The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity

doi:10.1016/j.mce.2012.01.001

Molecular and Cellular Endocrinology

Volume 354, Issues 1–2, 6 May 2012, Pages 74-84

https://doi.org/10.1016/j.mce.2012.01.001 Get rights and content

Abstract

There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.

Highlights

► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure influences adult body weight and metabolism. ► Effects of EDCs on body weight and on glucose homeostasis are seen at low doses.

Section snippets

Effects of exposure to estrogens in adulthood on adipose tissue

Estrogens and other sex hormones regulate the functioning of tissues in addition to those involved in reproduction in adults. The effects that occur when a hormone is present often do not occur after the hormone is withdrawn. These are termed “activational” effects. The typical view is that increased plasma concentrations of estrogens are associated with a reduction in food intake and body weight in adults, and that the loss of ovarian estrogen secretion related to menopause in women results in

Production and response to hormones in adipocytes

Fat tissue is now recognized to produce hormones that are critical for regulating metabolism and other processes. Leptin is produced by fat cells and impacts body weight via effects on the hypothalamus, and also impacts reproductive processes via effects on gonadotropin releasing hormone (GnRH) (Gao and Horvath, 2008, Donato et al., 2011). Adiponectin is produced by adipocytes and plays a role in regulating glucose uptake into cells (Ben-Jonathan et al., 2009). Interestingly, leptin and

Endocrine disrupting chemicals (EDCs): a paradigm shift in the study of environmental chemicals

A meeting held in 1991 (Colborn et al., 1992) brought to the attention of the scientific community and the public that chemicals present in household products, such as building materials, plastics, cleaning fluids, cosmetics and pesticides, previously considered safe by regulatory agencies, could interfere with endocrine signaling systems in the body. This discovery (Colborn et al., 1993) has led over the last two decades to an extensive amount of research on endocrine disrupting chemicals or

The adult phenotype due to intrauterine growth restriction (IUGR) is similar to developmental exposure to BPA

There is extensive epidemiological evidence showing that babies with intrauterine growth restriction (IUGR) who then experience a rapid “catch-up” growth spurt during childhood are at high risk for adult obesity and type 2 diabetes (as well as other aspects of metabolic syndrome), consistent with the DOHaD hypothesis (Heindel and vom Saal, 2009, Oken and Gillman, 2003). Thus, fetal growth rate interacts with childhood-adolescence growth rate in terms of whether IUGR leads to adult obesity and

Conclusions

At this time there is limited human data relating obesity with environmental chemicals, and specifically environmental chemicals that are estrogenic or otherwise disrupt estrogen homeostasis. However, there has been an increase in experimental animal research relating environmental chemical exposure to obesity, insulin and glucose dysregulation, and type 2 diabetes. Findings from these studies have led to an increased awareness that energy expenditure and components of diet, while important,

Disclosure statement

S.C.N., J.A.T., B.L.C. and B.M.A. have nothing to disclose. F.S.v.S. has been a consultant for attorneys involved in product labeling litigation.

Role of the funding source

Support during the preparation of this chapter was provided by grants to F.S.v.S. (ES018764) and to S.C.N. (HD056441). The study sponsors had no further part in the study or in the decision to submit the paper for publication.

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Synthetic chemicals are increasingly being recognized for potential independent contributions to preterm birth (PTB) and low birth weight (LBW). Bisphenols, parabens, and triclosan are consumer product chemicals that act via similar mechanisms including estrogen, androgen, and thyroid disruption and oxidative stress. Multiple cohort studies have endeavored to examine effects on birth outcomes, and systematic reviews have been limited due to measurement of 1–2 spot samples during pregnancy and limited diversity of populations.
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While many associations were modest and statistically imprecise, a 1-unit increase in log₁₀ pregnancy averaged concentration of benzophenone-3 and methylparaben were associated with decreases in birthweight, birthweight adjusted for gestational age and SGA. Increases in the odds of being SGA were 29% (95% CI: 5%, 58%) and 32% (95% CI: 3%, 70%), respectively. Bisphenol S in third trimester was also associated with SGA (OR 1.52, 95% CI 1.08, 2.13). Associations of benzophenone-3 and methylparaben with PTB and LBW were null. In addition, a 1-unit increase in log₁₀ pregnancy averaged concentration of 2,4-dichlorophenol was associated with 43% lower (95% CI: −67%, −2%) odds of low birthweight; the direction of effect was the same for the highly correlated 2,5-dichlorophenol, but with a smaller magnitude (-29%, 95% CI: −53%, 8%).
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Bisphenol A (BPA) is an endocrine disruptor widely existing in plastics and resins, which can accumulate in animals and human bodies, posing a potential threat to the physiological and biochemical reactions of human beings or other organisms. α-Chymotrypsin is a kind of proteolytic enzyme existing in humans and animals, which can cause diseases when its activity is excessive. However, there is a lack of research on the mechanism of endocrine disruptors affecting α-chymotrypsin activity. In this study, the interaction between BPA and α-chymotrypsin was proved via multiple spectroscopic approaches, enzyme activity change, isothermal titration calorimetry and molecular docking. Results showed that α-chymotrypsin’s polypeptide chains were unfolded, and protein skeletons were loosened with the exposure to BPA. α-Helix content increased and β-sheet content was decreased. The particle size of the BPA-α-chymotrypsin complex became smaller. Fluorescence sensitization may also be explained by a perturbation of the chromophore Trp 141. The thermodynamic parameters of the binding reaction were measured by isothermal titration calorimetry (ITC), which showed that there was hydrophobic interaction between BPA and α-chymotrypsin, which was consistent with the results of molecular docking. Moreover, BPA may stop near the active center of α-chymotrypsin and interact with the key residues His 57 and Ser 195. The above phenomenon explained the result that the activity of α-chymotrypsin increased to 139% when exposed to high dose BPA (40 μM). Taken together, the effects of BPA on the structure and function of α-chymotrypsin were clarified at the molecular level, which made up the gap in the mechanism of BPA on the proteolytic enzyme, and provided a reliable basis for disease avoidance and prevention.

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ReviewThe estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity

Abstract

Highlights

Section snippets

Effects of exposure to estrogens in adulthood on adipose tissue

Production and response to hormones in adipocytes

Endocrine disrupting chemicals (EDCs): a paradigm shift in the study of environmental chemicals

The adult phenotype due to intrauterine growth restriction (IUGR) is similar to developmental exposure to BPA

Conclusions

Disclosure statement

Role of the funding source

Reg. Tox. Pharm.

Mol. Cell Endocrinol.

Toxicol. Appl. Pharmacol.

Prog. Lipid Res.

Mol. Cell Endocrinol.

Int. J. Hyg. Environ. Health

Metabolism

Mol. Cell Endocrinol.

J. Biol. Chem.

Reprod. Toxicol.

Curr. Biol.

J. Steroid Biochem. Mol. Biol.

J. Lipid Res.

J. Steroid Biochem. Mol. Biol.

Life Sci.

Comp. Biochem. Physiol. C. Pharmacol. Toxicol. Endocrinol.

Dev. Biol.

J. Lipid Res.

Bone

Toxicol. In Vitro

Reprod. Toxicol.

Reprod. Toxicol.

Reprod. Toxicol.

Reprod. Toxicol.

Environ. Res.

Androgens regulate aromatase cytochrome P450 messenger ribonucleic acid in rat brain

Endocrinology

Rapid child growth raises blood pressure in adolescent boys who were thin at birth

Hypertension

Cellular and molecular aspects of adipose tissue development

Annu. Rev. Nutr.

Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells

Endocrinology

The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance

Environ. Health Perspect.

Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring

Environ. Health Perspect.

The effects of androgens and estrogens on preadipocyte proliferation in human adipose tissue: influence of gender and site

J. Clin. Endocrinol. Metab.

Endocrine disrupter bisphenol a increases in situ estrogen production in the mouse urogenital sinus

Biol. Reprod.

Chemical toxins: a hypothesis to explain the global obesity epidemic

J. Altern. Complement. Med.

The developmental origins of adult disease

J. Am. Coll. Nutr.

Pathways of adipose tissue androgen metabolism in women: depot differences and modulation by adipogenesis

Am. J. Physiol. Endocrinol. Metab.

Obesogens, stem cells and the maternal programming of obesity

J. Dev. Origins Health Dis.

Bisphenol A and children’s health

Curr. Opin. Pediatr.

Prenatal bisphenol A exposure and early childhood behavior

Environ. Health Perspect.

Maternal nutritional programming of fetal adipose tissue development: long-term consequences for later obesity

Birth Defects Res. C. Embryo Today

A phytoestrogen-rich diet increases energy expenditure and decreases adiposity in mice

Environ. Health Perspect.

Increased insulin and leptin sensitivity in mice lacking acyl CoA: diacylglycerol acyltransferase 1

J. Clin. Invest.

A new ‘crowded uterine horn’ mouse model for examining the relationship between foetal growth and adult obesity

Basic Clin. Pharmacol. Toxicol.

Developmental effects of endocrine-disrupting chemicals in wildlife and humans

Environ. Health Perspect.

The role of estrogens in adipocyte development and function

Exp. Biol. Med.

17-beta-estradiol increases mitogenic activity of medium from cultured preadipocytes of massively obese persons

J. Clin. Invest.

Expression of human GLUT4 in mice results in increased insulin action

Diabetologia

Review
The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity