Association of greenspace with hypertension in adult: a systematic review and meta-analysis of epidemiological studies.

BACKGROUND: Several studies have investigated the relationship of greenspace with blood pressure (BP) and hypertension, but the results were inconsistent. We aimed to assess the relationship of greenspace with BP/hypertension. METHODS: We searched PubMed, Embase and Web of Science on greenspace and BP/hypertension published before 5 April 2023. The methodological quality and risk of bias were evaluated. RESULTS: Twenty-seven articles were included. Our results suggested that higher normalized difference vegetation index (NDVI) was associated with lower odds of hypertension and levels of SBP [for every 10% increase of NDVI 500-m and NDVI 1000-m, the ORs were 0.95 (95% CI: 0.90-0.99) and 0.95 (95% CI: 0.90-0.99), the ꞵwas -1.32 (95% CI: -2.18, -0.45) and -1.41 (95% CI: -2.57, -0.25), respectively]. CONCLUSION: This study indicated that higher exposure to greenspace might be associated with lower levels of BP and risk of hypertension. Increase green spaces should be regarded as an important public health intervention..

Effect of flavonoid intake on circulating levels of adiponectin and leptin: A systematic review and meta-analysis of randomized controlled clinical trials.

This meta-analysis of randomized controlled trials (RCTs) was conducted to explore the effects of flavonoid intake on adiponectin and leptin levels. The PubMed, EMBASE, and Cochrane Library databases were searched on March 1, 2021. Random-effects, subgroup, sensitivity, and meta-regression analyses were conducted on 40 publications. Flavonoid intake significantly increased circulating adiponectin (0.54 µg/ml, 95% CI [0.20, 0.88], p = .002; I2  = 86.4%) and significantly reduced leptin levels (weighted mean difference: -0.79 ng/ml, 95% CI [-1.33, -0.25], p = .004; I2  = 87.7%). Subgroup analysis demonstrated that flavonoid intervention produced a significant elevation in adiponectin levels only in studies that lasted more than 12 weeks, conducted in Asian regions, were parallel-designed, involved obese or overweight participants and participants with type 2 diabetes mellitus (T2DM) or cardiovascular diseases, used tea catechins, and used a dietary supplement intervention. A significantly negative effect on leptin levels was observed in studies conducted in Asian countries, with healthy participants and participants with T2DM, used whole food interventions, and involved participants with lower baseline leptin levels. In conclusion, flavonoid intake significantly increased circulating adiponectin and decreased leptin levels; however, study heterogeneity was very high. Future well-designed trials are required to address heterogeneous study designs and clarify the efficacy of plants in regulating adiponectin and leptin levels.

Association of physical activity with chronic kidney disease: a systematic review and dose-response meta-analysis.

BACKGROUND: The relationship between physical activity (PA) and chronic kidney disease (CKD) risk was inconsistent. We therefore conducted a systematic review and dose-response meta-analysis to comprehensively evaluate the association of PA and CKD. RESULTS: A total of 14 studies from 13 articles with 353,975 participants were included. By comparing the highest vs. the lowest level of PA, we found that PA was inversely associated with CKD risk (odds ratio [OR] = 0.94, 95% confidence interval [CI] = 0.91-0.98). Seven studies from 6 articles were included in dose-response analysis. Restricted cubic splines showed no evidence of a nonlinear dose-response relationship of PA and CKD risk (Pnonlinearity = 0.135). The risk of CKD was reduced by 2% (OR = 0.98, 95% CI = 0.96-1.00) with each 10 metabolic equivalent h/week increment of PA. CONCLUSIONS: The findings demonstrated that the higher level of PA might have a protective effect against the risk of CKD. METHODS: Electronic databases PubMed and Embase were searched up to March 11, 2020. Observational studies investigated the relationship between PA and CKD risk with estimated effects (relative risk, hazard ratio, or OR) with 95 % CI among adults were included.

Mild-to-moderate iodine deficiency in a sample of pregnant women and salt iodine concentration from Zhejiang province, China.

Since 2011, Zhejiang province has eliminated iodine deficiency disorders (IDD) in its populations. Following this achievement, a new revised iodine concentration in iodised salt was implemented in Zhejiang in 2012. However, the re-emergence of iodine deficiency has been reported in pregnant women. Therefore, the aim of this study was to assess household salt iodine concentration and iodine status of pregnant women in Zhejiang province, China. We conducted a cross-sectional study between April 2018 and August 2018 in Quzhou, Zhejiang province. Pregnant women aged ≥ 18 years who did not have a history of thyroid disease were recruited into the study. They were asked to complete socio-demographic questionnaires including a food frequency questionnaire (FFQ). In addition, a spot urine sample and a household table salt sample were also provided by each participant. A total of 625 pregnant women agreed to participate. The overall median urinary iodine concentration (UIC) was 130 µg/L, indicating mild-to-moderate iodine deficiency in pregnant women. The coverage of iodised salt was 85.2%, and of these, the rate of adequately iodised salt was 98.1%. In conclusion, our results confirmed the re-emergence of iodine deficiency in pregnant women as reported by other studies conducted in Zhejiang province. Therefore, urgent public health actions are needed to improve iodine status of pregnant women in order to prevent the adverse consequences of IDD on the neurodevelopment of foetus.

Association Between Folate and Health Outcomes: An Umbrella Review of Meta-Analyses.

Background: There is no study that has systematically investigated the breadth and validity of the associations of folate and multiple health outcomes. We aimed to evaluate the quantity, validity, and credibility of evidence regarding associations between folate and multiple health outcomes by using umbrella review of meta-analysis. Methods: We searched the MEDLINE, EMBASE, and Cochrane Library databases from inception to May 20, 2018, to identify potential meta-analyses that examined the association of folate with any health outcome. For each included meta-analysis, we estimated the summary effect size and their 95% confidence interval using the DerSimonian and Laird random-effects model. We used the AMSTAR 2 (A Measurement Tool to Assess Systematic Reviews) to assess methodological quality and the GRADE (Grading of Recommendations, Assessment, Development, and Evaluation working group classification) to assess the quality of evidence for each outcome included in the umbrella review. Results: Overall, 108 articles reporting 133 meta-analyses of observational studies and 154 meta-analyses of randomized controlled trials (RCTs) were included in the study. Among them, 108 unique exposure-outcome-population triplets (referred to as unique meta-analyses hereafter) of RCTs and 87 unique meta-analyses of observational studies were reanalyzed. Beneficial effects of folate were observed in the all-cause mortality rate and in a number of chronic diseases, including several birth/pregnancy outcomes, several cancers, cardiovascular disease and metabolic-related outcomes, neurological conditions, and several other diseases. However, adverse effects of folate were observed for prostate cancer, colorectal adenomatous lesions, asthma or wheezing, and wheezing as an isolated symptom and depression. Conclusions: Current evidence allows for the conclusion that folate is associated with decreased risk of all-cause mortality and a wide range of chronic diseases. However, folate may be associated with an increased risk of prostate cancer. Further research is warranted to improve the certainty of the estimates.

Temporal trends in normal weight central obesity and its associations with cardiometabolic risk among Chinese adults.

Normal weight central obesity (NWCO), a distinct phenotype of obesity that is associated with a higher risk of cardiometabolic dysregulation, has received growing attention in the scientific literature. In this study, we aimed to report the prevalence of NWCO in the general Chinese adults and its secular trend from 1993 to 2011. The comorbid cardiometabolic risk of NWCO was also explored. Data from the China Health and Nutrition Survey (CHNS) 1993-2011 were obtained. NWCO was defined as the combination of a BMI of 18.5-23.9 kg/m2 and 1) a waist circumference (WC) of >85 cm in males or >80 cm in females (NWCO by WC); 2) a waist to height ratio (WHtR) of ≥0.5 (NWCO by WHtR); 3) a waist to hip ratio (WHR) of ≥0.9 in males or ≥0.85 in females (NWCO by WHR). We assessed the trend of NWCO prevalence with the generalized estimating equation method. The demographic, socioeconomic, geographic, behavioural and cardiometabolic predictors of NWCO were explored with multivariable logistic regression. From 1993 to 2011, the age-standardized prevalence of NWCO by WC increased from 6.65% (95% CI: 6.09-7.26) to 13.24% (95% CI: 12.58-13.93), and that of NWCO by WHtR and NWCO by WHR rose from 13.18% (95% CI: 12.41-13.98) to 17.06% (95% CI: 16.35-17.79) and from 16.14% (95% CI: 15.3-17.01) to 19.04% (95% CI: 18.25-19.85) respectively. The associated cardiometabolic factors of NWCO (by WC, WHtR and WHR) were hypertension, diabetes, insulin resistance, decreased insulin sensitivity, low high-density lipoprotein and elevated triglyceride. Moreover, NWCO by WC and NWCO by WHtR were associated with a decreased risk of impaired insulin secretion, and NWCO by WC was additionally linked to elevated total cholesterol. The prevalence of NWCO in the general Chinese adults increased significantly from 1993 to 2011. Effective strategies are needed to combat this epidemic and reduce its deleterious health outcomes.

Effects of green tea polyphenols on trace metals level of rats on food restriction and high-fat diet.

Little evidence showed the interplay between tea and diet in the regulation of trace metal. Here, we examined the effects of green tea polyphenols (GTPs) on the level of trace elements (TEs) in rats on food restriction or high-fat diet. Thirty-six rats (Wistar, male) were randomly divided into 6 groups and fed on standard diet, food restriction and high-fat diet with or without GTPs (200 mg/kg bw/day) supplementation, respectively. Levels of vanadium (V), manganese (Mn), iron (Fe), copper (Cu), zinc (Zn), selenium (Se), molybdenum (Mo) and cobalt (Co) in feed, whole blood, femur and urine were measured by inductively coupled plasma mass spectrometry (ICP-MS). Blood glucose, total cholesterol (TC), triglycerides (TG), high and low density lipoprotein-cholesterol (LDL-C, HDL-C) in serum were determined. Decreased daily intakes of TEs were observed in rats on food restriction and high-fat diet. Decreased whole blood level of Zn, femur level of Co and increase urinary excretion of Se were observed in rats fed on high-fat diet. GTPs altered the whole blood level of several TEs in rats on food restriction (V, Zn, Co) or high-fat diet (V, Se), respectively, but not in rats fed on standard diet. The level of several TEs in femur and the daily urinary excretion of V and Mo were altered by GTPs in rats on all of the three diets. In addition, rats fed on high-fat diet developed dyslipidemia, which was ameliorated by GTPs. The data indicated that diet status played a role in the effects of GTPs on TEs and lipid metabolism, and trace elements may play a role in the modulation of lipid metabolic disturbances by high-fat diet and GTPs.

Green Tea Polyphenols Ameliorate the Early Renal Damage Induced by a High-Fat Diet via Ketogenesis/SIRT3 Pathway.

SCOPE: Several reports in the literature have suggested the renoprotective effects of ketone bodies and green tea polyphenols (GTPs). Our previous study found that GTP consumption could elevate the renal expression of the ketogenic rate-limiting enzyme, which was decreased by a high-fat diet (HFD) in rats. Here, we investigated whether ketogenesis can mediate renoprotection by GTPs against an HFD. METHODS AND RESULTS: Wistar rats were fed a standard or HFD with or without GTPs for 18 weeks. The renal oxidative stress level, kidney function, renal expression, and activity levels of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2) and sirtuin 3(SIRT3) were detected. The increased renal oxidative stress and the loss of renal function induced by the HFD were ameliorated by GTPs. Renal ketogenesis and SIRT3 expression and activity levels, which were reduced by the HFD, were restored by GTPs. In vitro, HEK293 cells were transfected with the eukaryotic expression plasmid pcDNA HMGCS2. GTP treatment could upregulate HMGCS2 and SIRT3 expression. Although SIRT3 expression was not affected by HMGCS2 transfection, the 4-hydroxy-2-nonenal (4-HNE) level and the acetyl-MnSOD (K122)/MnSOD ratio were reduced in HMGCS2-transfected cells in the context of H2O2. CONCLUSION: The ketogenesis/SIRT3 pathway mediates the renoprotection of GTPs against the oxidative stress induced by an HFD.

Resveratrol and caloric restriction prevent hepatic steatosis by regulating SIRT1-autophagy pathway and alleviating endoplasmic reticulum stress in high-fat diet-fed rats.

BACKGROUND: Studies have demonstrated that resveratrol (a natural polyphenol) and caloric restriction activate Sirtuin-1 (SIRT1) and induce autophagy. Furthermore, autophagy is induced by the SIRT1-FoxO signaling pathway and was recently shown to be a critical protective mechanism against non-alcoholic fatty liver disease (NAFLD) development. We aimed to compare the effects of resveratrol and caloric restriction on hepatic lipid metabolism and elucidate the mechanism by which resveratrol supplementation and caloric restriction alleviate hepatosteatosis by examining the molecular interplay between SIRT1 and autophagy. METHODS AND RESULTS: Eight-week-old male Wistar rats (40) were divided into four groups: the STD group, which was fed a standard chow diet; the HFD group, which was fed a high-fat diet; HFD-RES group, which was fed a high-fat diet plus resveratrol (200 mg/kg.bw); and the HFD-CR group, which was fed a high-fat diet in portions containing 70% of the mean intake of the HFD group rats. The groups were maintained for 18 weeks. Metabolic parameters, Oil Red O and hematoxylin-eosin staining of the liver, and the mRNA and protein expression of SIRT1, autophagy markers and endoplasmic reticulum(ER) stress-associated genes in the liver were assessed after the 18-week treatment. We found that resveratrol (200 mg/kg bw) and caloric restriction (30%) partially prevented hepatic steatosis and hepatocyte ballooning, increased the expression of SIRT1 and autophagy markers while decreasing ER stress markers in the liver and alleviated lipid metabolism disorder. Moreover, caloric restriction provided superior protection against HFD-induced hepatic fatty accumulation compared with resveratrol and the effects were associated with decreased total energy intake and body weight. CONCLUSION: We conclude that the SIRT1-autophagy pathway and decreased ER stress are universally required for the protective effects of moderate caloric restriction (30%) and resveratrol (a pharmacological SIRT1 activator) supplementation against HFD-induced hepatic steatosis.

Effect of TCDD on the fate of epithelial cells isolated from human fetal palatal shelves (hFPECs).

Cleft palate is caused by the failure of palatal midline epithelial cells to disintegrate, which is necessary for palatal mesenchymal confluence. Although 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure is linked to cleft palate at a high rate, the mechanism remains to be elucidated. The present study was designed to determine the effects of TCDD on the fate of epithelial cell isolated from human fetal palatal shelves (hFPECs). We demonstrate that TCDD increased cell proliferation and promoted the progression of cells from G1 to S phase as well as increased the number of cells entering the G2/M phase. We found that TCDD has no measurable effect on apoptosis of hFPECs. The protein level assays revealed that TCDD increased cyclin-dependent kinases 4 (cdk4), cyclin D1, cyclin E and p21 (Waf1/Cip1) but not cdk2, bcl-2, cyclin B1 and cyclin A. Furthermore, TCDD activated PI3K/AKT signaling, and the PI3K inhibitor, LY294002, partially abrogated TCDD-induced cell proliferation and gene modulations. TCDD treatment increased CYP1A1 mRNA and protein levels, which indicated the activation of AhR signaling. Knockdown of the AhR with siRNA suppressed TCDD-induced cell proliferation and PI3K/AKT signaling activation. Taken together, these data demonstrated that TCDD is able to promote growth of hFPECs through AhR-dependent activation of the PI3K/AKT pathway, which may account for the underlying mechanism by which TCDD causes a failure of palatal fusion.

TCDD promoted EMT of hFPECs via AhR, which involved the activation of EGFR/ERK signaling.

One critical step of second palatal fusion is the newly formed medial epithelia seam (MES) disintegration, which involves apoptosis, epithelial to mesenchymal transition (EMT), and cell migration. Although the environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces cleft palate at high rates, little is known about the effects of TCDD exposure on the fate of palatal epithelial cells. By using primary epithelial cells isolated from human fetal palatal shelves (hFPECs), we show that TCDD increased cell proliferation and EMT, as demonstrated by increased the epithelial markers (E-cadherin and cytokeratin14) and enhanced the mesenchymal markers (vimentin and fibronectin), but had no effect on cell migration and apoptosis. TCDD exposure led to a dose-dependent increase in Slug protein expression. Coimmunoprecipitation revealed that TCDD promoted AhR to form a protein complex with Slug. ChIP assay confirmed that TCDD exposure recruited AhR to the xenobiotic responsive element of Slug promoter. Knockdown of AhR by siRNA remarkably weakened TCDD-induced binding of AhR to the XRE promoter of slug, thereby suppressed TCDD-induced vimentin. Further experiment showed that TCDD stimulated EGFR phosphorylation did not influence the TGFß3/Smad signaling; whereas TCDD increased phosphorylation of ERK1/2 and p38 with no effect on activation of JNK. By using varieties of inhibitors, we confirmed that TCDD promoted proliferation and EMT of hFPECs via activation of EGFR/ERK pathway. These data make a novel contribution to the molecular mechanism of cleft palate by TCDD.