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  1. Article ; Online: Environmental endocrine disruption of energy metabolism and cardiovascular risk.

    Kirkley, Andrew G / Sargis, Robert M

    Current diabetes reports

    2014  Volume 14, Issue 6, Page(s) 494

    Abstract: Rates of metabolic diseases have increased at an astounding rate in recent decades. Even though poor diet and physical inactivity are central drivers, these lifestyle changes alone fail to fully account for the magnitude and rapidity of the epidemic. ... ...

    Abstract Rates of metabolic diseases have increased at an astounding rate in recent decades. Even though poor diet and physical inactivity are central drivers, these lifestyle changes alone fail to fully account for the magnitude and rapidity of the epidemic. Thus, attention has turned to identifying novel risk factors, including the contribution of environmental endocrine disrupting chemicals. Epidemiologic and preclinical data support a role for various contaminants in the pathogenesis of diabetes. In addition to the vascular risk associated with dysglycemia, emerging evidence implicates multiple pollutants in the pathogenesis of atherosclerosis and cardiovascular disease. Reviewed herein are studies linking endocrine disruptors to these key diseases that drive significant individual and societal morbidity and mortality. Identifying chemicals associated with metabolic and cardiovascular disease as well as their mechanisms of action is critical for developing novel treatment strategies and public policy to mitigate the impact of these diseases on human health.
    MeSH term(s) Animals ; Atherosclerosis/chemically induced ; Atherosclerosis/epidemiology ; Atherosclerosis/etiology ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/toxicity ; Energy Metabolism ; Environmental Exposure/adverse effects ; Environmental Pollutants/toxicity ; Female ; Humans ; Male ; Models, Animal ; Obesity/chemically induced ; Obesity/epidemiology ; Obesity/etiology ; Phenols/toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects ; Prevalence ; Public Health ; Risk Factors ; Signal Transduction
    Chemical Substances Benzhydryl Compounds ; Endocrine Disruptors ; Environmental Pollutants ; Phenols ; bisphenol A (MLT3645I99)
    Language English
    Publishing date 2014-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2065167-3
    ISSN 1539-0829 ; 1534-4827
    ISSN (online) 1539-0829
    ISSN 1534-4827
    DOI 10.1007/s11892-014-0494-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5628: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  2. Article ; Online: Developmental exposure to the endocrine disruptor tolylfluanid induces sex-specific later-life metabolic dysfunction.

    Ruiz, Daniel / Regnier, Shane M / Kirkley, Andrew G / Hara, Manami / Haro, Fidel / Aldirawi, Hani / Dybala, Michael P / Sargis, Robert M

    Reproductive toxicology (Elmsford, N.Y.)

    2019  Volume 89, Page(s) 74–82

    Abstract: Endocrine-disrupting chemicals (EDCs) are implicated in the developmental mis-programming of energy metabolism. This study examined the impact of combined gestational and lactational exposure to the fungicide tolylfluanid (TF) on metabolic physiology in ... ...

    Abstract Endocrine-disrupting chemicals (EDCs) are implicated in the developmental mis-programming of energy metabolism. This study examined the impact of combined gestational and lactational exposure to the fungicide tolylfluanid (TF) on metabolic physiology in adult offspring. C57BL/6 J dams received standard rodent chow or the same diet containing 67 mg/kg TF. Offspring growth and metabolism were assessed up to 22 weeks of age. TF-exposed offspring exhibited reduced weaning weight. Body weight among female offspring remained low throughout the study, while male offspring matched controls by 17 weeks of age. Female offspring exhibited reduced glucose tolerance, markedly enhanced systemic insulin sensitivity, reduced adiposity, and normal gluconeogenic capacity during adulthood. In contrast, male offspring exhibited impaired glucose tolerance with unchanged insulin sensitivity, no differences in adiposity, and increased gluconeogenic capacity. These data indicate that developmental exposure to TF induces sex-specific metabolic disruptions that recapitulate key aspects of other in utero growth restriction models.
    MeSH term(s) Adiposity/drug effects ; Animals ; Endocrine Disruptors/toxicity ; Female ; Insulin Resistance ; Maternal Exposure/adverse effects ; Metabolic Diseases/chemically induced ; Metabolic Diseases/metabolism ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Prenatal Exposure Delayed Effects/metabolism ; Receptors, Glucocorticoid/metabolism ; Sex Characteristics ; Sulfonamides/toxicity ; Toluidines/toxicity
    Chemical Substances Endocrine Disruptors ; Receptors, Glucocorticoid ; Sulfonamides ; Toluidines ; N-dichlorofluoromethylthio-N',N'-dimethyl-N-p-tolylsulfamide (382277YXSG)
    Language English
    Publishing date 2019-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639342-1
    ISSN 1873-1708 ; 0890-6238
    ISSN (online) 1873-1708
    ISSN 0890-6238
    DOI 10.1016/j.reprotox.2019.06.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Arsenic Exposure Decreases Adiposity During High-Fat Feeding.

    Carmean, Christopher M / Kirkley, Andrew G / Landeche, Michael / Ye, Honggang / Chellan, Bijoy / Aldirawi, Hani / Roberts, Austin A / Parsons, Patrick J / Sargis, Robert M

    Obesity (Silver Spring, Md.)

    2020  Volume 28, Issue 5, Page(s) 932–941

    Abstract: Objective: Arsenic is an endocrine-disrupting chemical associated with diabetes risk. Increased adiposity is a significant risk factor for diabetes and its comorbidities. Here, the impact of chronic arsenic exposure on adiposity and metabolic health was ...

    Abstract Objective: Arsenic is an endocrine-disrupting chemical associated with diabetes risk. Increased adiposity is a significant risk factor for diabetes and its comorbidities. Here, the impact of chronic arsenic exposure on adiposity and metabolic health was assessed in mice.
    Methods: Male C57BL/6J mice were provided ad libitum access to a normal or high-fat diet and water +/- 50 mg/L of sodium arsenite. Changes in body weight, body composition, insulin sensitivity, energy expenditure, and locomotor activity were measured. Measures of adiposity were compared with accumulated arsenic in the liver.
    Results: Despite uniform arsenic exposure, internal arsenic levels varied significantly among arsenic-exposed mice. Hepatic arsenic levels in exposed mice negatively correlated with overall weight gain, individual adipose depot masses, and hepatic triglyceride accumulation. No effects were observed in mice on a normal diet. For mice on a high-fat diet, arsenic exposure reduced fasting insulin levels, homeostatic model assessment of insulin resistance and β-cell function, and systemic insulin resistance. Arsenic exposure did not alter energy expenditure or activity.
    Conclusions: Collectively, these data indicate that arsenic is antiobesogenic and that concentration at the source poorly predicts arsenic accumulation and phenotypic outcomes. In future studies, investigators should consider internal accumulation of arsenic rather than source concentration when assessing the outcomes of arsenic exposure.
    MeSH term(s) Adiposity/drug effects ; Animals ; Arsenic/pharmacology ; Arsenic/therapeutic use ; Diet, High-Fat/adverse effects ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/drug therapy
    Chemical Substances Arsenic (N712M78A8G)
    Language English
    Publishing date 2020-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2230457-5
    ISSN 1930-739X ; 1071-7323 ; 1930-7381
    ISSN (online) 1930-739X
    ISSN 1071-7323 ; 1930-7381
    DOI 10.1002/oby.22770
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    Zs.MG 87: Show issues

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  4. Article: Diet-dependence of metabolic perturbations mediated by the endocrine disruptor tolylfluanid.

    Regnier, Shane M / Kirkley, Andrew G / Ruiz, Daniel / Kamau, Wakanene / Wu, Qian / Kannan, Kurunthachalam / Sargis, Robert M

    Endocrine connections

    2017  Volume 7, Issue 1, Page(s) 159–168

    Abstract: ... a high-sucrose diet (HSD), with or without TF supplementation at 100 μg/g, for 12 weeks. Food intake ...

    Abstract Emerging evidence implicates environmental endocrine-disrupting chemicals (EDCs) in the pathogenesis of metabolic diseases such as obesity and diabetes; however, the interactions between EDCs and traditional risk factors in disease pathogenesis remain incompletely characterized. The present study interrogates the interaction of the EDC tolylfluanid (TF) and traditional dietary stressors in the promotion of metabolic dysfunction. Eight-week-old male C57BL/6 mice were fed a high-fat, high-sucrose diet (HFHSD) or a high-sucrose diet (HSD), with or without TF supplementation at 100 μg/g, for 12 weeks. Food intake, body weight and visceral adiposity were quantified. Glucose homeostasis was interrogated by intraperitoneal glucose and insulin tolerance tests at 9 and 10 weeks of exposure, respectively. After 12 weeks of dietary exposure, metabolic cage analyses were performed to interrogate nutrient handling and energy expenditure. In the background of an HFHSD, TF promoted glucose intolerance; however, weight gain and insulin sensitivity were unchanged, and visceral adiposity was reduced. In the background of an HSD, TF increased visceral adiposity; however, glucose tolerance and insulin sensitivity were unchanged, while weight gain was reduced. Thus, these analyses reveal that the metabolic perturbations induced by dietary exposure to TF, including the directionality of alterations in body weight gain, visceral adiposity and glucose homeostasis, are influenced by dietary macronutrient composition, suggesting that populations may exhibit distinct metabolic risks based on their unique dietary characteristics.
    Language English
    Publishing date 2017-11-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2668428-7
    ISSN 2049-3614
    ISSN 2049-3614
    DOI 10.1530/EC-17-0320
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Arsenic modifies serotonin metabolism through glucuronidation in pancreatic β-cells

    Carmean, Christopher M / Yokoi, Norihide / Takahashi, Harumi / Oduori, Okechi S / Kang, Christie / Kanagawa, Akiko / Kirkley, Andrew G / Han, Guirong / Landeche, Michael / Hidaka, Shihomi / Katoh, Miki / Sargis, Robert M / Seino, Susumu

    American journal of physiology. Endocrinology and metabolism

    2018  Volume 316, Issue 3, Page(s) E464–E474

    Abstract: In arsenic-endemic regions of the world, arsenic exposure correlates with diabetes mellitus. Multiple animal models of inorganic arsenic (iAs, as ... ...

    Abstract In arsenic-endemic regions of the world, arsenic exposure correlates with diabetes mellitus. Multiple animal models of inorganic arsenic (iAs, as As
    MeSH term(s) 5-Hydroxytryptophan/drug effects ; 5-Hydroxytryptophan/metabolism ; Adult ; Animals ; Arsenic/pharmacology ; Cell Line ; Diabetes Mellitus/metabolism ; Female ; Gene Knockdown Techniques ; Glucose/metabolism ; Glucuronosyltransferase/drug effects ; Glucuronosyltransferase/genetics ; Glucuronosyltransferase/metabolism ; Humans ; Insulin Secretion/drug effects ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Male ; Mice ; Mitochondria ; Oxygen Consumption ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Serotonin/metabolism
    Chemical Substances RNA, Messenger ; Serotonin (333DO1RDJY) ; 5-Hydroxytryptophan (C1LJO185Q9) ; Glucuronosyltransferase (EC 2.4.1.17) ; UDP-glucuronosyltransferase 1a6a, mouse (EC 2.4.1.17) ; Glucose (IY9XDZ35W2) ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2018-12-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00302.2018
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    Uc I Zs.89: Show issues Location:
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  6. Article ; Online: Arsenic exposure induces glucose intolerance and alters global energy metabolism.

    Kirkley, Andrew G / Carmean, Christopher M / Ruiz, Daniel / Ye, Honggang / Regnier, Shane M / Poudel, Ananta / Hara, Manami / Kamau, Wakanene / Johnson, Daniel N / Roberts, Austin A / Parsons, Patrick J / Seino, Susumu / Sargis, Robert M

    American journal of physiology. Regulatory, integrative and comparative physiology

    2017  Volume 314, Issue 2, Page(s) R294–R303

    Abstract: Environmental pollutants acting as endocrine-disrupting chemicals (EDCs) are recognized as potential contributors to metabolic disease pathogenesis. One such pollutant, arsenic, contaminates the drinking water of ~100 million people globally and has been ...

    Abstract Environmental pollutants acting as endocrine-disrupting chemicals (EDCs) are recognized as potential contributors to metabolic disease pathogenesis. One such pollutant, arsenic, contaminates the drinking water of ~100 million people globally and has been associated with insulin resistance and diabetes in epidemiological studies. Despite these observations, the precise metabolic derangements induced by arsenic remain incompletely characterized. In the present study, the impact of arsenic on in vivo metabolic physiology was examined in 8-wk-old male C57BL/6J mice exposed to 50 mg/l inorganic arsenite in their drinking water for 8 wk. Glucose metabolism was assessed via in vivo metabolic testing, and feeding behavior was analyzed using indirect calorimetry in metabolic cages. Pancreatic islet composition was assessed via immunofluorescence microscopy. Arsenic-exposed mice exhibited impaired glucose tolerance compared with controls; however, no difference in peripheral insulin resistance was noted between groups. Instead, early insulin release during glucose challenge was attenuated relative to the rise in glycemia. Despite decreased insulin secretion, pancreatic β-cell mass was not altered, suggesting that arsenic primarily disrupts β-cell function. Finally, metabolic cage analyses revealed that arsenic exposure induced novel alterations in the diurnal rhythm of food intake and energy metabolism. Taken together, these data suggest that arsenic exposure impairs glucose tolerance through functional impairments in insulin secretion from β-cells rather than by augmenting peripheral insulin resistance. Further elucidation of the mechanisms underlying arsenic-induced behavioral and β-cell-specific metabolic disruptions will inform future intervention strategies to address this ubiquitous environmental contaminant and novel diabetes risk factor.
    MeSH term(s) Animals ; Arsenites/toxicity ; Biomarkers/blood ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; Endocrine Disruptors/toxicity ; Energy Metabolism/drug effects ; Glucose Intolerance/blood ; Glucose Intolerance/chemically induced ; Glucose Intolerance/pathology ; Insulin/blood ; Insulin Resistance ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Male ; Mice, Inbred C57BL ; Secretory Pathway/drug effects ; Sodium Compounds/toxicity ; Water Pollutants, Chemical/toxicity
    Chemical Substances Arsenites ; Biomarkers ; Blood Glucose ; Endocrine Disruptors ; Insulin ; Sodium Compounds ; Water Pollutants, Chemical ; sodium arsenite (48OVY2OC72)
    Language English
    Publishing date 2017-11-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00522.2016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Dietary exposure to the endocrine disruptor tolylfluanid promotes global metabolic dysfunction in male mice.

    Regnier, Shane M / Kirkley, Andrew G / Ye, Honggang / El-Hashani, Essam / Zhang, Xiaojie / Neel, Brian A / Kamau, Wakanene / Thomas, Celeste C / Williams, Ayanna K / Hayes, Emily T / Massad, Nicole L / Johnson, Daniel N / Huang, Lei / Zhang, Chunling / Sargis, Robert M

    Endocrinology

    2015  Volume 156, Issue 3, Page(s) 896–910

    Abstract: Environmental endocrine disruptors are implicated as putative contributors to the burgeoning metabolic disease epidemic. Tolylfluanid (TF) is a commonly detected fungicide in Europe, and previous in vitro and ex vivo work has identified it as a potent ... ...

    Abstract Environmental endocrine disruptors are implicated as putative contributors to the burgeoning metabolic disease epidemic. Tolylfluanid (TF) is a commonly detected fungicide in Europe, and previous in vitro and ex vivo work has identified it as a potent endocrine disruptor with the capacity to promote adipocyte differentiation and induce adipocytic insulin resistance, effects likely resulting from activation of glucocorticoid receptor signaling. The present study extends these findings to an in vivo mouse model of dietary TF exposure. After 12 weeks of consumption of a normal chow diet supplemented with 100 parts per million TF, mice exhibited increased body weight gain and an increase in total fat mass, with a specific augmentation in visceral adipose depots. This increased adipose accumulation is proposed to occur through a reduction in lipolytic and fatty acid oxidation gene expression. Dietary TF exposure induced glucose intolerance, insulin resistance, and metabolic inflexibility, while also disrupting diurnal rhythms of energy expenditure and food consumption. Adipose tissue endocrine function was also impaired with a reduction in serum adiponectin levels. Moreover, adipocytes from TF-exposed mice exhibited reduced insulin sensitivity, an effect likely mediated through a specific down-regulation of insulin receptor substrate-1 expression, mirroring effects of ex vivo TF exposure. Finally, gene set enrichment analysis revealed an increase in adipose glucocorticoid receptor signaling with TF treatment. Taken together, these findings identify TF as a novel in vivo endocrine disruptor and obesogen in mice, with dietary exposure leading to alterations in energy homeostasis that recapitulate many features of the metabolic syndrome.
    MeSH term(s) Adiponectin ; Adiposity/drug effects ; Animals ; Circadian Rhythm ; Eating ; Endocrine Disruptors/toxicity ; Energy Metabolism/drug effects ; Gene Expression Regulation/drug effects ; Glucose Tolerance Test ; Insulin/metabolism ; Insulin Resistance ; Leptin ; Male ; Metabolic Diseases/chemically induced ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Mice ; Oligonucleotide Array Sequence Analysis ; RNA/genetics ; RNA/metabolism ; Sulfonamides/toxicity ; Toluidines/toxicity ; Weight Gain/drug effects
    Chemical Substances Adiponectin ; Endocrine Disruptors ; Insulin ; Leptin ; Sulfonamides ; Toluidines ; N-dichlorofluoromethylthio-N',N'-dimethyl-N-p-tolylsulfamide (382277YXSG) ; RNA (63231-63-0)
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2014-1668
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