Exercise-Induced Browning of White Adipose Tissue and Improving Skeletal Muscle Insulin Sensitivity in Obese/Non-obese Growing Mice: Do Not Neglect Exosomal miR-27a.

Exercise is considered as a favorable measure to prevent and treat childhood obesity. However, the underlying mechanisms of exercise-induced beneficial effects and the difference between obese and non-obese individuals are largely unclear. Recently, miR-27a is recognized as a central upstream regulator of proliferator-activated receptor γ (PPAR-γ) in contributing to various physiological and pathological processes. This study aims to explore the possible cause of exercise affecting white adipose tissue (WAT) browning and reversing skeletal muscle insulin resistance in obese/non-obese immature bodies. For simulating the process of childhood obesity, juvenile mice were fed with a basal diet or high-fat diet (HFD) and took 1 or 2 h swimming exercise simultaneously for 10 weeks. The obese animal model was induced by the HFD. We found that exercise hindered HFD-induced body fat development in growing mice. Exercise modified glucolipid metabolism parameters differently in the obese/non-obese groups, and the changes of the 2 h exercise mice were not consistent with the 1 h exercise mice. The level of serum exosomal miR-27a in the non-exercise obese group was increased obviously, which was reduced in the exercise obese groups. Results from bioinformatics analysis and dual-luciferase reporter assay showed that miR-27a targeted PPAR-γ. Exercise stimulated WAT browning; however, the response of obese WAT lagged behind normal WAT. In the HFD-fed mice, 2 h exercise activated the IRS-1/Akt/GLUT-4 signaling pathway in the skeletal muscles. In summary, our findings confirmed that exercise-induced beneficial effects are associated with exercise duration, and the response of obese and non-obese bodies is different. Exosomal miR-27a might be a crucial node for the process of exercise-induced browning of WAT and improving skeletal muscle insulin sensitivity.

[Study on secondary metabolic organ of echinacoside in herbs of Cistanche tubulosa].

OBJECTIVE: It could give some theory support of confirming the secondary metabolism organ and regulation of echinacoside in Cistanche tubulosa by searching parasitic growth of C. tubulosa ahd echinacoside variation in different organs of host and parasite. METHOD: The echinacoside content was analyzed by HPLC. The relationship between dry matter accumulation and echinacoside accumulation of C. tubulosa as the well as root diameter of host were comparatively analyzed. RESULT: With the increase of dry matter accumulation of C. tubulosa, echinacoside accumulation increased significantly, and both of them were in significantly positive correlated with the root diameter of host. Echinacoside content in haustorium phloem was 15.53%, higher than that of haustorium xylem, C. tubulosa plant and other organs. CONCLUSION: Haustorium phloem was probably the secondary metabolism organ of echinacoside in C. tubulosa.

[Inoculation experiments of Cistanche tubulosa on 8 introduced Tamarix species].

OBJECTIVE: To analyze the inoculation ratio and echinacoside content of Cistanche tubulosa and provide theoretical basis for Tamarix introduction, resource protection and screening of C. tubulosa. METHOD: 8 Tamarix species were introduced in the North China Plain and inoculation of C. tubulosa was conducted on all species. Phenylethanoid glycosides fingerprinting and echinacoside content of C. tubulosa were analyzed by using HPLC. RESULT: The adaptability of 8 Tamarix species were significantly different, phenylethanoid glycosides component of C. tubulosa on T. gansuensis and T. austromongolica were basically identical in contrast to T. chinensis, echinacoside content showed no obvious difference in C. tubulosa plant growing 4 months. CONCLUSION: T. gansuensis and T. Austromongolica are suitable for the host introduction plant of C. tubulosa resource protection and screening in North China Plain.

Analytical correction for multiple testing in admixture mapping.

Admixture mapping, using unrelated individuals from the admixture populations that result from recent mating between members of each parental population, is an efficient approach to localize disease-causing variants that differ in frequency between two or more historically separated populations. Recently, several methods have been proposed to test linkage between a susceptibility gene and a disease locus by using admixture-generated linkage disequilibrium (LD) for each of the genotyped markers. In a genome scan, admixture mapping usually tests 2,000 to 3,000 markers across the genome. Currently, either a very conservative Sidak (or Bonferroni) correction or a very time consuming simulation-based method is used to correct for the multiple tests and evaluate the overall p value. In this report, we propose a computationally efficient analytical approach for correction of the multiple tests and for calculating the overall p value for an admixture genome scan. Except for the Sidak (or Bonferroni) correction, our proposed method is the first analytical approach for correction of the multiple tests and for calculating the overall p value for a genome scan. Our simulation studies show that the proposed method gives correct overall type I error rates for genome scans in all cases, and is much more computationally efficient than simulation-based methods.