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

Effect of Pesticides on Peroxisome Proliferator-Activated Receptors (PPARs) and Their Association with Obesity and Diabetes

“…Since the biological effect of PPAR activation is directly related to the metabolism of lipids and carbohydrates, the main axis of biomarkers studied are the genes containing in their promoter the PPRE and the enzymes/proteins encoded by these genes in the main organs controlling the energetic homeostasis of the organism; the biomarkers used to monitoring PPAR activation through pesticides could be summarized as follows: the biological activation of the PPAR has been observed in adipose tissue by DDT, dieldrin, diazonin, fenthion, and fibronil through the accumulation of lipids as an effect of adipocyte maturation [22,33,38,50]. Also this activation has been observed with organophosphate flame retardants (OPFRs) in inducing adipogenesis as 2-ethylhexyl diphenyl phosphate (EHDPP) [114] and triphenyl phosphate (TPHP) [115]; however, by exploring the mechanism by which pesticides enable this accumulation, it has been shown that the role of PPARγ in this phenomenon is important and consistent, but not unique, as accumulation of lipids is still observed despite blocking the receptor, as in the case of qhizalofop-ethyl [39]; and even the direct role of other receptors in lipid accumulation has been reported, as in the case of dioxin: 2,3,7,8-tetrachlorodibenzo-p-dioxin, which is antagonistic to the aryl hydrocarbon receptor (AhR) and prevents lipid accumulation in association with a decrease in PPARγ [116]. Likewise, the mechanism of lipid accumulation has been shown to be 23 PPAR Research not only due to a process of direct activation of nuclear receptors, as is the case with chlorantraniliprole and pyraclostrobin, which increase oxidative stress in the ER and mitochondria, accordingly, caused by an increase in lipid peroxidation and ROS, and decrease the availability of ATP [23,40].…”

“…And that even the effect in the commercial presentation is much greater than in its pure state, as the presence of certain additives can enhance or even increase the activity, as in the case of glyphosate as an antagonist [56] or quizalofop-ethyl as an agonist [39], which has less activity in its pure state. Some additives that have been reported to activate PPARα are toximul [116], a pesticide surfactant, and piperonyl butoxide [118], a pesticide synergist that increases lipid accumulation as well as CYP4A10. Although it is important to highlight that the CYP4A gene contains a PPRE in its promoter, the LXR receptor can also activate this gene [119], revealing an alternative control mechanism and raising the possibility that other genes controlled by PPARs may have a similar mechanism.…”

Glabridin attenuates antiadipogenic activity induced by 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin in murine 3T3‐L1 adipocytes

“…Because AhR expression levels decrease during adipocyte differentiation (Ashida et al, ), we treated 3T3‐L1 adipocytes with TCDD or glabridin for the first 3 days of adipocyte differentiation and evaluated the effects of this compound on TCDD‐induced loss of lipid accumulation. To investigate the effects of TCDD on adipogenic differentiation, adipogenesis was induced in 3T3‐L1 cells in the presence of different concentrations of TCDD (5–100 n m ) for 3 days.…”