Nonylphenol aggravates non-alcoholic fatty liver disease in high sucrose-high fat diet-treated rats

Abstract

Exposure to environmental endocrine disruptors (EEDs) contributes to the pathogenesis of many metabolic disorders. Here, we have analyzed the effect of the EED-nonylphenol (NP) on the promotion of non-alcoholic fatty liver disease (NAFLD) in rats fed high sucrose-high fat diet (HSHFD). Fifty Sprague-Dawley rats were divided into five groups: controls fed a normal diet (C-ND); HSHFD-fed controls (C-HSHFD); and rats fed a HSHFD combined with NP at doses of 0.02 μg/kg/day (NP-L-HSHFD), 0.2 μg/kg/day (NP-M-HSHFD), and 2 μg/kg/day (NP-H-HSHFD). Subchronic exposure to NP coupled with HSHFD increased daily water and food intake (p < 0.05), hepatic echogenicity and oblique liver diameter (p < 0.05), and plasma levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, triglycerides, and low density lipoprotein cholesterol (p < 0.05). Combined exposure to NP and HSHFD induced macrovesicular steatosis with dilation and congestion of the central vein, liver inflammatory cell infiltration, and expression of genes regulating lipid metabolism, SREBP-1C, FAS, and Ucp2. These results demonstrate that NP aggravates NAFLD in HSHFD-treated rats by up-regulating lipogenic genes, and that HSHFD increases the toxic effects of NP. Thus subchronic NP exposure may lead to NAFLD, especially when combined with a high-sucrose/high-fat diet.

In vivo and in vitro effects of chronical exposure to nonylphenol on lipid metabolism

“…The results of animal experiments in this study showed that the body weight of rats increased during 1 to 17 weeks of NP exposure, while the weight of rats increased significantly from 21 to 26 weeks and presented a positive relationship with NP dose. NP-induced weight gain in rats has also been demonstrated in multiple studies [25,28,29]. In this study, the serum cholesterol, triglyceride, and low-density lipoprotein contents of the rats in the exposed group were higher than these in the control group, which was consistent with the results of Zhang et al [30].…”

“…Moreover, the mRNA expression levels of the four regulatory factors were also higher than these of the control group. Some studies had consistent results to this animal experiment, such as the increase of SREBP-1C and FAS mRNA expression in non-alcoholic fatty liver was caused by NP subchronic exposure [29]. Continuous exposure from the 6th day of pregnancy to the 21st day after birth, the expression levels of FAS, PPARγ, and SREBP1 mRNA in liver tissues of F 1 and F 2 rats were higher than those in the control group, and the increase was proportional to the dose of NP [30]; NP exposure during the development period could increase PPARγ mRNA expression in adult male offspring [6].…”

Effects of Lactobacillus Casei YBJ02 on Lipid Metabolism in Hyperlipidemic Mice

“…It is essential for the adipocyte expression in fat differentiation, which is mainly expressed in adipose tissue and can control fat oxidation (Yamashita, Mitani, Wang, & Ashida, ). FAS converts the nutrients absorbed in mice into fatty acids, which can significantly increase the amount of triglyceride synthesis (Yu et al., ).…”

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“…The liver and kidney tissues were weighed, and hepatosomatic index and renal index were calculated as follows 11,12 Hepatosomatic Index (HSI) = Liver weight × 100 / Bodyweight Renal Index = Kidney weight (right and left) × 100 / Bodyweight Antioxidant Enzymes and Oxidative Stress in Tissues: After dissecting the rat, the liver and kidney tissues were excised out and washed in normal saline. 10% w/v tissues were then homogenized in 50 mM phosphate buffer saline, pH 7.4.…”