Background Because consumption of conventional yogurt has beneficial effects in a healthy population, and insulin resistance (IR) is the mutual pathogenesis in nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS), we hypothesized that yogurt would ameliorate IR in patients with NAFLD and MetS. Objectives The aim of this study was to investigate the effects of yogurt on IR and secondary endpoints including liver fat, gut microbiota, and serum biomarkers of inflammation and oxidative stress in obese women with NAFLD and MetS. Methods One hundred obese women aged 36–66 y with both NAFLD and MetS were randomly assigned to consume 220 g/d of either conventional yogurt or milk for 24 wk. At baseline and week 24, we measured anthropometric indices, serum glucose, insulin, lipids, and cytokines in all participants, and liver fat and gut microbiota in 20 participants randomly selected from each group. Results Forty-eight participants from the yogurt group and 44 from the milk group completed the intervention. Compared with milk, yogurt significantly decreased the homeostasis model assessment of insulin resistance (−0.53; 95% CI: −1.03, −0.02), fasting insulin (−2.77 mU/L; 95% CI: −4.91, −0.63 mU/L), 2-h insulin (−25.5 mU/L; 95% CI: −33.0, −17.9 mU/L), 2-h area under the curve for insulin (−29.4 mU/L · h; 95% CI: −44.0, −14.8 mU/L · h), alanine aminotransferase (−4.65 U/L; 95% CI: −8.67, −0.64 U/L), intrahepatic lipid (−3.44%; 95% CI: −6.19%, −0.68%), and hepatic fat fraction (−3.48%; 95% CI: −6.34%, −0.63%). Yogurt also decreased serum LPS (−0.31 EU/mL; 95% CI: −0.48, −0.14 EU/mL), fibroblast growth factor 21 (−57.76 pg/mL; 95% CI: −86.32, −29.19 pg/mL), lipids, and biomarkers of inflammation and oxidative stress, and altered gut microbiota composition. Mediation analysis showed that yogurt may improve IR by reducing serum lipids, inflammation, oxidative stress, and LPS. Conclusions Yogurt was better than milk at ameliorating IR and liver fat in obese Chinese women with NAFLD and MetS, possibly by improving lipid metabolism, reducing inflammation, oxidative stress, and LPS, and changing the gut microbiota composition. This trial was registered at www.chictr.org.cn as ChiCTR-IPR-15006801.

Mitochondrial dysfunction is considered a crucial therapeutic target for early brain injury following subarachnoid hemorrhage (SAH). Emerging evidence indicates that docosahexaenoic acid (DHA), an essential omega-3 fatty acid, protects mitochondria in various chronic diseases. This study aimed to investigate the neuroprotective effects of DHA on mitochondrial dynamic dysfunction after EBI using in vivo and in vitro approaches. For in vivo experiments, the rat endovascular perforation SAH model was performed, whereby DHA was administered intravenously 1 h after induction of SAH. Primary cultured neurons treated with oxyhemoglobin (OxyHb) for 24 h were used to mimic SAH in vitro. Our results demonstrated that DHA improved neurological deficits and reduced brain edema in rats with SAH, and attenuated OxyHb-induced neuronal death in primary cultured cells. DHA reduced the amount of reactive oxygen species-positive cells and improved cell viability when compared to the SAH + vehicle group in vitro. DHA attenuated malondialdehyde levels and superoxide dismutase stress, increased Bcl2 and Bcl-xl, and decreased Bax and cleaved caspase-3 in vivo. Additionally, DHA ameliorated mitochondrial dysfunction, upregulated the mitochondrial fusion-related protein Optic Atrophy 1, and downregulated the mitochondrial fission-related protein Dynamin-Related-Protein 1 (Drp1) and Serine 616 phosphorylated Drp1 after SAH both in vitro and in vivo. Taken together, our current study demonstrates that DHA might prevent oxidative stress-based apoptosis after SAH. The characterization of the underlying molecular mechanisms may further improve mitochondrial dynamics-related signaling pathways.

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Mdivi-1 is a selective inhibitor of mitochondrial fission protein, Drp1, and can penetrate the blood-brain barrier. Previous studies have shown that Mdivi-1 improves neurological outcomes after ischemia, seizures and trauma but it remains unclear whether Mdivi-1 can attenuate early brain injury after subarachnoid hemorrhage (SAH). We thus investigated the therapeutic effect of Mdivi-1 on early brain injury following SAH. Rats were randomly divided into four groups: sham; SAH; SAH + vehicle; and SAH + Mdivi-1. The SAH model was induced by standard intravascular perforation and all of the rats were subsequently sacrificed 24 h after SAH. Mdivi-1 (1.2 mg/kg) was administered to rats 30 min after SAH. We found that Mdivi-1 markedly improved neurologic deficits, alleviated brain edema and BBB permeability, and attenuated apoptotic cell death. Mdivi-1 also significantly reduced the expression of cleaved caspase-3, Drp1 and p-Drp1, attenuated the release of Cytochrome C from mitochondria, inhibited excessive mitochondrial fission, and restored the ultra-structure of mitochondria. Furthermore, Mdivi-1 reduced levels of MDA, 3-NT, and 8-OHdG, and improved SOD activity. Taken together, our data suggest that Mdivi-1 exerts neuroprotective effects against cell death induced by SAH and the underlying mechanism may be inhibition of Drp1-activated mitochondrial fission and oxidative stress.

Hyperperfusion syndrome (HPS) is a rare but potentially devastating postoperative complication developing after endarterectomy and carotid stenting. Limited information is available about this complication. The aim of this study was to assess the incidence of HPS and risk factors leading to its development. We retrospectively reviewed 178 consecutive cases of patients who underwent stenting of intracranial artery revascularization. We analyzed the association between HPS and patient's age, collateral vascular supply of the lesion, the interval between operation and the last occurrence of ischemic symptom, adequacy of blood pressure control after the operation, and other risk factors such as diabetes, smoking, hypertension, and gender. Of 178 included patients, we found HPS in six cases (3.4%). Failure to strictly control postoperative blood pressure, a less than 3-week long interval between operation and the last occurrence of ischemic symptom, and poor collateral circulation were significantly associated with the development of HPS. The aforementioned factors are predictors for HPS. We argue that nitroprusside should not be used to control blood pressure after the operation because its use permits considerable blood pressure fluctuations.