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Effects of DEHP exposure in the early life and the lifelong groups on PPARγ (A) mRNA and (B) protein expression (C) immunoblot images in white adipose tissue (n = 8 per group). The expression level of PPARγ mRNA was determined by real-time RT-PCR and normalized with GAPDH level, and the protein expression was determined by Western blotting. The PPARγ mRNA expression levels were significantly increased in the early life group (P = 0.0409) and the lifelong group (P = 0.0100). The lifelong group showed a statistically significant increase in PPARγ mRNA expression compared to that in the early life group (P = 0.0156). The immunoblot analysis showed similar significant results of PPARγ mRNA expression (P = 0.0495 in the early life and the lifelong groups). Values are mean and standard errors of three replicates. (
Contexts in source publication
Context 1
... early life and the lifelong groups showed 1.5-and 3.8-fold higher relative PPARγ mRNA expression levels than those in the control group, respectively (P = 0.0409 and P = 0.0100, respectively) ( Figure 3A). The difference in the PPARγ mRNA expression between the early life and the lifelong group was statistically significant (P = 0.0156). ...
Context 2
... difference in the PPARγ mRNA expression between the early life and the lifelong group was statistically significant (P = 0.0156). The PPARγ protein expression in WAT was also increased in the early life and the lifelong groups compared to that in the control group (P = 0.0495 and P = 0.0495, respectively) ( Figure 3B and 3C). In the lifelong group, the PPARγ protein expression tended to be higher than that in the early life group, although the difference was not statistically significant. ...
Citations
... The details of administration schedule were described in our previous study. 19 At the end of our experiment (PND 69), the animals were fasted overnight with free access to water. Male offspring were sacrificed under isophorone anesthesia via inhalation on the morning of PND 70. ...
Introduction
Di-(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer in consumer products and medical devices. It is also suspected to exacerbate the development of fatty liver. However, the mechanisms underlying excessive lipid synthesis and its deposition in the liver are yet to be identified. This study was aimed to evaluate the molecular mechanisms of hepatic lipid accumulation in adult male offspring after perinatal exposure to DEHP.
Method
Corn oil and DEHP (0.75 mg/kg/day) were administered once per day to dam from gestation day 6 to postnatal day (PND) 21 by oral gavage. After the weaning period, DEHP treated male pups were categorized into early life stage- and lifelong period group. Male rats both control and early life stage group administered corn oil, and lifelong period group administered DEHP from PND 22 to 70. Histological examination and triglyceride (TG) levels in the liver were analyzed. Expressions of transcription factors associated with lipid accumulation in the liver were analyzed.
Results
Both early life stage- and lifelong period group, hepatic TG levels, and mRNA and protein expression of diacylglycerol acyltransferase 1 (DGAT1) were significantly higher than control (TG: all p < 0.05, mRNA & protein: p < 0.05 and p < 0.001, respectively). The average body weight from PND 35 to 63, and mRNA and protein expression of sterol regulatory element binding protein 1c in lifelong period group were significantly lower than control (all p < 0.05); however, alanine transaminase were significantly higher than control (p < 0.01).
Conclusion
Perinatal exposure to DEHP may induce the hepatic lipid accumulation through up-regulation of DGAT1 expression.
... Previous studies have focused on the development and reproductive toxicity after phthalate exposure [18,19]. Recent studies have suggested that phthalates can induce obesity, insulin resistance, and metabolic disorders [20][21][22][23][24][25]. ...
... The occurrence of metabolic diseases after phthalate exposure might be linked to the activation of peroxisome proliferator-activated receptors (PPARs) [25,26], which are modulated by the sterol regulatory element binding proteins (SREBPs) [27]. In experimental studies, the disruption of gene expression related to fatty acid metabolism was suggested as a plausible mechanism in the development of NAFLD after phthalate exposure [28][29][30][31][32][33][34]. ...
... Phthalates were classified as obesogen based on the previous animal studies on obesity and metabolic derangement [25,38,39]. Although NAFLD is closely associated with obesity [4], it also occurs in non-obese people [40,41]. ...
The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Recent experimental studies suggested that phthalates might induce NAFLD. Therefore, this study aimed to investigate the relationship between phthalates metabolites and NAFLD in the human population. This cross-sectional analysis was performed using data from the Korean National Environmental Health Survey II (2012–2014) among Korean adults (n = 5800). NAFLD was diagnosed using the hepatic steatosis index (HSI) in the absence of other causes of chronic liver diseases. Among the participants (mean age 46 years, 47.5% male), the prevalence of NAFLD was associated with urinary levels of mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono-(2-ethyl-5-oxohexyl) phthalate, mono-(2-ethyl-5-carboxypentyl) phthalate, mono-benzyl phthalate (MBzP), and mono-n-butyl phthalate (MnBP) compared to the reference group. In the multivariate model, the odds ratios (ORs), 95% confidence interval (CI) for NAFLD were 1.33 (1.00–1.78) and 1.39 (1.00–1.92) in the 3rd and 4th quartile of MEHHP, respectively. Based on the study findings, high levels of urinary phthalates are associated with the prevalence of NAFLD in Korean adults. Further investigation is required to elucidate the causal relationship.
