PMID: 

J Nutr. 2019 Dec 20. Epub 2019 Dec 20. PMID: 31858105

Abstract Title: 

Niacin Ameliorates Hepatic Steatosis by Inhibiting De Novo Lipogenesis Via a GPR109A-Mediated PKC-ERK1/2-AMPK Signaling Pathway in C57BL/6 Mice Fed a High-Fat Diet.

Abstract: 

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hepatic de novo lipogenesis (DNL) has been suggested to contribute to the pathogenesis of NAFLD. Recent studies have demonstrated that niacin (NA) modulates hepatic DNL through GPR109A. However, the underlying mechanism remains largely unknown.OBJECTIVES: This study aims to elucidate the potential molecular mechanism by which GPR109A inhibits hepatic DNL.METHODS: C57BL/6 wild-type (WT) and Gpr109a knockout (KO) mice (male, 5 wk old) were fed a high-fat diet (60% energy from fat) firstly for 6 wk to generate a diet-induced obese model. Subsequently, they were randomly divided into 4 groups for the next 8-9 wk: WT mice with oral water [WT + vehile (VE)], WT mice with oral NA (50 mM, dissolved in water) (WT + NA), KO mice with oral water (KO + VE), and KO mice with oral NA (50 mM) (KO + NA). Mechanisms were examined in HepG2 cells. Body composition, liver histology, biomarkers of hepatic function, lipid accumulation, and lipid synthesis signals in HepG2 cells were measured.RESULTS: Upon activation, GPR109A apparently protected against obesity and hepatic steatosis (P 

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PMID: 

Arterioscler Thromb Vasc Biol. 2019 Sep ;39(9):1776-1786. Epub 2019 Jul 25. PMID: 31340670

Abstract Title: 

Diesel Exhaust Induces Mitochondrial Dysfunction, Hyperlipidemia, and Liver Steatosis.

Abstract: 

OBJECTIVE: Air pollution is associated with increased cardiovascular morbidity and mortality, as well as dyslipidemia and metabolic syndrome. Our goal was to dissect the mechanisms involved. Approach and Results: We assessed the effects of exposure to air pollution on lipid metabolism in mice through assessment of plasma lipids and lipoproteins, oxidized fatty acids 9-HODE (9-hydroxyoctadecadienoic) and 13-HODE (13-hydroxyoctadecadienoic), lipid, and carbohydrate metabolism. Findings were corroborated, and mechanisms were further assessed in HepG2 hepatocytes in culture. ApoE knockout mice exposed to inhaled diesel exhaust (DE, 6 h/d, 5 days/wk for 16 weeks) exhibited elevated plasma cholesterol and triglyceride levels, increased hepatic triglyceride content, and higher hepatic levels of 9-HODE and 13-HODE, as compared to control mice exposed to filtered air. A direct effect of DE exposure on hepatocytes was demonstrated by treatment of HepG2 cells with a methanol extract of DE particles followed by loading with oleic acid. As observed in vivo, this led to increased triglyceride content and significant downregulation of ACAD9 mRNA expression. Treatment of HepG2 cells with DE particles and oleic acid did not alter de novo lipogenesis but inhibited total, mitochondrial, and ATP-linked oxygen consumption rate, indicative of mitochondrial dysfunction. Treatment of isolated mitochondria, prepared from mouse liver, with DE particles and oleic acid also inhibited mitochondrial complex activity andβ-oxidation.CONCLUSIONS: DE exposure leads to dyslipidemia and liver steatosis in ApoE knockout mice, likely due to mitochondrial dysfunction and decreased lipid catabolism.

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PMID: 

Gastroenterol Res Pract. 2019 ;2019:1484598. Epub 2019 Dec 11. PMID: 31885541

Abstract Title: 

Systematic Review with Meta-Analysis: The Effects of Probiotics in Nonalcoholic Fatty Liver Disease.

Abstract: 

Background and Aims: Probiotics was considered as a potential therapy for nonalcoholic fatty liver disease (NAFLD) without approval and comprehensive assessment in recent years, which call for a meta-analysis.Methods: We performed electronic and manual searches including English and Chinese databases published before April 2019, with the use of mesh term and free text of"nonalcoholic fatty liver disease"and"probiotics."Clinical trials evaluating the efficacy of probiotic therapy in NAFLD patients were included according to the eligibility criteria. With the use of random effects models, clinical outcomes were presented as weighted mean difference (WMD) with 95% confidence interval (CI), while heterogeneity and meta-regression were also assessed.Results: 28 clinical trials enrolling 1555 criterion proven NAFLD patients with the use of probiotics from 4 to 28 weeks were included. Overall, probiotic therapy had beneficial effects on body mass index (WMD: -1.46, 95% CI: [-2.44, -0.48]), alanine aminotransferase (WMD: -13.40, 95% CI: [-17.03, -9.77]), aspartate transaminase (WMD: -13.54, 95% CI: [-17.86, -9.22]), gamma-glutamyl transpeptidase (WMD: -9.88, 95% CI: [-17.77, -1.99]), insulin (WMD: -1.32, 95% CI: [-2.43, -0.21]), homeostasis model assessment-insulin resistance (WMD: -0.42, 95% CI: [-0.73, -0.12]), and total cholesterol (WMD: -15.38, 95% CI: [-26.50, -4.25]), but not in fasting blood sugar, lipid profiles, or tumor necrosis factor-alpha.Conclusion: The systematic review and meta-analysis support that probiotics are superior to placebo in NAFLD patients and could be utilized as a common complementary therapeutic approach.

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PMID: 

Med Oral Patol Oral Cir Bucal. 2020 Jan 1. Epub 2020 Jan 1. PMID: 31893476

Abstract Title: 

Effect of probiotics as a complement to non-surgical periodontal therapy in chronic periodontitis: a systematic review.

Abstract: 

BACKGROUND: To improve the results of the classic periodontal treatment, probiotics have been suggested recently to decrease the number of bacteria and the expression of mediators of inflammation. This systematic review aimed to assess the literature for the effectiveness of different probiotic strains as adjuvants to non-surgical periodontal therapy.MATERIAL AND METHODS: The electronic database of MEDLINE (via Pubmed) was searched up to December 2017 for randomised clinical trials in English comparing non-surgical periodontal treatment and probiotics versus periodontal treatment and placebo. The primary outcome investigated was reduction in pocket probing depth. Secondary outcomes were bleeding on probing, plaque index reduction and bacteria counts.RESULTS: Nine trials were included. A narrative data synthesis did not result in any major improvement of overall pocket probing depth but moderate pockets from 4 to 6 mm showed larger reductions in study groups, which could decrease the need for surgery. Sites with bleeding on probing and presence of plaque decreased after treatment. For periimplant mucositis, there was a small tendency to better results in the study group.CONCLUSIONS: With the available data, it is concluded that probiotics may provide an additional benefit to manual debridement in chronic periodontitis. More studies are required on dose, route of administration and strains of probiotics used.

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PMID: 

Adv Sci (Weinh). 2019 Sep 18 ;6(18):1900972. Epub 2019 Jul 22. PMID: 31559135

Abstract Title: 

Probiotics Ameliorate Colon Epithelial Injury Induced by Ambient Ultrafine Particles Exposure.

Abstract: 

Diesel exhaust particles (DEPs) are common airborne ultrafine particles (UFPs); however, few studies have examined their effects on the gastrointestinal tract. To investigate the interaction of gut microbiota and DEPs-induced colonic injury, adult C57BL/6 mice are kept in whole-body inhalation chambers and exposed to filtered room air (FRA) or DEPs (300µg m) 1 h per day for 28 consecutive days. DEPs exposure results in colon epithelial injury with inflammatory cell infiltration and mucus depletion. Abundance ofin murine feces is transiently increased following 7-day DEPs exposure and then decreased until the end of 28-day exposure. A reduction of the colonic mucus layer thickness is observed in mice receiving gut microbiota from DEPs-exposed mice. Mechanistically, RNA-sequencing suggests disruption of the nitrogen metabolism pathway in DEPs-exposed NCM460 cells. Upregulation of carbonic anhydrase 9 (CA9) expression levels is observed in epithelia following DEPs exposure both in vivo and in vitro. Oral administration of probiotics protects the mice against DEPS-induced colon epithelial injury. The results strongly suggest the involvement of gut microbiota in response to DEPs exposure and subsequently epithelial injury in vivo. Supplementation with probiotic may be a potential way to protect against UFPs-induced colon epithelial injury.

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PMID: 

Int J Mol Sci. 2019 Nov 9 ;20(22). Epub 2019 Nov 9. PMID: 31717476

Abstract Title: 

Diesel Exhaust Particle Exposure Compromises Alveolar Macrophage Mitochondrial Bioenergetics.

Abstract: 

Diesel exhaust particles (DEPs) are known pathogenic pollutants that constitute a significant quantity of air pollution. Given the ubiquitous presence of macrophages throughout the body, including the lungs, as well as their critical role in tissue and organismal metabolic function, we sought to determine the effect of DEP exposure on macrophage mitochondrial function. Following daily DEP exposure in mice, pulmonary macrophages were isolated for mitochondrial analyses, revealing reduced respiration rates and dramatically elevated HOlevels. Serum ceramides and inflammatory cytokines were increased. To determine the degree to which the changes in mitochondrial function in macrophages were not dependent on any cross-cell communication, primary pulmonary murine macrophages were used to replicate the DEP exposure in a cell culture model. We observed similar changes as seen in pulmonary macrophages, namely diminished mitochondrial respiration, but increased HOproduction. Interestingly, when treated with myriocin to inhibit ceramide biosynthesis, these DEP-induced mitochondrial changes were mitigated. Altogether, these data suggest that DEP exposure may compromise macrophage mitochondrial and whole-body function via pathologic alterations in macrophage ceramide metabolism.

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PMID: 

Mediators Inflamm. 2019 ;2019:3437104. Epub 2019 Nov 15. PMID: 31827376

Abstract Title: 

Involvement of Oxidative Stress and the Epidermal Growth Factor Receptor in Diesel Exhaust Particle-Induced Expression of Inflammatory Mediators in Human Mononuclear Cells.

Abstract: 

Exposure to diesel exhaust particles (DEPs) has been associated with increased incidence of cardiopulmonary diseases. This study is aimed at examining the proinflammatory effects of DEP on primary human peripheral blood mononuclear cells (PBMC) and the underlying mechanisms using a human mononuclear cell line, THP-1. DEPs were incubated with the PBMC and THP-1 cells for 24 h, respectively. The supernatants were collected and subjected to measurement of proinflammatory mediators including interleukin 8 (IL-8) or tumor necrosis factor(TNF) by ELISA. Levels of reactive oxygen species (ROS) were determined using flow cytometry. Phosphorylation of the epidermal growth factor receptor (EGFR) was examined with immunoblotting. Exposure to DEP induced a concentration-dependent increase in the expression of IL-8 and TNFin the PBMC and THP-1 cells. Further mechanistic studies with THP-1 cells indicated that DEP stimulation increased intracellular levels of ROS, an indicator of oxidative stress, and phosphorylation of the EGFR, indicative of EGFR activation. Pretreatment of THP-1 cells with the antioxidant N-acetyl-L-cysteine (NAC) markedly blunted DEP-induced EGFR phosphorylation, indicating that oxidative stress was involved in DEP-induced EGFR activation. Furthermore, the pretreatment of THP-1 cells with either NAC or a selective EGFR inhibitor significantly blocked DEP-induced IL-8 expression, implying that oxidative stress and subsequent EGFR activation mediated DEP-induced inflammatory response. In summary, DEP stimulation increases the expression of proinflammatory mediators in human mononuclear cells, which is regulated by oxidative stress-EGFR signaling pathway.

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PMID: 

Environ Health. 2019 10 10 ;18(1):84. Epub 2019 Oct 10. PMID: 31601202

Abstract Title: 

Low concentrations of fine particle air pollution and mortality in the Canadian Community Health Survey cohort.

Abstract: 

BACKGROUND: Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM). In general, cohort studies of mortality and outdoor PMconcentrations have limited information on individuals exposed to low levels of PMas well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PMexposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM.METHODS: Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PMexposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PMconcentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates.RESULTS: In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PMconcentrations were low (i.e. 5.9 μg/m, s.d. 2.0) and each 10 μg/mincrease in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04-1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/musing a shape constrained health impact function. Mortality risks associated with exposure to PMwere increased for males, those under age 65, and non-immigrants. Hazard ratios for PMand mortality were attenuated when gaseous pollutants were included in models.CONCLUSIONS: Outdoor PMconcentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PMconcentrations.

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PMID: 

Int J Hyg Environ Health. 2020 01 ;223(1):171-178. Epub 2019 Sep 20. PMID: 31548162

Abstract Title: 

Association between ambient particulate matter and hospitalization for anxiety in China: A multicity case-crossover study.

Abstract: 

AIMS: Evidence concerning the impact of ambient particulate matter (PM) on mental health is just emerging and inconsistent. Air pollution with high PM levels has been frequently reported in China, however, no Chinese study has determined the association between PM exposures and anxiety hospitalizations. We examined the potential association between PM concentrations and anxiety admissions in 26 Chinese cities from January 2014 to December 2015.
METHODS: A time-stratified case-crossover design was employed in the study. Anxiety hospitalizations were identified according to ICD-10 from the electronic hospitalization summary reports system in China. Conditional logistic regression was applied to estimate the relation between PM levels and anxiety admissions, stratified by age and sex.
RESULTS: Positive associations between PM/PMand admitted anxiety cases were observed. PMhad the largest effect estimate at lag 5 days, with a per 10 μg/mincrease corresponding to a 0.63% (95% CI, 0.26-1.00) increase in anxiety admissions. PM's largest effect estimate was observed at lag 3 days, increasing 0.37% (95% CI, 0.12-0.62) anxiety admissions per 10 μg/m. Females were more sensitive to PM/PMconcentrations than males, however, the effect modification by age was not significant. A marginally significant distinction in anxiety hospitalizations was found in patients with and without CVDs when they were exposed to PM.
CONCLUSIONS: Our findings indicate that short-term exposure to increased concentrations of PM/PMexacerbates risks of anxiety hospitalizations in 26 Chinese cities. We observed effect modification by sex, with significantly stronger associations in female patients. This study offers the promise that reducing PM air pollution could probably reduce the huge disease burden from anxiety disorders.

PMID: 

Chemosphere. 2019 Dec ;237:124510. Epub 2019 Aug 6. PMID: 31549641

Abstract Title: 

Short-term effects of ambient particulate matter on blood pressure among children and adolescents:A cross-sectional study in a city of Yangtze River delta, China.

Abstract: 

Several studies have demonstrated associations between short-term exposure to particulate matter (PM) and blood pressure (BP) among various adults groups, but evidence in children and adolescents is still rare. In 2016, a cross-sectional survey was conducted among 194 104 participants aged 6-17 years in Suzhou, China. Daily concentrations of particulate matters with an aerodynamic diameter of ≤10 μg/m(PM) and aerodynamic diameter≤2.5 μg/m(PM) on 0-6 days preceding BP examination were collected from nearby air monitoring stations. Using generalized linear mixed-effects models, short-term effects of PM on personal BP were estimated. A 10 μg/mincrement in the 0-6 day mean of PMwas significantly associated with elevation of 0.20 mmHg [95% confidence interval (95% CI) 0.16-0.23] in systolic BP (SBP), 0.49 mmHg (95% CI 0.45-0.53) in diastolic BP (DBP), respectively. Similarly, 0.14 mmHg (95% CI 0.12-0.16) higher SBP and 0.32 mmHg (95% CI 0.30-0.34) higher DBP were found for each 10 μg/mincrease in 0-6 day mean of PM. More apparent associations were observed in females than in males. Odds ratio (95%CI) of for PMexposure at 0-6 d mean was 1.06 (1.03-1.08) in females, while it was 1.01 (0.99-1.03) in males. Participants with young ages, underweight and obesity were also associated with increased susceptibility to PM-induced BP effects. Short-term exposure in PM was significantly associated with elevated BP in children, indicating a need to control PM levels and protect children from PM exposure in China.

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