Low‐dose food contaminants trigger sex‐specific, hepatic metabolic changes in the progeny of obese mice

Naville, Danielle; Pinteur, Claudie; Véga, Nathalie; Menade, Yoan; Vigier, Michèle; Bourdais, A; Labaronne, Emmanuel; Debard, Cyrille; Luquain-Costaz, Céline; Bégeot, Martine; Vidal, Hubert; Magueresse-Battistoni, Brigitte Le

doi:10.1096/fj.13-231670

Cited by 61 publications

(85 citation statements)

References 59 publications

(95 reference statements)

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“…DEHP was delivered at 0.05 and 500 mg/kg/day. The lower dose (0.05 mg/kg/day) is considered to be a 'safe dose' for humans and is within the tolerable daily intake (TDI) (21). In contrast, the higher dose (500 mg/kg/day) has caused adverse reproductive and developmental effects in previous animal studies (22).…”

Section: Discussionmentioning

confidence: 99%

In utero exposure to di-(2-ethylhexyl) phthalate induces metabolic disorder and increases fat accumulation in visceral depots of C57BL/6J mice offspring

Liu

Wang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract.Excessive visceral fat accumulation is associated with metabolic disorders. Di-(2-ethylhexyl) phthalate (DEHP), a candidate environmental obesogen, affects lipid metabolism and adipogenesis. Perinatal exposure to DEHP may be associated with metabolic disorders of dams and offspring. The aim of the present study was to explore the effects of exposure of pregnant dams to DEHP on the metabolism and fat distribution of their offspring, and to determine the mechanisms for these effects. Pregnant C57BL/6J mice were administered DEHP via gavage (0.05 or 500 mg/kg/day) from gestational days 1-19. Pups were sacrificed at nine weeks of age. Serum leptin, insulin, lipid and fasting glucose levels, and the weights of the inguinal (subcutaneous) and gonadal (visceral) fat pads were determined. mRNA expression levels of two developmental genes, T-box 15 (Tbx15) and glypican 4 (Gpc4) were detected in fat tissues. A 100% abortion rate was exhibited in 500 mg/kg DEHP-treated dams, whereas exposure to 0.05 mg/kg DEHP did not affect reproductive outcomes. Pups from the 0.05 mg/kg exposure group were used for subsequent experimentation. Serum leptin, insulin, lipid and fasting glucose concentrations in these pups were significantly higher than those of control pups (P<0.05). Although no significant change in body weight was detected, the visceral fat weights of DEHP-exposed pups were significantly higher than those of control pups (P<0.05). Compared with controls, mRNA expression levels of Tbx15 in subcutaneous fat and Gpc4 in visceral fat were significantly increased among DEHP-exposed pups (P<0.01). The present results suggest that in utero exposure to an environmentally safe dose of DEHP may lead to excessive visceral fat accumulation and metabolic disorders in offspring and that aberrant expression of Tbx15 and Gpc4 may have an important role in these effects.

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Section: Discussionmentioning

confidence: 99%

In utero exposure to di-(2-ethylhexyl) phthalate induces metabolic disorder and increases fat accumulation in visceral depots of C57BL/6J mice offspring

Liu

Wang

et al. 2016

Experimental and Therapeutic Medicine

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“…Subchronic exposure to BPA induces functional and structural changes such as a significantly increased frequency of edema and parenchymal degeneration in the liver [31]. Naville et al [32] recently described that some chemical food contaminants, including BPA, at low dose may induce hepatic metabolic dysfunction in the progeny of obese mice. Specifically, this study showed that male mice fed on high fat diet and exposed to the pollutants had an increased peroxisome proliferator-activated receptors γ (PPARγ) and liver X receptor α (LXRα) mRNA levels in the liver.…”

Section: Bpa Effects In Liver Functionsmentioning

confidence: 99%

Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

Menale¹,

Mita²,

Diano³

et al. 2016

TOBIOTJ

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Bisphenol A (BPA) is used as basic chemical compound in the production of polycarbonate food containers or epoxy resins coating metallic cans for food and beverages conservation. Its xeno-estrogenic activity alters endocrine-metabolic pathways modulating glucose metabolism and increasing the risk of developing diabetes, insulin resistance, and obesity. Based on in vitro and in vivo experimental research, here we report some of the major BPA adverse effects on tissues that play a key role in the regulation on the whole body's metabolism. Evidences have shown that BPA is able to exert its endocrine disrupting action altering glucose metabolism and contributing to the onset of metabolic disorders, acting on liver functions and affecting insulin production by the pancreas. Exposure to BPA has been reported also to modulate glucose utilization in muscles, as well as to interfere with adipose tissue endocrine function. In addition, to peripheral tissues, recent studies have shown that BPA by acting in the Central Nervous System affects neuroendocrine regulation of glucose metabolism, promoting glucose metabolism dysfunction such as glucose intolerance and insulin resistance. Thus, exposure to BPA seems to be an important risk factor in the onset of obesity and metabolic syndrome. However, its mechanisms of action need to be further investigated to provide a major evaluation of risk assessment.

show abstract

Section: Bpa Effects In Liver Functionsmentioning

confidence: 99%

Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

Menale¹,

Mita²,

Diano³

et al. 2015

TOBIOTJ

View full text Add to dashboard Cite

Bisphenol A (BPA) is used as basic chemical compound in the production of polycarbonate food containers or epoxy resins coating metallic cans for food and beverages conservation. Its xenoestrogenic activity alters endocrine-metabolic pathways modulating glucose metabolism and increasing the risk of developing diabetes, insulin resistance, and obesity. Based on in vitro and in vivo experimental research, here we report some of the major BPA adverse effects on tissues that play a key role in the regulation on the whole body's metabolism. Evidences have shown that BPA is able to exert its endocrine disrupting action altering glucose metabolism and contributing to the onset of metabolic disorders, acting on liver functions and affecting insulin production by the pancreas. Exposure to BPA has been reported also to modulate glucose utilization in muscles, as well as to interfere with adipose tissue endocrine function. In addition, to peripheral tissues, recent studies have shown that BPA by acting in the Central Nervous System affects neuroendocrine regulation of glucose metabolism, promoting glucose metabolism dysfunction such as glucose intolerance and insulin resistance. Thus, exposure to BPA seems to be an important risk factor in the onset of obesity and metabolic syndrome.However, its mechanisms of action need to be further investigated to provide a major evaluation of risk assessment.

show abstract

Low‐dose food contaminants trigger sex‐specific, hepatic metabolic changes in the progeny of obese mice

Cited by 61 publications

References 59 publications

In utero exposure to di-(2-ethylhexyl) phthalate induces metabolic disorder and increases fat accumulation in visceral depots of C57BL/6J mice offspring

In utero exposure to di-(2-ethylhexyl) phthalate induces metabolic disorder and increases fat accumulation in visceral depots of C57BL/6J mice offspring

Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

Adverse Effects of Bisphenol A Exposure on Glucose Metabolism Regulation

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