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Although the relationship between socio‐economic status (SES) and prosocial practices has been extensively studied, little is known about the role that social capital plays in this relationship. This study examines the mediating effect of different forms of social capital, including informal neighbourhood capital, membership in voluntary associations, and professional connection, on the relationship between SES and prosocial practices. A total of 3,300 urban samples and 2,170 rural samples from the Chinese General Social Survey (CGSS) 2012 were selected to conduct two‐group structural equation modelling. Our results suggested that (a) all three forms of social capital mediated the effect of SES on donating, but only informal neighbourhood capital and membership mediated the effect of SES on volunteering, and (b) SES had a different relationship with social capital in urban China than in rural China. SES had a weak positive correlation with informal neighbourhood capital in rural areas but a negative one in urban areas. SES also had a stronger relationship with membership in voluntary associations in rural areas. Our analyses support the notion that higher SES promotes prosocial practices through social capital. [ABSTRACT FROM AUTHOR]

Objectives: This study investigates the impact of pension on depressive symptoms among Chinese older adults. Additional effort is made to test the mediating effect of multidimensional downward intergenerational support and the moderating effect of age on this relationship. Methods: A total of 1828 Chinese older community‐dwellers who met our inclusion criteria are drawn from the 2018 China Health and Retirement Longitudinal Study. Multivariate regression modeling is applied to analyze the effect of pensions on depressive symptoms of older adults. Additionally, bootstrap method with resampling strategies is used to estimate the mediating effect of three dimensions of downward intergenerational support (instrumental, emotional, and financial support). Further, Johnson‐Neyman technique is employed to analysis and visualize the moderating effect of age. Results: The findings reveal a significant inverse relationship between pension levels and depressive symptoms (B = −6.664, SE = 2.826, p < 0.05). The analysis shows that downward intergenerational emotional support (B = −0.195, Boot SE = 0.103, 95% Boot CI [−0.404, −0.003]) serves as a partial mediator in this relationship. Furthermore, the results highlight the moderating role of age in the linkage between pension and depressive symptoms (B = 0.065, SE = 0.039, p < 0.1). Discussion: This investigation is pioneering in simultaneously assessing the mediating role of multidimensional downward intergenerational support and the moderating effect of age in the context of pension and depressive symptoms. The study underscores the necessity of an interdisciplinary approach in devising comprehensive intervention strategies. These should encompass pension policy consultation, respite services, and other crucial elements aimed at mitigating the severity or reducing the risk of depressive symptoms among the older adults. Key points: We discovered a moderating effect of age on the relationship between pension benefits and depressive symptoms in older adults, and further elucidated this effect using the Johnson‐Neyman method.Concurrently, we employed bootstrapping methods to validate the mediating effect of downward intergenerational support between pension benefits and depressive symptoms in older adults. [ABSTRACT FROM AUTHOR]

Background Overproduction of reactive oxygen species is associated with the development of alcoholic liver disease ( ALD). Plant polyphenols have been used as dietary interventions for multiple diseases including ALD. The objective of this study was to determine whether dietary supplementation with fisetin, a novel flavonoid, exerts beneficial effect on alcohol-induced liver injury. Methods C57 BL/6J mice were pair-fed with the Lieber-DeCarli control or ethanol (EtOH) diet for 4 weeks with or without fisetin supplementation at 10 mg/kg/d. Results Alcohol feeding induced lipid accumulation in the liver and increased plasma alanine aminotransferase and aspartate aminotransferase activities, which were attenuated by fisetin supplementation. The EtOH concentrations in the plasma and liver were significantly elevated by alcohol exposure but were reduced by fisetin supplementation. Although fisetin did not affect the protein expression of alcohol metabolism enzymes, the aldehyde dehydrogenase activities were significantly increased by fisetin compared to the alcohol alone group. In addition, fisetin supplementation remarkably reduced hepatic NADPH oxidase 4 levels along with decreased plasma hydrogen peroxide and hepatic superoxide and 4-hydroxynonenal levels after alcohol exposure. Alcohol-induced apoptosis and up-regulation of Fas and cleaved caspase-3 in the liver were prevented by fisetin. Moreover, fisetin supplementation attenuated alcohol-induced hepatic steatosis through increasing plasma adiponectin levels and hepatic protein levels of p- AMPK, ACOX1, CYP4A, and MTTP. Conclusions This study demonstrated that the protective effect of fisetin on ALD is achieved by accelerating EtOH clearance and inhibition of oxidative stress. The data suggest that fisetin has a therapeutical potential for treating ALD. [ABSTRACT FROM AUTHOR]

Background Peroxisome proliferator-activated receptor gamma ( PPAR γ) signaling has been shown to regulate lipogenesis and lipid accumulation. Previous studies have shown that hepatic PPAR γ is up-regulated in steatotic liver of both animal and human. However, the effects of hepatic PPAR γ signaling on alcoholic liver disease ( ALD) remain elusive. Methods To determine the role of hepatic PPAR γ signaling on ALD, wild-type ( WT) and hepatocyte-specific PPAR γ knockdown ( PPAR γ∆ Hep) mice were fed a modified Lieber- De Carli alcohol or isocaloric maltose dextrin control liquid diet for 8 weeks to induce ALD. Blood parameters, hepatic steatosis, and inflammation were measured after 8-week alcohol feeding. Results Alcohol feeding to WT mice resulted in liver damage (alanine aminotransferase [ ALT], 94.68 ± 17.05 U/L; aspartate aminotransferase [ AST], 55.87 ± 11.29 U/L), which was significantly alleviated by hepatic PPAR γ knockdown ( ALT, 57.36 ± 14.98 U/L; AST, 38.06 ± 3.35 U/L). Alcohol feeding led to marked lipid accumulation and up-regulation of lipogenic genes including fatty acid transport protein 1 ( FATP1), acetyl- Co A carboxylase ( ACC), fatty acid synthase ( FASN), lipin1 (LIPIN1), diacylglycerol acyltransferase 1 ( DGAT1), and diacylglycerol acyltransferase 2 ( DGAT2) in the livers of WT mice. Knockdown of hepatic PPAR γ significantly alleviated alcohol-induced lipid accumulation and abolished the up-regulation of FASN, DGAT1, and DGAT2. Silencing of PPAR γ in FL83 B cells significantly decreased ethanol ( Et OH)-, linoleic acid-, and Et OH plus linoleic acid-induced lipid accumulation. Knockdown of hepatic PPAR γ also significantly reduced alcohol-induced inflammatory chemokine (monocyte chemotactic protein 1 [ MCP1], keratinocyte-derived chemokine [ KC], interferon gamma-induced protein 10 [ IP-10]) and inflammatory infiltration (lymphocyte antigen 6 complex, locus G [ Ly6 G], and F4/80). Conclusions The results suggest that hepatic PPAR γ signaling contributes to alcohol-induced liver injury by promoting hepatic steatosis and inflammation. [ABSTRACT FROM AUTHOR]

Background Chronic alcohol exposure causes lipid dyshomeostasis at the adipose-liver axis, reducing lipid storage in white fat and increasing lipid deposit in the liver. Previous studies have shown that visceral fat, rather than subcutaneous fat, is a risk factor for metabolic diseases. This study was conducted to determine whether chronic alcohol exposure differentially affects lipid metabolism in visceral (epididymal) and subcutaneous fat, and the mechanisms underlying the alcohol effects. Methods Male Wistar rats were pair-fed the Lieber-DeCarli control or alcohol liquid diet for 12 weeks to determine the effects of alcohol on the white fat. Tissue explants culture and 3T3-L1 culture were conducted to define the role of acetaldehyde in alcohol-induced adipose tissue dysfunction. Results Chronic alcohol feeding significantly reduced visceral fat mass and down-regulated peroxisome proliferator activator receptor- γ and CCAAT/enhancer binding protein- α, 2 important transcription factors in regulation of lipogenesis. The protein levels of lipogenic enzymes including phospho- ATP-citrate lyase, acetyl-CoA carboxylase, fatty acid synthase, lipin1, and diacylglycerol acyltransferase 2 in the visceral fat were reduced. In contrast, chronic alcohol exposure did not affect subcutaneous fat mass and had less effect on the protein levels of lipogenic enzymes and regulators. Accordingly, the visceral fat showed a lower protein level of aldehyde detoxification enzymes compared to the subcutaneous fat. Acetaldehyde treatment to either visceral fat explants or 3T3-L1 adipocytes produced similar effects on lipogenic enzymes and regulators as observed in animal model. Conclusions These results demonstrated that visceral fat is more susceptible to alcohol toxicity compared to subcutaneous fat, and disruption of adipose lipogenesis contributes to the pathogenesis of alcoholic lipodystrophy. [ABSTRACT FROM AUTHOR]