Maternal exposure to phenanthrene during gestation disturbs glucose homeostasis in adult mouse offspring

Guo, Jianzhong; Huang, Jie; Wang, Qian; Fang, Lü; Zhang, Shenli; Li, Bingshui; Lv, Liangju; Chen, Meng; Wang, Chonggang

doi:10.1016/j.chemosphere.2020.128635

Cited by 12 publications

(3 citation statements)

References 60 publications

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“…Prenatal phenanthrene exposure in mice was also shown to impair adipokine levels through the alteration of adiponectin and resistin gene DNA methylation, thus promoting glucose intolerance [130]. Another adipose tissue-targeted mechanism contributing to insulin resistance upon PAH exposure may involve an increase in insulin receptor substrate 2 methylation [131].…”

Section: Polycyclic Aromatic Hydrocarbons (Pahs)mentioning

confidence: 99%

The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies

Aaseth

Javorac

Djordjevic

et al. 2022

Toxics

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Persistent organic pollutants (POPs) are considered as potential obesogens that may affect adipose tissue development and functioning, thus promoting obesity. However, various POPs may have different mechanisms of action. The objective of the present review is to discuss the key mechanisms linking exposure to POPs to adipose tissue dysfunction and obesity. Laboratory data clearly demonstrate that the mechanisms associated with the interference of exposure to POPs with obesity include: (a) dysregulation of adipogenesis regulators (PPARγ and C/EBPα); (b) affinity and binding to nuclear receptors; (c) epigenetic effects; and/or (d) proinflammatory activity. Although in vivo data are generally corroborative of the in vitro results, studies in living organisms have shown that the impact of POPs on adipogenesis is affected by biological factors such as sex, age, and period of exposure. Epidemiological data demonstrate a significant association between exposure to POPs and obesity and obesity-associated metabolic disturbances (e.g., type 2 diabetes mellitus and metabolic syndrome), although the existing data are considered insufficient. In conclusion, both laboratory and epidemiological data underline the significant role of POPs as environmental obesogens. However, further studies are required to better characterize both the mechanisms and the dose/concentration-response effects of exposure to POPs in the development of obesity and other metabolic diseases.

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Section: Polycyclic Aromatic Hydrocarbons (Pahs)mentioning

confidence: 99%

The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies

Aaseth

Javorac

Djordjevic

et al. 2022

Toxics

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“…Beyond adverse health impacts on mothers and women of child-bearing age, EDC exposures have been linked to long-term adverse health outcomes in their offspring, including, but not limited to childhood obesity and insulin resistance, delayed growth, cognitive and behavioral disorders, congenital abnormalities including heart defects, urogenital defects, and certain cancers ( Wang et al, 2019 ; Park, 2020 ; Wang et al, 2018 ; Chatzi et al, 2019 ; Doherty et al, 2019 ; Tinkelman et al, 2020 ; Ren et al, 2018 ; Rankin et al, 2009 ; Fetita et al, 2006 ; Guo et al, 2021 ; Evans et al, 2019 ; Jacobson et al, 2018 ). During the preconception period, gametes are vulnerable to enduring, EDC-related epigenetic modifications that can be passed between generations ( Stephenson et al, 2018 ; Marcho et al, 2020 ; Xin et al, 2015 ; Brehm and Flaws, 2019 ).…”

Section: Overview Of Edcs: Phthalates and Phenolsmentioning

confidence: 99%

Lifestyle interventions to reduce endocrine-disrupting phthalate and phenol exposures among reproductive age men and women: A review and future steps

Martin

First

Mustieles

et al. 2022

Environment International

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“…Obesity has become a global health challenge reaching alarming prevalence and being a cause of chronic metabolic diseases, including type 2 diabetes (T2DM) (1)(2)(3). The etiology of obesity implicates multiple factors involving environmental, genetic, and epigenetic modification (4)(5)(6)(7). Clinical, epidemiological, and experimental studies consistently demonstrate that abnormal maternal caloric intake or environment disturbance during the perinatal period favors the development of cardiometabolic diseases in the offspring (6,8).…”

Section: Introductionmentioning

confidence: 99%

Maternal exposure to air pollution alters energy balance transiently according to gender and changes gut microbiota

et al. 2023

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IntroductionThe timing of maternal exposure to air pollution is crucial to define metabolic changes in the offspring. Here we aimed to determine the most critical period of maternal exposure to particulate matter (PM2.5) that impairs offspring's energy metabolism and gut microbiota composition.MethodsUnexposed female and male C57BL/6J mice were mated. PM2.5 or filtered air (FA) exposure occurred only in gestation (PM2.5/FA) or lactation (FA/PM2.5). We studied the offspring of both genders.ResultsPM2.5 exposure during gestation increased body weight (BW) at birth and from weaning to young in male adulthood. Leptin levels, food intake, Agrp, and Npy levels in the hypothalamus were also increased in young male offspring. Ikbke, Tnf increased in male PM2.5/FA. Males from FA/PM2.5 group were protected from these phenotypes showing higher O2 consumption and Ucp1 in the brown adipose tissue. In female offspring, we did not see changes in BW at weaning. However, adult females from PM2.5/FA displayed higher BW and leptin levels, despite increased energy expenditure and thermogenesis. This group showed a slight increase in food intake. In female offspring from FA/PM2.5, BW, and leptin levels were elevated. This group displayed higher energy expenditure and a mild increase in food intake. To determine if maternal exposure to PM2.5 could affect the offspring’s gut microbiota, we analyzed alpha diversity by Shannon and Simpson indexes and beta diversity by the Linear Discriminant Analysis (LDA) in offspring at 30 weeks. Unlike males, exposure during gestation led to higher adiposity and leptin maintenance in female offspring at this age. Gestation exposure was associated with decreased alpha diversity in the gut microbiota in both genders.DiscussionOur data support that exposure to air pollution during gestation is more harmful to metabolism than exposure during lactation. Male offspring had an unfavorable metabolic phenotype at a young age. However, at an older age, only females kept more adiposity. Ultimately, our data highlight the importance of controlling air pollution, especially during gestation.

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Maternal exposure to phenanthrene during gestation disturbs glucose homeostasis in adult mouse offspring

Cited by 12 publications

References 60 publications

The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies

The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies

Lifestyle interventions to reduce endocrine-disrupting phthalate and phenol exposures among reproductive age men and women: A review and future steps

Maternal exposure to air pollution alters energy balance transiently according to gender and changes gut microbiota

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