The endocrine disruptor mono-(2-ethylhexyl)phthalate promotes adipocyte differentiation and induces obesity in mice

Hao, Chanjuan; Cheng, Xuejia; Xia, Hong-Fei; Ma, Xu

doi:10.1042/bsr20120042

Cited by 169 publications

(106 citation statements)

References 53 publications

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“…Moreover, di(2-ethylhexyl) phthalate (DEHP) or its metabolite mono-(2-ethylhexyl) phthalate (MEHP) increased adipocyte differentiation in 3T3-L1 cells, (142) (115), murine mesenchymal stem cells (44), and in vivo (142) (62). Few human studies have addressed effects of BFRs on obesity and metabolic syndrome; however, adipocyte differentiation was increased by the BFRs PDBE (397) and BDE-47 (185).…”

Section: Effects Of Pops On At Functionmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

142

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We examine the role of adipose tissue, typically considered an energy storage site, as a potential site of toxicant accumulation. Although the production of most persistent organic pollutants (POPs) was banned years ago, these toxicants persist in the environment due to their resistance to biodegradation and widespread distribution in various environmental forms (e.g., vapor, sediment, water). As a result, human exposure to these toxicants is inevitable. Largely due to their lipophilicity, POPs bioaccumulate in adipose tissue, resulting in greater body burdens of these environmental toxicants with obesity. POPs of major concern include polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDDs/PCDFs), and polybrominated biphenyls and diphenyl ethers (PBBs/PBDEs), among other organic compounds. In this review, we 1) highlight the physical characteristics of toxicants that enable them to partition into and remain stored in adipose tissue, 2) discuss the specific mechanisms of action by which these toxicants act to influence adipocyte function, and 3) review associations between POP exposures and the development of obesity and diabetes. An area of controversy relates to the relative potential beneficial versus hazardous health effects of toxicant sequestration in adipose tissue.

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Section: Effects Of Pops On At Functionmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

142

View full text Add to dashboard Cite

show abstract

“…DEHP was recently reported to be a ligand for activation of PPARs and thus might be implicated in adiposity induced by DEHP (Latini et al 2006;Viana Abranches et al 2011). DEHP disrupts the metabolism of fatty acids in adipocytes and thereby promotes their differentiation, ultimately leading to obesity (Desvergne et al 2009;Hao et al 2012;Chiang et al 2015). However, how maternal DEHP exposure induces adiposity in offspring and whether a PPAR-dependent mechanism is involved in this process in our in vivo system remain for further investigation.…”

Section: Discussionmentioning

confidence: 94%

Maternal exposure to di-(2-ethylhexyl) phthalate exposure deregulates blood pressure, adiposity, cholesterol metabolism and social interaction in mouse offspring

et al. 2015

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Long-term exposure to di-(2-ethylhexyl) phthalate (DEHP) is highly associated with carcinogenicity, fetotoxicity, psychological disorders and metabolic diseases, but the detrimental effects and mechanisms are not fully understood. We investigated the effect of exposing mouse mothers to DEHP, and the underlying mechanism, on blood pressure, obesity and cholesterol metabolism as well as psychological and learning behaviors in offspring. Tail-cuff plethysmography was used for blood pressure measurement; Western blot used was for phosphorylation and expression of protein; hematoxylin and eosin staining, Nissl staining and Golgi staining were used for histological examination. The serum levels of cholesterol, triglycerides and glucose were measured by blood biochemical analysis. Hepatic cholesterol and triglyceride levels were assessed by colorimetric assay kits. Offspring behaviors were evaluated by open-field activity, elevated plus maze, social preference test and Morris water maze. Maternal DEHP exposure deregulated the phosphorylation of endothelial nitric oxide synthase and upregulated angiotensin type 1 receptor in offspring, which led to increased blood pressure. It led to obesity in offspring by increasing the size of adipocytes in white adipose tissue and number of adipocytes in brown adipose tissue. It increased the serum level of cholesterol in offspring by decreasing the hepatic capacity for cholesterol clearance. The impaired social interaction ability induced by maternal DEHP exposure might be due to abnormal neuronal development. Collectively, our findings provide new evidence that maternal exposure to DEHP has a lasting effect on the physiological functions of the vascular system, adipose tissue and nerve system in offspring.

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“…mesenchymal stem cells C3H/10T1/2. Mono-(2-ethylhexyl), a metabolite of DEHP, also increased LPL expression in mice adipose tissue (Hao et al, 2012b). However, DEHP caused a significant increase of TAGs (24 h) and PCs (48 and 72 h exposure), particularly of highly unsaturated PCs (>5) of 38 and 40 C atoms, which is in agreement with other studies that reported DEHP (50 M) to enhance the accumulation of PCs in HRP-1 trophoblastic cells after 24 h exposure (Xu et al, 2006).…”

Section: Discussionmentioning

confidence: 95%