Background Chronic liver disease poses an escalating health challenge on a global scale. It has been suggested that prolonged exposure to heavy metals could potentially contribute to the development of non-alcoholic fatty liver disease (NAFLD). Our study aimed to assess the correlation between urinary levels of specific heavy metals, including Ba, Cd, Co, Cs, Hg, Mo, Pb, Sb, Sn, Ti, and Ur, and the occurrence of NAFLD and advanced liver fibrosis within the general population of the United States. Methods In our study, we conducted a thorough analysis using data from the NHANES spanning from 2013 to 2018. To examine the correlation between urinary heavy metal concentration and the prevalence of NAFLD and advanced liver fibrosis, we employed a multivariable analysis that accounted for various factors such as sociodemographic characteristics, lifestyle factors, hypertension, and T2DM. This allowed us to control for potential confounding variables and obtain reliable findings regarding the association between urinary heavy metal concentration and the occurrence of NAFLD and advanced liver fibrosis. Results We employed multiple logistic regression models to examine the data, and the results revealed noteworthy findings. Higher levels of urinary Ba, Cd, Co, Pb, Sb, Sn, Tu, and Ur exhibited a significant positive association with NAFLD. Additionally, as the concentration of Cd, Pb, Sb, and Sn increased in urine, the likelihood of advanced liver fibrosis also significantly increased. These findings underscore the significant positive associations between the levels of specific heavy metals in urine and both NAFLD and advanced liver fibrosis. Conclusion The findings of this study suggest a significant association between elevated urinary Ba, Cd, Co, Pb, Sb, Sn, Tu, Ur concentration and NAFLD while a significant correlation was also found between higher urinary levels of Cd, Pb, Sb, Sn and advanced liver fibrosis.
Background: Nonalcoholic fatty liver disease (NAFLD) is the highest incidence of chronic liver disease worldwide, seriously endangering human health, and its pathogenesis is still unclear. In the recent years, increasing evidence has shown that intestinal flora plays an important role in the occurrence and development of NAFLD. Synbiotics can alter gut microbiota and may be a treatment option for NAFLD in the future. Objectives: To systematically investigate the therapeutic effect of synbiotic supplementation on NAFLD patients. Design: A systematic review and meta-analysis were conducted. Data sources and methods: We conducted a search on four databases (PubMed, Embase, Cochrane Library, and Web of Science) to identify relevant studies. Eligible studies were then screened, and data from the included studies were extracted, combined, and analyzed. Result: This study analyzed 10 randomized controlled trials involving 634 patients with NAFLD. The results showed that synbiotic supplementation could significantly reduce the level of alanine aminotransferase (mean difference (MD) = −8.80; (95% CI [−13.06, −4.53]), p < 0.0001), aspartate aminotransferase (MD = −9.48; 95% CI [−12.54, −6.43], p < 0.0001), and γ-glutamyl transferase (MD = −12.55; 95% CI [−19.40, −5.69], p = 0.0003) in NAFLD patients. In the field of metabolism, synbiotic supplementation could significantly reduce the level of total cholesterol (MD = −11.93; 95% CI [−20.43, −3.42], p = 0.006) and low-density lipoprotein cholesterol (MD = −16.2; 95% CI [−19.79, −12.60], p < 0.0001) and increase the level of high-density lipoprotein cholesterol (MD = 1.56; 95% CI [0.43, 2.68], p = 0.007) in NAFLD patients. In addition, synbiotic supplementation could significantly reduce liver stiffness measurement indicator (MD = −1.09; 95% CI [−1.87, −0.30], p = 0.006) and controlled attenuation parameter indicator (MD = −37.04; 95% CI [−56.78, −17.30], p = 0.0002) in NAFLD patients. Conclusion: Based on the current evidence, synbiotic supplementation can improve liver function, adjust lipid metabolism, and reduce the degree of liver fibrosis in patients with NAFLD, but these effects need to be confirmed by further studies.
Polycystic ovary syndrome (PCOS) is one of the most common hormonal disorders among premenopausal women. PCOS is accompanied by many other reproductive, endocrinal, and metabolic disorders thus amassing the difficulties encountered by the women affected. However, there is limited information on its molecular etiology. Synoviolin (SYVN1) is an E3 ubiquitin ligase that is thought to participate in the pathology of PCOS. However, the expression and function of SYVN1 in PCOS are unknown. In this study, we found that downregulation of SYVN1 expression was followed by increased apoptosis in the granulosa cells (GCs) of patients with PCOS. Subsequent in vitro experiments indicated that the overexpression of SYVN1 inhibited apoptosis and mitochondrial fission. Furthermore, using immunoprecipitation and western blotting, we identified that SYVN1 promoted the degradation of Drp1 via the proteasome-dependent pathway. Additionally, we generated a PCOS model in female Sprague Dawley rats and treated them with an SYVN1 inhibitor, LS-102. We observed that the inhibition of SYVN1 increased Drp1 levels and exacerbated the degeneration of GCs in the PCOS rat model. Finally, in vitro and in vivo experiments showed that SYVN1 inhibits apoptosis and mitochondrial fission by promoting Drp1 degradation in GCs. These results highlight the function of SYVN1 in PCOS and provide a potential target for the clinical treatment of PCOS.
Selection and peer-review under responsibility of the scientific committee of the 11th Int. Conf. on Applied Energy (ICAE2019).
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