Involvement of SREBPs in 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced disruption of lipid metabolism in male guinea pig

Luteolin suppresses TCDD-induced wasting syndrome in a cultured adipocyte model

“…7). This result was consistent with our previous in vivo study using TCDD-dosed guinea pig adipose tissue [13]. In the current study, we found that TCDD decreased DNA binding of C/EBPβ and C/EBPδ by ChIP assay (Fig.…”

“…TCDD decreased the protein expression levels of C/EBPα and PPARγ in 3T3-L1 adipocytes and adipose tissue of animals [9,10,12,13]. In this study, we also confirmed that protein expression of PPARγ and C/EBPα was decreased by treatment with TCDD (Fig.…”

“…TCDD was shown to decrease the levels of CCAAT/enhancer binding protein (C/EBP) α and peroxisome proliferator activated receptor (PPAR) γ in 3T3-L1 adipocytes and murine adipose tissue [9][10][11][12]. In our previous in vivo study [13], it was confirmed that TCDD decreased expression of the late stage adipocyte differentiation markers C/EBPα, PPARγ and GLUT4 in adipose tissue of guinea pigs, whereas expression of early stage factors C/EBPβ and C/EBPδ, remained unchanged. TCDD also reduced expression of the lipogenesis-related factors sterol regulatory element binding protein (SREBP) -1 and -2, and down-regulated their DNA binding activity in adipose tissue.…”

“…TCDD also reduced expression of the lipogenesis-related factors sterol regulatory element binding protein (SREBP) -1 and -2, and down-regulated their DNA binding activity in adipose tissue. A decrease in expression of SREBPs by TCDD would lead to disruption of lipid metabolism as is seen in wasting syndrome [13].…”

Attenuation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Toxicity by Resveratrol: A Comparative Study with Different Routes of Administration

“…Although the mechanism of TCDD-induced steatosis is still unclear, it is suggested that this symptom is caused by an increase in lipid uptake by hepatocytes and/or a reduction in lipid metabolism by AhR activation. [34][35][36][37] On the other hand, since a putative link between oxidative stress and steatosis has been demonstrated (see review of Mantena et al 38) ), an alternative mechanism may involve oxidative stress that contributes to the production and progression of TCDD-induced steatosis. However, the observation that oral resveratrol had no effect on TBARS elevation by TCDD, even although it is protective against steatosis, does not support the above view.…”