Effects of endocrine disruptors on obesity

Newbold, Retha R.; Padilla-Banks, Elizabeth; Jefferson, Wendy N.; Heindel, Jerrold J.

doi:10.1111/j.1365-2605.2007.00858.x

Cited by 294 publications

(188 citation statements)

References 34 publications

Supporting

Mentioning

178

Contrasting

Unclassified

Order By: Relevance

“…There is evidence that some environmental contaminants disrupt endocrine systems, and may play a role in the obesity epidemic [6,[107][108]. Consistent with human findings, the animal study also showed that rats exposed to POPs clearly developed visceral obesity [6].…”

Section: +supporting

confidence: 76%

Are Environmental Contaminants Responsible for ‘Globesity’?

Filipiak‐Florkiewicz¹,

Topolska²,

Florkiewicz³

et al. 2017

Pol. J. Environ. Stud.

View full text Add to dashboard Cite

Section: +supporting

confidence: 76%

Are Environmental Contaminants Responsible for ‘Globesity’?

Filipiak‐Florkiewicz¹,

Topolska²,

Florkiewicz³

et al. 2017

Pol. J. Environ. Stud.

View full text Add to dashboard Cite

“…Moreover, recent interest has emerged from the idea of an association between EDCs and the metabolic syndrome. Regarding this issue, an increasing number of studies reports that exposure to chemicals during critical periods of differentiation, at low environmentally-relevant doses, alters developmental programming, resulting in obesity (Newbold et al, 2008). Furthermore, some persistent organic pollutants (POPs) have been reported to be linked to the prevalence of type 2 diabetes and insulin resistance .…”

Section: E2 and Bpa Are Equally Effective Through A Non-classical Estmentioning

confidence: 99%

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

Nadal

Alonso-Magdalena

Soriano

et al. 2009

Molecular and Cellular Endocrinology

255

187

View full text Add to dashboard Cite

. The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes. Molecular and Cellular Endocrinology, Elsevier, 2009, 304 (1-2) Please cite this article as: Nadal, A., Alonso-Magdalena, P., Soriano, S., Quesada, I., Ropero, A.B., The pancreatic ␤-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. THE PANCREATIC -CELL AS A TARGET OF ESTROGENS AND XENOESTROGENS: IMPLICATIONS FOR BLOOD GLUCOSE HOMEOSTASIS AND DIABETESAngel Rosen & Spiegelman, 2006;Fritsche et al., 2008). During the fasting state, insulin remains at low levels because plasma glucose concentration is low. In this situation, the levels of the counter-regulatory hormones, glucagon, adrenaline and corticosteroids are increased to promote hepatic glucose production. In contrast, insulin, the only hormone in the body able to decrease blood glucose levels, is increased during the fed state. Insulin decreases blood glucose by promoting adipocyte and muscle glucose uptake, as well as by preventing the liver from producing glucose by suppressing glycogenolysis and gluconeogenesis (Fritsche et al., 2008). neurotransmitters, hormones and nutrients, among which glucose is the most important.Normally, in response to short glucose stimulation, insulin biosynthesis is regulated by the increased translation of the preproinsulin transcript. After a prolonged glucose exposure, however, it is regulated via the insulin gene transcription (Orland et al., 1985;Permutt & Rotwein, 1983;Poitout et al., 2006). Both transcriptional and translational regulation of insulin biosynthesis is essential to maintain the intracellular stores of insulin on a long term basis.The secretory response of -cells depends on their electrical activity. This consists of oscillations of the membrane potential that range from electrically silent periods to depolarised plateaus on which Ca 2+ -action potentials originate (Rorsman et al., 2000).The classical stimulus-secretion coupling that drives insulin release involves the closure of K ATP channels by increasing the intracellular ATP/ADP ratio (Ashcroft et al., 1984) and diadenosine polyphosphates concentration (DPs) (Ripoll et al., 1996) oscillatory pattern is originated (Nadal et al., 1999;Santos et al., 1991;Valdeolmillos et al., 1989), which triggers a pulsatile insulin secretion (Barbosa et al., 1998;Gilon et al., 1993;Dyachok et al., 2008). Estrogens, estrogen receptors and blood glucose homeostasisT...

show abstract

“…Recent works suggests that several changes in the chemical environment over the past 40 years may play a role in the recent global obesity epidemic. [7][8][9][10] These provocative hypotheses predict the existence of 'environmental obesogens', which disrupt or interfere with critical pathways involved in energy balance, adipogenesis and lipid metabolism. Hence, an exposure to EDCs in utero or during lifetime might predispose to or even cause obesity.…”

Section: Edcs and Obesitymentioning

confidence: 99%

“…In addition, a current hypothesis is that some EDCs may act as 'obesogens', possibly contributing to the current epidemic of obesity. [7][8][9][10] In this review we will focus on the endocrine disruption mediated by EDCs interacting with the lipid-activated nuclear receptors, peroxisome proliferator-activated receptors (PPARs) and their potential role as metabolic disruptors.…”

Section: Introductionmentioning

confidence: 99%

Interference of pollutants with PPARs: endocrine disruption meets metabolism

2008

View full text Add to dashboard Cite

The concept of endocrine disruption emerged over a decade ago with the observation that several natural or industrial compounds can interfere with estrogen and androgen signaling, and thereby affect both male and female reproductive functions. Since then, many endocrine-disrupting chemicals (EDCs) have been identified and the concept has been broadened to receptors regulating other aspects of endocrine pathways. In that context, interference of EDCs with receptors regulating metabolism has been proposed as a factor that could contribute to metabolic diseases such as obesity and diabetes. We review recent studies showing that several pollutants, including phthalates and organotins, interfere with PPAR (peroxisome proliferator-activated receptors) nuclear receptors and may thereby affect metabolic homeostasis. Particular emphasis is given on the mechanisms of action of these compounds. However, unlike what has been suspected, we provide evidence from mouse models suggesting that in utero exposure to the phthalate ester di-ethyl-hexyl-phthalate most likely does not predispose to obesity. Collectively, these studies define a subclass of EDCs that perturb metabolic signaling and that we propose to define as metabolic disruptors.

show abstract

Effects of endocrine disruptors on obesity

Cited by 294 publications

References 34 publications

Are Environmental Contaminants Responsible for ‘Globesity’?

Are Environmental Contaminants Responsible for ‘Globesity’?

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

Interference of pollutants with PPARs: endocrine disruption meets metabolism

Contact Info

Product

Resources

About