Endocrine disrupters as obesogens

Grün, Felix; Blumberg, Bruce

doi:10.1016/j.mce.2009.02.018

Cited by 490 publications

(345 citation statements)

References 266 publications

(182 reference statements)

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“…Obesogens can also act indirectly by altering the basal metabolic rate, by shifting the energy balance to favour storage of calories, alter lipid metabolism and alter hormonal control of appetite and satiety Schug et al, 2011). Many known obesogens are endocrine disrupting chemicals (EDCs) that may mimic or block hormones and disrupt the normal function of the body (De Coster and van Larebeke, 2012;Elobeid and Allison, 2008;Grün and Blumberg, 2009). EDCs may also be implicated in cancer (Soto and Sonnenschein, 2010) .…”

Section: Introductionmentioning

confidence: 99%

In utero exposure to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) did not increase body weight or intestinal tumorigenesis in multiple intestinal neoplasia (Min/+) mice

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Hetland

Sabaredzovic

et al. 2014

Environmental Research

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We examined whether perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) had obesogenic effects and if they increased spontaneous intestinal tumorigenesis in the mouse model C57BL/6J-Min/+ (multiple intestinal neoplasia) after in utero exposure. The dams were exposed to PFOA or PFOS (0.01, 0.1 or 3.0 mg/kg bw/day) by po gavage on GD1-17. TheMin/+ and wild-type offspring were terminated at week 11 for examination of intestinal tumorigenesis or at week 20 for obesogenic effect, respectively. Body weights of the dams and pups were recorded throughout life. Food intake was determined at week 6 and 10. Blood glucose (non-fasted) was measured at week 6 and 11. No obesogenic effect of PFOA or PFOS was observed up to 20 weeks of age. PFOA or PFOS did not increase the incidence or number of tumors in the small intestine or colon of the Min/+ mice or affect their location along the intestines. Feed intake was not affected. There were some indications of toxicity of PFOA, but not of PFOS. There was lower survival of pups after 3.0 mg/kg PFOA, lower body weight in pups after 3.0 and possibly 0.1 mg/kg PFOA, and increased relative liver weight after 0.01 and possibly 0.1 mg/kg PFOA. Plasma glucose was lower after 0.01 and 0.1 mg/kg PFOA. In conclusion, exposure to PFOA and PFOS in utero with the doses used did not have obesogenic effect on either Min/+ or wild-type mice, at least not up to 11 or 20 weeks of age, nor increased intestinal tumorigenesis in Min/+ mice.

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Section: Introductionmentioning

confidence: 99%

In utero exposure to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) did not increase body weight or intestinal tumorigenesis in multiple intestinal neoplasia (Min/+) mice

Ngo

Hetland

Sabaredzovic

et al. 2014

Environmental Research

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“…Exposure to endocrine disrupting POPs has recently emerged as a potential contributor to the pandemic of both type 2 diabetes mellitus and obesity (3,28). Our study relates a range of POPs to detailed anthropometric measures and glucose and insulin levels (basal and postglucose load).…”

Section: Resultsmentioning

confidence: 99%

“…man-made chemicals, described as persistent organic pollutants (POPs) (2,3). POPs are a group of diverse substances, including polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs), that are resistant to biodegradation and ubiquitously present in our environment.…”

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confidence: 99%

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Exposure to Persistent Organic Pollutants: Relationship With Abnormal Glucose Metabolism and Visceral Adiposity

et al. 2014

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OBJECTIVE The contribution of persistent organic pollutants (POPs) to the pandemic of type 2 diabetes mellitus and obesity has been assumed but remains speculative. Our study aimed at investigating the relationship of POP levels with detailed markers of glucose metabolism and body composition. RESEARCH DESIGN AND METHODS Glucose tolerance was determined in a group of normal-weight and obese individuals. Fat distribution was assessed with abdominal computed tomography (CT) scanning, determining subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). Selected POPs (28 polychlorinated biphenyls [PCBs] and the pesticide p,p’-dichlorodiphenyldichloroethylene [p,p’-DDE]) were measured in serum. In a subset of obese individuals undergoing bariatric surgery, POPs were also measured in adipose tissue. RESULTS Among obese participants, serum and adipose tissue levels of POPs were significantly correlated to glucose levels during an oral glucose tolerance test. Logistic regression using a model including age, age2, sex, family history of diabetes, BMI, CT-VAT, smoking behavior, physical activity level score, and a POP level identified serum levels of PCB153, the sum of PCBs and p,p’-DDE as significant predictors of abnormal glucose tolerance (odds ratio 4.6, 4.8, and 3.4, respectively; P < 0.05). Adipose tissue levels of p,p’-DDE were also significant predictors (odds ratio 81.6; P < 0.05). Serum levels of PCBs were inversely related to BMI, while serum and adipose tissue levels of all POPs were positively related to the CT-VAT/SAT ratio, suggesting an important role for the visceral fat compartment in POP dynamics. CONCLUSIONS Our findings further sustain the theory that exposure to environmentally relevant levels of POPs may exert both a diabetogenic and obesogenic effect.

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“…The various chemicals known or presumed to disrupt endocrine systems may also be regarded as important contributors to this disease [8][9].…”

mentioning

confidence: 99%

Are Environmental Contaminants Responsible for ‘Globesity’?

Filipiak‐Florkiewicz¹,

Topolska²,

Florkiewicz³

et al. 2017

Pol. J. Environ. Stud.

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Endocrine disrupters as obesogens

Cited by 490 publications

References 266 publications

In utero exposure to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) did not increase body weight or intestinal tumorigenesis in multiple intestinal neoplasia (Min/+) mice

In utero exposure to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) did not increase body weight or intestinal tumorigenesis in multiple intestinal neoplasia (Min/+) mice

Exposure to Persistent Organic Pollutants: Relationship With Abnormal Glucose Metabolism and Visceral Adiposity

Are Environmental Contaminants Responsible for ‘Globesity’?

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