaptic plasticity as well as via anti-oxidative effects. In conclusion, GTEs might ameliorate unhealthy diet-induced brain dysfunction that develops with aging

    Simulations of systematic effects arising from cosmic rays in the LiteBIRD space telescope, and effects on the measurements of CMB B-modes

    No full text
    International audienceSystematic effects arising from cosmic rays have been shown to be a significant threat to space telescopes using high-sensitivity bolometers. The LiteBIRD space mission aims to measure the polarised Cosmic Microwave Background with unprecedented sensitivity, but its positioning in space will also render it susceptible to cosmic ray effects. We present an end-to-end simulator for evaluating the expected scale of cosmic ray effects on the LiteBIRD space mission, which we demonstrate on a subset of detectors on the 166 GHz band of the Low Frequency Telescope. The simulator couples the expected proton flux at L2 with a model of the thermal response of the LFT focal plane and the electrothermal response of its superconducting detectors, producing time-ordered data which is projected into simulated sky maps and subsequent angular power spectra

    Blood glucose, plasma insulin, HOMA-IR, and serum LECT2 concentrations in SAMP8 mice.

    No full text
    <p>Blood glucose levels were analyzed at dissection after 5 h of fasting by ACCU-CHEK Aviva described in Materials and Methods (A). Plasma insulin (B) and serum LECT2 (D) concentrations were analyzed after serum and plasma sample collection by enzyme-linked immuno-sorbent assay. HOMA-IR was calculated as described in the Materials and Methods (C). Data are means ± S.D. One-way ANOVA followed by Tukey’s post-hoc test was used for comparison among groups. *, <i>P</i> < 0.05; **, <i>P</i> < 0.01; ***, <i>P</i> < 0.001.</p

    Phosphorylation of kinases involved in insulin signaling in skeletal muscle of adult (6M) SAMP8 mice.

    No full text
    <p>Representative western blot images (upper panels, all images provided in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195753#pone.0195753.s001" target="_blank">S1 Appendix</a>) and quantification of phosphorylation (lower graphs) are shown for Akt (A) and S6K (B). Data are means ± S.D. One-way ANOVA followed by Tukey’s post-hoc test was used for comparison among groups. *, <i>P</i> < 0.05.</p

    Body weight and skeletal muscle weight in aging SAMR1 and SAMP8 mice.

    No full text
    <p>Body weight (A) and skeletal muscle weight (B) were measured in young (2M) and adult (6M) mice fed a Cont diet. Skeletal muscle weight increased in SAMR1 mice concomitantly with body weight gain, but did not increase in SAMP8 mice. Data are means ± S.D. (8 to 16 mice per group). Statistical significance of the interaction between mouse strain (SAMR1 and SAMP8) and age (2M and 6M) was determined by two-way factorial ANOVA without replication, and Student’s <i>t</i>-test was used for comparison between the two age groups. *, <i>P</i> < 0.05; ***, <i>P</i> < 0.001.</p

    Body weight and skeletal muscle weight in SAMP8 mice on different diets.

    No full text
    <p>Body weight (A); skeletal muscle weight (B). Skeletal muscle loss with aging was exacerbated by an HF diet (2M Cont vs. 6M HF; <i>P</i> = 0.016) but was significantly prevented by GTEs in the HFGT group (HF vs. HFGT; <i>P</i> = 0.002). Data are means ± S.D. (8 to 16 mice per group). One-way ANOVA followed by Tukey’s post-hoc test was used for comparison among groups. *, <i>P</i> < 0.05; **, <i>P</i> < 0.01; ***, <i>P</i> < 0.001.</p
    corecore