Age and sex differences in childhood and adulthood obesity association with phthalates: Analyses of NHANES 2007–2010

Buser, Melanie C.; Murray, Hannah; Scinicariello, Franco

doi:10.1016/j.ijheh.2014.02.005

Cited by 163 publications

(111 citation statements)

References 30 publications

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“…LMW metabolites, including MnBP, MEP, and MiBP, have been associated with childhood obesity (77) (145) (388) (59) (48). Conversely, HMW metabolites have been associated with lower weight gain and lower BMI z-scores in boys but higher BMI in girls (406).…”

Section: Associations Between Pop Exposures and The Development Of Obmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

123

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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: Associations Between Pop Exposures and The Development Of Obmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

123

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show abstract

“…For example, male children and adolescents are at high risk for obesity associated with urinary low molecular weight phthalate metabolites, whereas adults are at high risk for obesity associated with high molecular weight phthalate metabolites (9). Moreover, associations were positive for low molecular weight phthalate metabolites with BMI z-score in boys >10 years of age, but no association was detected in girls <10 years of age (10).…”

Section: In Utero Exposure To Di-(2-ethylhexyl) Phthalate Induces Metmentioning

confidence: 99%

“…ences in the association between phthalate exposure and obesity (9,10). For example, male children and adolescents are at high risk for obesity associated with urinary low molecular weight phthalate metabolites, whereas adults are at high risk for obesity associated with high molecular weight phthalate metabolites (9).…”

Section: In Utero Exposure To Di-(2-ethylhexyl) Phthalate Induces Metmentioning

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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“…Among results of human studies investigating the effects of phthalate exposure on obesity, data from the National Health and Nutrition Examination Survey (NHANES) 1999–2002 evidenced a positive association between urinary excretion of phthalates metabolites and waist circumference in both male and female adults was found [65], while more recent studies from NHANES 2007–2010 found that phthalates were associated with higher odds for obesity in both adults and children of both gender [66]. …”

Section: Phthalatesmentioning

confidence: 99%

Endocrine Aspects of Environmental “Obesogen” Pollutants

Nappi

Barrea

Somma

et al. 2016

IJERPH

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Growing evidence suggests the causal link between the endocrine-disrupting chemicals (EDCs) and the global obesity epidemics, in the context in the so-called “obesogenic environment”. Dietary intake of contaminated foods and water, especially in association with unhealthy eating pattern, and inhalation of airborne pollutants represent the major sources of human exposure to EDCs. This is of particular concern in view of the potential impact of obesity on chronic non-transmissible diseases, such as type 2 diabetes, cardiovascular disease, and hormone-sensitive cancers. The key concept is the identification of adipose tissue not only as a preferential site of storage of EDCs, but also as an endocrine organ and, as such, susceptible to endocrine disruption. The timing of exposure to EDCs is critical to the outcome of that exposure, with early lifetime exposures (e.g., fetal or early postnatal) particularly detrimental because of their permanent effects on obesity later in life. Despite that the mechanisms operating in EDCs effects might vary enormously, this minireview is aimed to provide a general overview on the possible association between the pandemics of obesity and EDCs, briefly describing the endocrine mechanisms linking EDCs exposure and latent onset of obesity.

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Age and sex differences in childhood and adulthood obesity association with phthalates: Analyses of NHANES 2007–2010

Cited by 163 publications

References 30 publications

Adipose Tissue as a Site of Toxin Accumulation

Adipose Tissue as a Site of Toxin Accumulation

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

Endocrine Aspects of Environmental “Obesogen” Pollutants

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