Metabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association of gut microbiota with metabolic diseases. However, the effects of glucose-lowering agents on gut microbiota are poorly understood. Several studies revealed that these agents affect the composition and diversity of gut microbiota and consequently improve glucose metabolism and energy balance. Possible underlying mechanisms include affecting gene expression, lowering levels of inflammatory cytokines, and regulating the production of short-chain fatty acids. In addition, gut microbiota may alleviate adverse effects caused by glucose-lowering agents, and this can be especially beneficial in diabetic patients who experience severe gastrointestinal side effects and have to discontinue these agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus.
20(S)-Ginsenoside Rg3 (20(S)-Rg3) has been shown to induce apoptosis by interfering with several signaling pathways. Furthermore, it has been reported to have anticancer and antidiabetic effects. In order to detect the protective effect of 20(S)-Rg3 on diabetic kidney disease (DKD), diabetic rat models which were established by administering high-sugar, high-fat diet combined with intraperitoneal injection of streptozotocin (STZ), and age-matched wild-type (WT) rat were given 20(S)-Rg3 for 12 weeks, with three groups: control group (normal adult rats with saline), diabetic group (diabetic rats with saline), and 20(S)-Rg3 treatment group (diabetic rats with 20(S)-Rg3 (10 mg/kg body weight/day)). The biochemical indicators and the changes in glomerular basement membrane and mesangial matrix were detected. TUNEL staining was used to detect glomerular and renal tubular cell apoptosis. Immunohistochemical staining was used to detect the expression of fibrosis factors and inflammation factors in rat kidney tissues. Through periodic acid-Schiff staining, we observed that the change in renal histology was improved and renal tubular epithelial cell apoptosis decreased significantly by treatment with 20(S)-Rg3. Plus, the urine protein decreased in the rats with the 20(S)-Rg3 treatment. Fasting blood glucose, creatinine, total cholesterol, and triglyceride levels in the 20(S)-Rg3 treatment group were all lower than those in the diabetic group. Mechanistically, 20(S)-Rg3 dramatically downregulated the expression of TGF- β 1, NF- κ B65, and TNF- α in the kidney. These resulted in a significant prevention of renal damage from the inflammation. The results of the current study suggest that 20(S)-Rg3 could potentially be used as a novel treatment against DKD.
Insulin-like growth factor binding protein-2 (IGFBP-2) has been implicated in the etiology of insulin resistance. And previous studies have pointed that IGFBP-2 overexpression could prevent age-related hypertension. The present study was aimed to document the modulation of dual vascular actions of IGFBP-2 in human umbilical vein endothelial cells (HUVECs). HUVECs at passage 4-6 were cultured with either 20 μM hydrogen peroxide (H2O2) or 2mM glucosamine (GLU) to induce insulin resistance, which declined the expression of IGFBP-2 in HUVECs and resulted in endothelial nitric oxide (NO) and endothelin-1 (ET-1) production were reduced significantly compare to those control cells (p<0.01), the suppression of NO production was more notable. The insulin-induced phosphorylation of Akt at The3and endothelial NO synthase (eNOS) at Ser1177 were also slightly decreased in IGFBP-2 down-regulated HUVECS. Coherently, insulin-induced phosphorylated eNOS and extracellular signal-related kinase 1/2 (ERK1/2) were 3.5 (p<0.01) and 1.5 (p<0.05) folds increased by an overnight IGFBP-2 treatment, respectively. As the production of ET-1 was mediated by ERK1/2 and the secretion of NO was regulated by eNOS, we suspected that IGFBP-2 played an important role on endothelial diastolic and systolic function, may robustly improved vasodilation more than vasoconstriction in insulin resistant HUVECs. Disclosure Z. Li: None. Y. Lv: None. W. Guo: None. G. Wang: None.
A W-band sheet beam extended interaction klystron (SBEIK) with three five-gap cavities is designed and optimized in this paper. The cold-test simulation results shows that the stable $\mathbf{TM}_{\mathbf{11}}-\mathbf{2}\boldsymbol{\pi}$ operating mode is achieved at 93. 8GHz. The particle-in-cell (PIC) simulation results shows that the continuous wave output power of the EIK is 496.3W and an electronic efficiency is 3.19%, driven by a 14.1kV,1.2A sheet beam in a 0.5T magnetic field respectively.
Gut hormones are known to play an important role in long-term weight loss maintenance after bariatric surgery. However, the interplay between gut hormones and diet-induced weight changes remains unclear. Our aims were to evaluate the alterations of gut hormones in diet-induced weight loss, weight maintenance, and weight regain periods. Available studies were searched on MEDLINE, EMASE, ClinicalTrials.gov, the Cochrane Library, and Web of science from inception to October 2016. After selection, 16 studies with 656 participants were included. Based on current evidence, we found significant alterations of gut hormones induced by different diets. In weight-loss diets, decreased fasting total PYY, GLP-1, CCK, GIP, PP, and amylin along with increased ghrelin levels were observed in most studies. After weight loss, the persistent decreases of fasting total PYY and GLP-1 levels as well as increased appetite were reported, suggesting the profound impact of altered gut hormones on later weight regain after dietary intervention. The differences between diet-induced changes in gut hormones and other treatments such as bariatric surgery and exercise are also discussed in this review. Although significant alterations of gut hormones were found during weight changes, huge heterogeneity exists in methods and populations. More large-scale studies with elaborate design addressing the gut hormone alterations in dietary weight regulation are required in the future.
To investigate the effect of lipopolysaccharides(LPS) extracted from Porphyromonas endodontalis(P.e) on the expression of CD14 in osteoblast.Under the condition with or without serum, MC3T3-E1 cells were stimulated with 10 μg/mL P.e-LPS for 24 hours, then the expression of CD14 was measured using flow cytometry; the membrane CD14 mRNA was detected at different time point (0, 1, 3, 6, 12, 24 h) by RT-PCR. Statistical analysis was performed using two-sample t test, one-way ANOVA and Dunnett t test with SPSS13.0 software package.Flow cytometry showed that CD14 protein increased after the stimulation of P.e-LPS for 24 h, while the non-serum group demonstrated more increase; the membrane CD14 mRNA level was up-regulated by 10 μg/mL P.e-LPS at 1 hour, and reached the maximum at 3 h and declined after 6 h.P.e-LPS can induce the expression of CD14 in osteoblast MC3T3-E1, which indicates that P.e-LPS may play an important role in osteoblast through CD14.
Since December 2019, COVID-19 has aroused global attention. Studies show the link between obesity and severe outcome of influenza and COVID-19. Thus, we aimed to compare the impacts of obesity on the severity and mortality of influenza and COVID-19 by performing a meta-analysis. A systematic search was performed in MEDLINE, EMASE, ClinicalTrials.gov, and Web of Science from January 2009 to July 2020. The protocol was registered onto PROSPERO (CRD42020201461). After selection, 46 studies were included in this meta-analysis. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were analyzed. We found obesity was a risk factor for the severity and mortality of influenza (ORsevere outcome = 1.56, CI: 1.28-1.90; ORmortality = 1.99, CI: 1.15-3.46). For COVID-19, obesity was a significant risk factor only for severe outcome (OR = 2.07, CI: 1.53-2.81) but not for mortality (OR = 1.57, CI: 0.85-2.90). Compared with obesity, morbid obesity was linked with a higher risk for the severity and mortality of both influenza (OR = 1.40, CI: 1.10-1.79) and COVID-19 (OR = 3.76, CI: 2.67-5.28). Thus, obesity should be recommended as a risk factor for the prognosis assessment of COVID-19. Special monitoring and earlier treatment should be implemented in patients with obesity and COVID-19.
Introduction: The efficacy of myo-inositol supplementation to prevent gestational diabetes onset remains controversial. We conducted a systematic review and meta-analysis to explore the influence of myo-inositol supplementation on the incidence of gestational diabetes.Methods: We search PubMed, Embase, Web of science, EBSCO, and Cochrane Library databases through November 2017 for randomized controlled trials (RCTs) assessing the effect of myo-inositol supplementation on gestational diabetes onset. This meta-analysis is performed using the random-effect model.Results: Five randomized controlled trials (RCTs) are included in the meta-analysis. Compared with control group in pregnant women, myo-inositol supplementation is associated with significantly reduced incidence of gestational diabetes (risk ratio (RR) = 0.43; 95%CI = 0.21–0.89; p = .02), and preterm delivery (RR = 0.36; 95%CI = 0.17–0.73; p = .005), but has no substantial impact on 2-h glucose oral glucose tolerance test (OGTT) (mean difference (MD) = −6.90; 95%CI = −15.07 to 1.27; p = .10), gestational age at birth (MD = 0.74; 95%CI = −1.06 to 2.54; p = .42), birth weight (MD = −5.50; 95%CI = −116.99 to 105.99; p = .92), and macrosomia (RR = 0.65; 95%CI = 0.20–2.11; p = .47).Conclusions: Myo-inositol supplementation has some ability to reduce the incidence of gestational diabetes and preterm delivery in pregnant women.
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