Exercise Reduces Insulin Resistance in Type 2 Diabetes Mellitus via Mediating the lncRNA MALAT1/MicroRNA-382-3p/Resistin Axis.

Insulin resistance (IR) is the primary pathological mechanism underlying type 2 diabetes mellitus (T2DM). Here, the study aimed to ascertain whether and how exercise mediates IR in T2DM. An in vivo mouse model of high-fat diet-induced IR and an in vitro high-glucose-induced IR model were constructed. High long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression was detected in T2MD and was positively correlated with HOMA-IR and resistin levels. Then, short hairpin RNA targeting MALAT1 (sh-MALAT1) or pcDNA-MALAT1 was delivered into human umbilical vein endothelial cells (HUVECs) to knock down or upregulate its expression, respectively. Silencing of MALAT1 resulted in reduced levels of resistin, Ang II, tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), endothelin-1 (ET-1), and p-insulin receptor substrate-1 (p-IRS)/ISR-1, and decreased cell migration, as well as enhanced glucose uptake and levels of nitric oxide (NO) and p-Akt/Akt. In the IR mouse model, exercise was observed to downregulate MALAT1 to reduce resistin, whereby exercise reduced homeostatic model assessment-insulin resistance (HOMA-IR). Besides, exercise also elevated microRNA-382-3p (miR-382-3p) expression in the serum of IR mice. Dual-luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays identified that MALAT1 could bind to miR-382-3p to upregulate resistin. Collectively, the key observations of the study provide evidence that inhibition of MALAT1 elevates miR-382-3p to repress resistin, which consequently underlies the mechanism of exercise protecting against IR, highlighting a direction for T2DM therapy development.

Aerobic Exercise Prevents Insulin Resistance Through the Regulation of miR-492/Resistin Axis in Aortic Endothelium.

Previously, we found that miR-492 delayed the progression of atherosclerosis (AS) by acting as an up-stream regulator of resistin. Therefore, we hypothesized that the anti-atherogenic effects of exercise are related to miR-492-mediated downregulation of resistin and repair of endothelial injury. In this study, we investigated the effects of the miR-492/resistin axis on improving endothelial injury in ApoE-/- mice (ApoE-deficient/knockout in C57BL/6 mice) through swimming exercises. Our results showed that the severity of AS and insulin resistance (IR) in these mice were significantly reduced by swimming exercises. In addition, miR-492 expression in the aortic endothelium of ApoE-/- mice was decreased, in addition to increased levels of resistin. Interestingly, swimming exercises increased miR-492 expression while decreasing that of resistin. Taken together, swimming exercises delayed the progression of AS, possibly by upregulating miR-492 and downregulating resistin in aortic endothelium. Therefore, exercises modulated glucose and lipid metabolism, alleviated endothelial IR, and repaired endothelial injury.

The rural carbonaceous aerosols in coarse, fine, and ultrafine particles during haze pollution in northwestern China.

The carbonaceous aerosol concentrations in coarse particle (PM10: Dp ≤ 10 µm, particulate matter with an aerodynamic diameter less than 10 µm), fine particle (PM2.5: Dp ≤ 2.5 µm), and ultrafine particle (PM0.133: Dp ≤ 0.133 µm) carbon fractions in a rural area were investigated during haze events in northwestern China. The results indicated that PM2.5 contributed a large fraction in PM10. OC (organic carbon) accounted for 33, 41, and 62 % of PM10, PM2.5, and PM0.133, and those were 2, 2.4, and 0.4 % for EC (elemental carbon) in a rural area, respectively. OC3 was more abundant than other organic carbon fractions in three PMs, and char dominated EC in PM10 and PM2.5 while soot dominated EC in PM0.133. The present study inferred that K(+), OP, and OC3 are good biomass burning tracers for rural PM10 and PM2.5, but not for PM0.133 during haze pollution. Our results suggest that biomass burning is likely to be an important contributor to rural PMs in northwestern China. It is necessary to establish biomass burning control policies for the mitigation of severe haze pollution in a rural area.