The adverse effects of chronic low-dose exposure to nonylphenol on type 2 diabetes mellitus in high sucrose-high fat diet-treated rats

Yu, Jian; Yang, Jin; Luo, Yi; Yang, Gangyi; Li, Wen-Mei; Yang, Yu; He, Ling

doi:10.1080/19382014.2017.1404211

Cited by 14 publications

(11 citation statements)

References 27 publications

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“…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].…”

Section: Discussionsupporting

confidence: 91%

“…These studies were consistent with these in vitro results, which suggested that NP exposure had an effect on adipocyte lipid metabolism. The results of the above cell experiments and animal experiments have confirmed our previous research findings that NP exposure could cause 2-diabetes [28], alcoholic fatty liver [29], and metabolic syndrome [27].…”

Section: Discussionsupporting

confidence: 87%

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

Tang

et al. 2020

Environ Sci Eur

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Background: The incidence of obesity has soared over the last several decades. There is mounting evidence suggesting that the increased presence of environmental endocrine disruptors (EEDs), including nonylphenol (NP), plays an important role in the incidence of lipid metabolism disorders. The aim of this work was to determine whether chronical exposure to NP could induce obesity and lipid metabolism disorders, both in vivo in Sprague-Dawley rats, and in vitro in 3T3-L1 preadipocytes. Forty rats (n = 10 per group) were gavaged with NP in corn oil at dose levels of 0.02 μg/kg/day (low dose, L), 0.2 μg/kg/day (middle dose, M), and 2.00 μg/kg/day (high dose, H) or corn oil alone (vehicle control, C) for 180 days. In vitro study, 3T3-L1 preadipocytes were exposed to NP at concentrations of 0, 40 pM, 40 nM, or 40 μM for 12 days. Results: In vivo, the fat weight (F = 103.605, P < 0.001) and fat coefficient (F = 169.807, P < 0.001) of NP-exposed rats were higher than those of control group rats. The serum levels of TC (F = 3.798, P < 0.05), LDL-C (F= 4.946,P < 0.05), and TG (F = 14.117,P < 0.05) in the H group were higher than those in the control group. Protein concentrations of CEBPα (F = 189.104, P < 0.001), FAS (F = 51.011, P < 0.001), PPARγ (F = 114.306,P < 0.001), and SREBP1 (F = 30.432,P < 0.001) in serum in the NP group were higher than those in the control group. The concentration of NP in adipose tissues of rats increased with an increase in NP exposure dose in a dose-response manner (F = 561.353,P < 0.001). The numbers of adipocytes in the M and H groups decreased, and the volume of a single cell increased with cells' membranes ruptured. With the increase in NP exposure dose, the number of adipocytes per microscope decreased gradually (F = 85.873, P < 0.001). The expression levels of PPARγ (F = 169.936, P < 0.001) and FAS (F = 295.249, P < 0.001) proteins in the H group were higher than those in the control group. CEBPα (F = 101.086, P < 0.001) mRNA expression was up-regulated in the M and H groups; and FAS (F = 439.600, P < 0.001), PPARγ (F = 10.540, P < 0.001), and SREBP1 (F = 123.499, P < 0.001) mRNA expression in NP-exposed groups were significantly higher than those in the control group. In vitro, compared with the control group, the Oil Red Staining of adipocytes in the NP groups was darker, the fat cells were more densely distributed, and some of them fused into large lipid droplets. Expressions of CEBPα (F = 539.103, P < 0.001), FAS (F = 715.740, P < 0.001), PPARγ(F = 114.783, P < 0.001), and SREBP1 (F = 139.600, P < 0.001) proteins in 3T3-L1 preadipocytes were higher in group exposed to 40 μM NP than those in the control group. Conclusions: The results of this in vivo and in vitro experiment were consistent, and both have demonstrated that NP exposure interfered with the expression of proteins and/or mRNAs of lipid metabolism-related regulators (CEBPα, FAS, SREBP1, PPARγ), promoted the proliferation and differentiation of adipocytes and intracellular accumulation of lipids, and eventually lead to blo...

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 87%

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

Tang

et al. 2020

Environ Sci Eur

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“…Low-dose effects were defined by the National Toxicology Program (NTP) as those that occur in the range of human exposures or effects observed at doses below those used for traditional toxicological studies (Vandenberg et al, 2012). Actually, there is growing evidence to support low-dose effects of NP (Melnick et a., 2002; Di et al, 2018; Patino-Garcia et al, 2018; Yu et al, 2018). Nonmonotonic dose-response curves, a nonlinear relationship between dose and effect where the slope of the curve changes sign somewhere within the range of doses examined, is best explanation for the low-dose (i.e.…”

Section: Discussionmentioning

confidence: 99%

Adverse Effect of Nonylphenol on the Reproductive System in F1 Male Mice: A Subchronic Low-Dose Exposure Model

Kim¹,

Cheon²,

Lee³

2019

Dev. Reprod.

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Nonylphenols (NPs) are widely used industrial materials, and are considered as potent endocrine disrupting chemical. Present study was undertaken to clarify the effect of subchronic low-dose NP exposure to F1 generation male mice. Mice were divided into 2 groups; (1) CON, control animals and (2) NP-50 (50 μg/L), animals were treated with NP via drinking water. NP exposures were continuously conducted from parental pre-mating period until the postnatal day (PND) 55 of F1 offsprings. Mice were sacrificed on PND 55 and the tissue weights were measured. The initial body weights (at PND 21) and terminal body weights (PND 55) of the NP-50 animals were significantly lower than those of control animals ( p< 0.05). NP exposure induced a significant increase in the absolute weight of the testes ( p< 0.05). Conversely, the NP exposure caused significant decrease in the absolute weights of the epididymis ( p< 0.01), prostate ( p< 0.05) and seminal vesicle ( p< 0.05). Histopathological studies revealed that NP-treated animals exerted decreased seminiferous tubule diameters, reduced luminal area, and lower number of germ cells. Also some sloughing morphologies in the tubules were observed. In the caudal epididymis, fewer mature sperms and swollen epithelial cells were found in the NP-treated group. Our results confirmed that the subchronic low-dose NP exposure altered some male parameters and induced histopathological abnormalities in testis and epididymis of F1 mice. Since the NP dose used in this study is close to the average human daily NP exposure, our results could provide practically meaningful understanding of adverse effect of EDC in human.

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“…Interestingly, a large number of human studies and experimental animal models demonstrated that adverse environmental exposures experienced by their parents during intrauterine or early postnatal life significantly influenced health of the next generations (Dong et al, 2019; Lund et al, 2019; Zhang et al, 2019). More specifically, poor early-life exposures robustly increased the risks of developing chronic metabolic diseases in adult life, including glucose intolerance, T2DM and obesity (Csongova et al, 2018; Kearney et al, 2018; Wen et al, 2018; Yu et al, 2018; Chang et al, 2019). This association has been conceptualized by the fetal programming hypothesis and the developmental origins of health and disease, which propose that environmental stimuli during critical windows of development programmed permanent changes in later life (Aris et al, 2018; Velazquez et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Maternal Genistein Intake Mitigates the Deleterious Effects of High-Fat Diet on Glucose and Lipid Metabolism and Modulates Gut Microbiota in Adult Life of Male Mice

et al. 2019

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Adverse early-life exposures program increased risk of chronic metabolic diseases in adulthood. However, the effects of genistein supplementation in early life on metabolic health in later life are largely unclear. Our objective was to investigate whether maternal genistein intake could mitigate the deleterious influence of a maternal high-fat diet on glucose and lipid metabolism in offspring and to explore the role of gut microbiota in mediating the transgenerational effects. C57BL/6 female mice were fed either a high-fat diet (HF), high-fat diet with genistein (0.6 g /kg diet) (HFG) or normal control diet (C) for 3 weeks before pregnancy and throughout pregnancy and lactation. The male offspring had ad libitum access to normal chow diet from weaning to 24 weeks of age. Then the content of inguinal subcutaneous adipose tissue (SAT) and epididymal visceral adipose tissue (VAT) were weighed. Glucose tolerance test (GTT), the level of serum insulin and lipid profiles were analyzed. The caecal contents were collected for 16S rDNA sequencing. The results showed that maternal genistein intake could significantly reduce blood glucose levels during GTT, fasting insulin levels, VAT mass and serum triglyceride levels as well as increase high-density lipoprotein cholesterol in adult male offspring. Significant decrease of germs from the Tenericutes phylum and enrichment of Rikenella as well as SCFA (short-chain fatty acid)-producing bacteria, including Alloprevotella, Odoribacter , and Clostridium XlVa , in offspring of genistein fed dams might play crucial roles in the improvement of glucose and lipid metabolism. Overall, early-life genistein intake attenuated the harmful effects of maternal HF on metabolism in adult offspring and the protective effects were associated with the alterations in gut microbiota, which provides new evidence and targets for mitigate the poor effects of adverse early-life exposures on metabolic health in later life.

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The adverse effects of chronic low-dose exposure to nonylphenol on type 2 diabetes mellitus in high sucrose-high fat diet-treated rats

Cited by 14 publications

References 27 publications

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

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

Adverse Effect of Nonylphenol on the Reproductive System in F1 Male Mice: A Subchronic Low-Dose Exposure Model

Maternal Genistein Intake Mitigates the Deleterious Effects of High-Fat Diet on Glucose and Lipid Metabolism and Modulates Gut Microbiota in Adult Life of Male Mice

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