Many previous studies have indicated the adverse effects of bisphenol A (BPA) on sperm production and quality; however, the mechanisms underlying BPA male reproductive toxicity have yet to be elucidated. The main purpose of this study was to investigate the effect of perinatal exposure to BPA on the spermatogenic capacity of male offspring, and to explore the possible influence of inflammatory responses in BPA reproductive toxicity. Twenty-one pregnant C57BL/6mice were randomly divided into three groups: a control group, a group receiving 0.2 μg/mL (LBPA), and a group receiving 2 μg/mL of BPA (HBPA), all via drinking water from gestational day 6 to the end of lactation. After weaning, one male mouse was randomly selected from each group (n = 7/group); these three mice were fed a normal diet and drinking water for 1 month. Levels of serum testosterone (T) and tumor necrosis factor (TNF)-α were then measured in all mice. Sperm count and the proportion of sperm malformation were also determined. The levels of Toll-like receptor 4 (TLR4), nuclear factor (NF)-κB, and aryl hydrocarbon receptor (AhR) protein expression in the testis tissue were determined. Analysis showed that the proportion of sperm malformation increased in the LBPA and HBPA groups (p < 0.05). Sperm count significantly decreased only in the HBPA group (p < 0.05), while the levels of serum TNF-α increased in the LBPA and HBPA groups (p < 0.05). Levels of serum T decreased significantly in the HBPA group, compared with controls (p < 0.05). Levels of TLR4 and NF-κB protein expression in the testis were significantly higher in the LBPA and HBPA groups (p < 0.05 or p < 0.01), while AhR protein expression was higher and seminiferous tubules in the testis showed more damage in the HBPA group compared to controls (p < 0.05 and p < 0.01, respectively). Our results showed that perinatal exposure to low or high doses of BPA decreased the capacity for spermatogenesis in male offspring, which may be associated with an inflammatory response activated by the TLR4/ NF-κB and AhR signaling pathways in the testis.

The aim of this study was to investigate whether combined exposure to fructose and bisphenol A (BPA) has a synergistic effect on abnormal lipid metabolism in the liver of developmental male rats and its possible mechanism. Fifty weaned male Wistar rats were divided into five groups: the control, 13% fructose, 20% fructose, 1 µg/mL BPA, and 13% fructose + 1 µg/mL BPA (combined exposure). Rats were exposed to fructose and/or BPA through drinking water for eight weeks. Genes or proteins regulating lipid metabolism include sterol regulatory element binding protein 1 (SREBP1), adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FAS), zinc α 2 glycoprotein (ZAG) and estrogen receptor α (ERα), and the expression of proteins regulating inflammatory response, such as TLR4 and NF-κB, were determined. Serum total cholesterol (T-CHO), triglyceride (TG), low, high density lipoprotein cholesterol (LDL-C, HDL-C), blood glucose, insulin, IL-17 and TNF-α levels were also measured. Liver tissue morphology was observed by H&E staining. The results showed that the levels of gene and protein catalyzing lipogenesis were increased (SREBP1, ACC1 and FAS), while those catalyzing lipolysis were decreased (ATGL, HSL and ZAG), accompanied by dyslipidemia, insulin resistance and hepatic fat accumulation, and there were higher expression of TLR4 and NF-κB protein and lower expression of ERα protein in liver, and increased serum IL-17 and TNF-α levels in fructose and/or BPA exposed rats compared with controls. Moreover, the above indicators were more serious in combined exposure group than in single exposure group. Therefore, abnormal lipid metabolism in the liver of developmental rats could be exacerbated by combined exposed to fructose and BPA.

Background: Metabolic dysfunction–associated fatty liver disease and steatotic liver disease (SLD) have emerged as one of the fastest-growing liver complications over recent decades; this study evaluated trends in SLD prevalence among Chinese adults and its variation across demographic groups. Methods: A multicenter, retrospective study analyzed health examination data from 600,536 Chinese adults across 10 provinces between 2015 and 2023. Participants (≥18 y) with complete data on age, sex, weight, waist circumference, ultrasound, and biochemical tests were included. SLD was defined as hepatic steatosis with at least 1 metabolic disorder. Age-adjusted SLD prevalence was calculated using direct standardization, and trends were assessed through Joinpoint regression. Logistic regression models examined associations between SLD and demographic/metabolic factors. Results: Of 501,017 participants (mean age: 43.39±12.89 y, 54.8% male), the age-standardized SLD prevalence rose from 36.24% in 2015 to 48.11% in 2023 (estimated annual percentage change=3.38, p=0.002). Metabolic dysfunction–associated SLD (MASLD) prevalence also increased from 30.01% to 43.17% (estimated annual percentage change=4.48, p<0.001). Subgroup analysis revealed significant increases in individuals aged 18–40, and higher prevalence in older adults, with the highest risk in those aged 41–64. Males had a higher risk than females (53.0% vs. 18.6%, adjusted prevalence ratio=1.97). Participants from North China had a higher risk of both SLD and MASLD compared with South China. Laborers had a lower risk of SLD compared with farmers, while administrative personnel had a higher risk of MASLD. Conclusions: The prevalence of SLD and MASLD significantly increased from 2015 to 2023, with notable variations across demographic groups, highlighting the need for targeted public health strategies to address the growing burden of SLD in China.