IntroductionDyslipidemia is associated with increased rho-associated kinase 2 (ROCK2) concentration. Whether moderate aerobic exercise could attenuate leukocyte ROCK2 concentration is unknown.Material and methodsOne hundred subjects with dyslipidemia and without statin treatment were enrolled and assigned to exercise and control groups. In the exercise group, at least 30 min of moderate aerobic exercise per day 5 times weekly was recommended. In the control group, participants were recommended to undertake exercise of the same intensity as the exercise group but not mandatorily. At baseline and 3 months later, between-group differences were compared.ResultsAt baseline, dyslipidemia in both groups was characterized by increased serum levels of total cholesterol and low density lipoprotein cholesterol (LDL-C). Serum high-sensitivity C-reactive protein (hs-CRP) level was comparably increased too, and the average daily exercise time was extremely low: 5.8 ±2.7 min and 6.2 ±3.1 min respectively. Leukocyte ROCK2 concentration in the two groups was 38.4 ±7.5 mg/ml and 40.2 ±8.2 mg/ml respectively. Three months later, compared with the control group, average daily exercise time was significantly longer in the exercise group (37.4 ±4.3 min vs. 16.5 ±7.5 min, p < 0.05). Leukocyte ROCK2 concentration was also significantly reduced (27.6 ±4.3 mg/ml vs. 34.6 ±5.2 mg/ml, p < 0.05). Serum nitric oxide (NO) concentration in the exercise group was significantly higher than the control group (p < 0.05). Multivariate linear regression analysis revealed that NO and exercise time were significantly associated with leukocyte ROCK2 concentration after adjusting for traditional risk factors.ConclusionsModerate aerobic exercise could effectively attenuate leukocyte ROCK2 concentration in subjects with dyslipidemia.

Using this dual-parameter screening method, we acquired a strain with GOD activity of 3126 U l, which was 146% higher than the original strain. Its secretion rate of GOD was 83, 32% higher than the original strain.

Objective Here, Our study aimed to find the plasma biomarkers related to the diagnosis of multiple sclerosis (MS) through Liquid chromatography Mass Spectrometry (LC/MS) technology. Methods Tandem mass tag (TMT) quantitative LC/MS proteomics method was used to determine the differentially expressed proteins (DEPs) in the plasma samples of 22 MS patients and 22 healthy controls. and the functional annotations of the DEPs were analyzed by GO and IPA. The candidate protein was validated by ELISA. The receiver operating characteristic (ROC) curves were used to determine the predictive potential of the biomarker. Results LC/MS analysis of plasma proteomic identified 88 DEPs among the quantified 375 proteins, of which 39 proteins were up-regulated and 49 proteins were down-regulated. These proteins are involved in immunity/inflammation and Neurological diseases related pathways. A protein panel consisting of Alpha-1-antitrypsin (SERPINA1) and Protein S100-A9 (S100A9) were with an area under the curve (AUC) of 0.991. A MS treatment related protein, DPP4, was validated by ELISA. Conclusion DEPs related to MS can be found in the plasma proteome, which may become biomarkers for MS diagnosis. Our study layed the foundation for the further application plasma proteomics in the diagnosis of MS.

Background: That cells sense extracellular amino acids to regulate intracellular lipid metabolism has been a heated debate in terms of the study on amino acid nutrition. T1R1 is a membrane G protein-coupled receptor that senses amino acids in a variety of cells. In our study, T1R1-KO mice was used to explore the function of umami taste receptor in lipid metabolism. Results: Compared with wild-type mice, T1R1-KO mice showed Significantly lighter adipose tissue weight, reduced serum triglycerides (TG) and total cholesterol (TC), as well as higher glucose tolerance on chow diet. Moreover, there were less lipid accumulation in adipose and liver tissue and shrink of the adipocyte size in T1R1-KO mice. And a decreased expression of lipogenesis genes (PPARγ, CEBPα, SREBP1) was found in both adipose and liver tissue. To further study the mechanism of T1R1 regulating liver lipid metabolism, proteomics analysis was introduced and the up-regulated proteins were enriched in lipid and steroid metabolism pathways of T1R1-KO mice. Further PRM verification analysis showed that the ablation of T1R1 reduced the de novo synthesis of lipids through BCKDHA and BCKDHB, and promoted lipid metabolism through CYP7B1 and IGFBP2. Conclusions: Our results showed that the disruption of T1R1 in mice could reduce body lipid accumulation, and our data clarifies the role of umami receptors in lipid metabolism and could provide a basis for the research on nutrition and obesity.