The current findings suggest that treadmill running provides a nonpharmacological means to combat cognitive declines due to AD pathology.

[Purpose]The aim of this study was to investigate the effects of aerobic exercise training on a high fat diet (HFD)-induced fatty liver and its metabolic complications in C57BL/6 mice.[Methods]Mice at 5-month old (n = 30) were randomly assigned to standard chow (SC + CON, n = 10) and high-fat diet (HFD, n = 20), and they were subjected to SC and HFD, respectively, for 23-week. After 15-week of HFD, mice in the HFD group were further assigned to HFD (HFD + CON, n = 10) or exercise training (HFD + EX, n = 10) groups. The HFD + EX mice were subjected to aerobic treadmill running during the last 8-week of the 23-week HFD course. Outcomes included hepatic steatosis, insulin resistance, and expression of genes involved in mitochondrial function and/or fatty oxidation as well as de novo lipogenesis and/or triacylglycerol (TAG) synthesis.[Results]Treadmill running ameliorated impaired glucose tolerance and insulin resistance secondary to the HFD. The beneficial effects of treadmill running were associated with enhanced molecular markers of mitochondrial function and/or fatty acids oxidation (i.e., PPARα and CPT1a mRNAs, pAMPK/AMPK, pACC, and SIRT1 protein) as well as suppressed expression of de novo lipogenesis and/or TAG synthesis (i.e., SREBP1c, lipin1 and FAS mRNAs) in the liver.[Conclusion]The current findings suggest that aerobic exercise training is an effective and non-pharmacological means to combat fatty liver and its metabolic complications in HFD-induced obese mice.

The variation in the biological function of proteins plays an important role in plasma medicine and sterilization. Several non-thermal plasma sources with different feeding gases are used worldwide for plasma treatment, including dielectric barrier discharge (DBD) and atmospheric-pressure plasma jet (APPJ) as the most commonly used sources. Therefore, in the present work, we used both DBD and APPJ plasma sources with N2 and air as feeding gases to evaluate the effects on the structural, thermodynamic, and activity changes of enzymes. In the current work, we used lysozyme as a model enzyme and verified the structural changes using circular dichroism (CD), fluorescence, and X-ray crystallography. In addition, we investigated the lysozyme thermodynamics using CD thermal analysis and changes in the B-factor from X-ray crystallography. The results showed that lysozyme activity decreased after the plasma treatment. From these analyses, we concluded that N2-feeding gas plasma disturbs the structure and activity of lysozyme more than Air feeding gas plasma in our experimental studies. This study provides novel fundamental information on the changes to enzymes upon plasma treatment, which has been absent from the literature until now.

Animals have to cope with starvation. The molecular mechanisms by which animals survive long-term starvation, however, are not clearly understood. When they hatch without food, C. elegans arrests development at the first larval stage (L1) and survives more than two weeks. Here we show that the survival span of arrested L1s, which we call L1 longevity, is a starvation response regulated by metabolic rate during starvation. A high rate of metabolism shortens the L1 survival span, whereas a low rate of metabolism lengthens it. The longer worms are starved, the slower they grow once they are fed, suggesting that L1 arrest has metabolic costs. Furthermore, mutants of genes that regulate metabolism show altered L1 longevity. Among them, we found that AMP-dependent protein kinase (AMPK), as a key energy sensor, regulates L1 longevity by regulating this metabolic arrest. Our results suggest that L1 longevity is determined by metabolic rate and that AMPK as a master regulator of metabolism controls this arrest so that the animals survive long-term starvation.

Background Little information is available about molecular markers for sarcopenia and osteoporosis in Asian populations. Objective This study investigated the association of the ACTN3 polymorphism with sarcopenia and osteoporotic status in older Korean adults. Methods Older Korean 62 men and 270 women (mean age 73.7 ± 6.6 years) participated in this study. Body mass index, percent body fatness, appendicular skeletal muscle mass, and bone mineral density of the lumbar spine, femur, and total body were analyzed with dual-energy X-ray absorptiometry. ACTN3 R/X genotyping was determined using TaqMan probes. Results Determination of odds ratios (ORs) and 95% confidence intervals (CIs) using binary logistic regression analyses showed that XX homozygotes were at a significantly higher risk of sarcopenia (OR = 2.056, 95%  CI = 1.024–4.127, p = 0.043) and osteoporosis (OR = 2.794, 95%  CI = 1.208–5.461, p = 0.016) than RR homozygotes (reference group, OR = 1). The OR of XX homozygotes for having sarcopenia remained significant (OR = 2.237, 95%  CI = 1.044–4.836, p = 0.038) after adjustments for age, gender, body fatness, and serum vitamin D. The OR of XX homozygotes for having osteoporosis was no longer significant (OR = 2.682, 95%  CI = 0.960–7.942, p = 0.075) after adjustments for the covariates. Conclusion Our findings suggest that the ACTN3 R577X genotype may influence decline in muscle and bone health phenotypes in older Korean adults.