Butyltin contamination in Northern Chilean coast: Is there a potential risk for consumers?

Mattos, Yasna; Stotz, Wolfgang; Estrella, Soledad; Bravo, Manuel; Fillmann, Gilberto; Castro, Ítalo Braga

doi:10.1016/j.scitotenv.2017.03.264

Cited by 68 publications

(23 citation statements)

References 66 publications

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“…Adult mice exposed to TBT in utero displayed increased lipid accumulation in adipose depots, livers, and testis (76; 85). Although epidemiological studies of TBT levels and its associated effects are scant, TBT continues to be found in house dust (79) and in seafood, (86) and at least one study shows increased ponderal index in human infants with the highest prenatal TBT exposure (87).…”

Section: Causes Of Obesitymentioning

confidence: 99%

Environmental Obesogens: Mechanisms and Controversies

Heindel

Blumberg

2019

Annu. Rev. Pharmacol. Toxicol.

227

159

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Obesity is a worldwide pandemic in adults as well as children and adds greatly to health care costs through its association with type 2 diabetes, metabolic syndrome, cardiovascular disease, and cancers. The prevailing medical view of obesity is that it results from a simple imbalance between caloric intake and energy expenditure. However, numerous other factors are important in the etiology of obesity. The obesogen hypothesis proposes that environmental chemicals termed obesogens promote obesity by acting to increase adipocyte commitment, differentiation, and size by altering metabolic set points or altering the hormonal regulation of appetite and satiety. Many obesogens are endocrine disrupting chemicals that interfere with normal endocrine regulation. Endocrine disrupting obesogens are abundant in our environment, used in everyday products from food packaging to fungicides. In this review, we explore the evidence supporting the obesogen hypothesis, as well as the gaps in our knowledge that are currently preventing a complete understanding of the extent to which obesogens contribute to the obesity pandemic. Expected final online publication date for the Annual Review of Pharmacology and Toxicology Volume 59 is January 6, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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Section: Causes Of Obesitymentioning

confidence: 99%

Environmental Obesogens: Mechanisms and Controversies

Heindel

Blumberg

2019

Annu. Rev. Pharmacol. Toxicol.

227

159

View full text Add to dashboard Cite

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“…78,79 Adult mice exposed to TBT in utero displayed increased lipid accumulation in adipose depots, livers and testis 70,81 and treatment of adolescent or adult mice, rats, goldfish and zebrafish led to increased fat deposition and hepatic steatosis. 82,83 Very few epidemiological studies of TBT levels exist, yet TBT continues to be found in house dust 73 and in seafood, 86 and at least one study shows increased ponderal index in human infants with the highest prenatal TBT exposure. 87 Several other chemicals have been identified as obesogens, in vivo.…”

Section: Stem Cell Fatementioning

confidence: 99%

Transgenerational effects of obesogens

Lee

Blumberg

2019

Basic Clin Pharma Tox

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Obesity and associated disorders are now a global pandemic. The prevailing clinical model for obesity is overconsumption of calorie‐dense food and diminished physical activity (the calories in—calories out model). However, this explanation does not account for numerous recent research findings demonstrating that a variety of environmental factors can be superimposed on diet and exercise to influence the development of obesity. The environmental obesogen model proposes that exposure to chemical obesogens during in utero and/or early life can strongly influence later predisposition to obesity. Obesogens are chemicals that inappropriately stimulate adipogenesis and fat storage, in vivo either directly or indirectly. Numerous obesogens have been identified in recent years and some of these elicit transgenerational effects on obesity as well as a variety of health end‐points after exposure of pregnant F0 females. Prenatal exposure to environmental obesogens can produce lasting effects on the exposed animals and their offspring to at least the F4 generation. Recent results show that some of these transgenerational effects of obesogen exposure can be carried across the generations via alterations in chromatin structure and accessibility. That some chemicals can have permanent effects on the offspring of exposed animals suggests increased caution in the debate about whether and to what extent exposure to endocrine‐disrupting chemicals and obesogens should be regulated.

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“…1995 ; Kannan et al. 1996 ; Mattos et al. 2017 ), which suggests that human exposure may be widespread.…”

Section: Introductionmentioning

confidence: 99%

Effects of Perinatal Exposure to Dibutyltin Chloride on Fat and Glucose Metabolism in Mice, and Molecular Mechanisms, in Vitro

Chamorro-García

Shoucri

Willner

et al. 2018

Environ Health Perspect

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Background:The organotin dibutyltin (DBT) is used in the manufacture of polyvinyl chloride (PVC) plastics, in construction materials, and in medical devices. Previous animal studies showed detrimental effects of DBT during in utero development at relatively high doses, but little was known about the effects of DBT exposure at environmentally relevant doses on endpoints such as obesity and metabolic disease.Objectives:We tested the potential obesogenic effects of DBT using in vitro and in vivo models.Methods.We evaluated the effects of DBT on nuclear receptor activation and adipogenic potential using human and mouse multipotent mesenchymal stromal stem cells (MSCs). We also evaluated the effects of perinatal exposure to environmentally relevant doses of DBT in C57BL/6J mice.Results:DBT activated human and mouse PPARγ and RXRα in transient transfection assays, increased expression of adipogenic genes, promoted adipogenic differentiation and increased lipid accumulation in mouse and human MSCs, in vitro. DBT-induced adipogenic differentiation was abolished by the PPARγ antagonist T0070907, indicating that DBT was acting primarily through PPARγ. Perinatal exposure to low doses of DBT led to increased fat storage, decreased glucose tolerance, and increased circulating leptin levels in male, but not female, mice.Conclusions:DBT acted as an obesogen by inducing lipid accumulation in human and mouse MSCs through a PPARγ-dependent pathway. In vivo exposure to biologically relevant doses of DBT during perinatal development led to increased fat storage, elevated leptin levels in plasma, and glucose intolerance in mice. Based on these findings, we posit that monitoring of DBT levels in human samples may aid in understanding and potentially preventing the rising rates of metabolic disorders in human populations. https://doi.org/10.1289/EHP3030

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Butyltin contamination in Northern Chilean coast: Is there a potential risk for consumers?

Cited by 68 publications

References 66 publications

Environmental Obesogens: Mechanisms and Controversies

Environmental Obesogens: Mechanisms and Controversies

Transgenerational effects of obesogens

Effects of Perinatal Exposure to Dibutyltin Chloride on Fat and Glucose Metabolism in Mice, and Molecular Mechanisms, in Vitro

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