Fwd: CHE diabetes/obesity: New science this week

[Sarah Howard]

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View this email in your browser CHE Diabetes and Obesity News and Updates   Reviews Environmental Chemicals: Human Studies Environmental Chemicals: Laboratory Studies Air Pollution Type 1 Diabetes Reviews Chemical Compounds and Ambient Factors Affecting Pancreatic Alpha-Cells Mass and Function: What Evidence? Reviews the effects of chemical, biological, and physical environmental factors on alpha cells, and found studies on air pollutants, compounds of known toxicity present in common objects, pharmacological agents, and compounds present in food. Mannino et al. Int J Environ Res Public Health. Environmental Chemicals: Human Studies Influence of BPA exposure, measured in saliva, on childhood weight BPA exposure in saliva (from dental sealants) was associated with an increased risk of overweight/obesity in children (Spain). Heras-González et al. Front Endocrinol (Lausanne).  The association between serum cadmium and diabetes in the general population: A cross-sectional study from NHANES (1999-2020) Serum cadmium was negatively associated with diabetes in those with normal levels of cadmium exposure, but there was no association in the high exposure group (U.S.). Gong et al. Front Nutr. Altered Metal Homeostasis Associates with Inflammation, Oxidative Stress, Impaired Glucose Metabolism, and Dyslipidemia in the Crosstalk between Childhood Obesity and Insulin Resistance "The most important disturbances in childhood obesity were related to elevated circulating copper levels, decreased content of plasmatic proteins containing chromium, cobalt, iron, manganese, molybdenum, selenium, and zinc, as well as the sequestration of copper, iron, and selenium within erythrocytes" (Spain). González-Domínguez et al. Antioxidants (Basel). Serum glycolipids mediate the relationship of urinary bisphenols with NAFLD: analysis of a population-based, cross-sectional study Higher BPA and BPS exposure levels were associated with a higher risk of non-alcoholic fatty liver disease (NAFLD) (U.S. NHANES). Peng et al. Environ Health. Prenatal exposure to persistent organic pollutants and changes in infant growth and childhood growth trajectories PCB-153 was associated with increased and p,p'-DDE with decreased infant growth to age 2, but there were no associations between any of the exposures and growth trajectories to age 8 (Belgium). Cai et al. Chemosphere. Environmental Chemicals: Laboratory Studies Impact of Glyphosate on the Development of Insulin Resistance in Experimental Diabetic Rats: Role of NFκB Signalling Pathways The pesticide glyphosate can cause insulin resistance and increase glucose and insulin levels in rats by affecting insulin signaling in the liver. Prasad et al. Antioxidants (Basel). Acute and chronic effects of the organophosphate malathion on the pancreatic α and β cell viability, cell structure, and voltage-gated K+ currents High concentrations of the pesticide malathion increased cell death in rat islet cells, while low concentrations caused damage in pancreatic α and β cells. Martins et al. Environ Toxicol Pharmacol. Preconception exposure of adult male rats to bisphenol S impairs insulin sensitivity and glucose tolerance in their male offspring Paternal exposure to BPS for 2 months before mating did not alter the metabolic status of sires or female offspring. Male offspring (of  the low dose, but not high dose exposure group) had increased body weight and body fat/lean ratio, increased insulin resistance, and increased glucose-induced insulin secretion and glucose intolerance as adults. Gong et al. Chemosphere. Synergetic effects of concurrent chronic exposure to a mixture of OCPs and high-fat diets on type 2 diabetes and beneficial effects of caloric restriction in female zebrafish The group exposed to a high fat diet and organochlorine pesticides had a significant increase in glucose levels, whereas those also calorie-restricted maintained normal glucose levels. Lee et al. J Hazard Mater. Intergenerational Arsenic Exposure on the Mouse Epigenome and Metabolic Physiology Exposure to arsenic during pregnancy affected two generations of offspring with changes in weight, body composition and glucose metabolism that persisted from early life to adulthood within both generations. Colwell et al. Environ Mol Mutagen. Untargeted Lipidomics Revealed the Protective Effects of Cyanidin-3- O-glucoside on Bisphenol A-Induced Liver Lipid Metabolism Disorder in Rats The flavonoid cyanidin-3-O-glucoside ameliorated the effects of BPA on cholesterol and triglyceride levels in rats. Liu et al. J Agric Food Chem. Air Pollution Long-Term Exposure to Air Pollution and the Occurrence of Metabolic Syndrome and Its Components in Taiwan Higher annual exposure to fine particulate matter was associated with an increased risk of abdominal obesity, hypertriglyceridemia, low HDL cholesterol, hypertension, and elevated fasting blood glucose. Also, PM2.5 and NO2 may increase the risk of developing metabolic syndrome among people who already have some components of metabolic syndrome. Chen et al. EHP. Type 1 Diabetes and Autoimmunity Effect of polycyclic aromatic hydrocarbons on immunity Reviews the impact of PAHs on the immune system and some related diseases, including type 1 diabetes. Yu et al. J Transl Autoimmun. Do trace elements influence the course of newly diagnosed type 1 diabetes mellitus? Selenium, arsenic, and copper levels were increased in children newly diagnosed with type 1 diabetes. Neuro Endocrinol Lett. Additional articles on type 1 diabetes/autoimmunity: Development of Type 1 Diabetes may occur through a Type 2 Diabetes mechanism Autoimmune reaction against pancreatic beta cells in children and adolescents with simple obesity A randomized trial of oral gamma aminobutyric acid (GABA) or the combination of GABA with glutamic acid decarboxylase (GAD) on pancreatic islet endocrine function in children with newly diagnosed type 1 diabetes Projections of Type 1 and Type 2 Diabetes Burden in the U.S. Population Aged <20 Years Through 2060: The SEARCH for Diabetes in Youth Study New Drug Delays Type 1 Diabetes Onset   To see how these studies relate to existing research, or for more on environmental chemicals and diabetes/obesity, visit www.diabetesandenvironment.org Collaborative on Health and the Environment in...@healthandenvironment.org | www.healthandenvironment.org Copyright © 2023 Collaborative on Health and the Environment, All rights reserved. You are receiving this email because you opted in to the Diabetes Obesity Scienceserv Our mailing address is: Collaborative on Health and the Environment PO Box 316 Bolinas, CA 94924 Add us to your address book

[Sarah Howard]

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View this email in your browser CHE Diabetes and Obesity News and Updates

Environmental Chemicals: Human Studies Environmental Chemicals: Laboratory Studies Air Pollution

Environmental Chemicals: Human Studies

The association analysis between exposure to volatile organic chemicals and obesity in the general USA population: A cross-sectional study from NHANES program In U.S. adults, higher exposure to volatile organic chemicals (VOCs) was associated with a higher risk of obesity or abdominal obesity. Lei et al. Chemosphere. Prospective association between phthalate exposure in childhood and liver function in adolescence: the Ewha Birth and Growth Cohort Study Exposure to phthalates during childhood led to higher liver enzyme levels in adolescence; elevated liver enzymes are linked to the development of metabolic syndrome (Korea). Lee et al. Environ Health. Effect of lifestyle-based lipid lowering interventions on the relationship between circulating levels of per-and polyfluoroalkyl substances and serum cholesterol PFAS levels as well as cholesterol levels significantly decreased following a 6-month lipid-lowering lifestyle-based intervention (U.S.). Morgan et al. Environ Toxicol Pharmacol. Associations between mercury exposure with blood pressure and lipid levels: A cross-sectional study of dental professionals Higher mercury levels in urine were associated with higher LDL cholesterol levels. Xu et al. Environ Res. The effects of phthalate exposure on metabolic parameters in polycystic ovary syndrome Phthalate metabolite levels were associated with BMI, waist circumference/visceral adiposity, leptin, fasting glucose, insulin resistance, LDL cholesterol, and triglyceride levels (Serbia). Milankov et al. Clin Chim Acta.

Environmental Chemicals: Laboratory Studies

Screening of Metabolism-Disrupting Chemicals on Pancreatic α-Cells Using In Vitro Methods BPA and TBT decreased α-cell viability, while PFOA, TPP, TCS, and DDE negatively affected glucagon secretion. Dos Santos et al. Int J Mol Sci. Perfluorooctane sulfonate-induced oxidative stress contributes to pancreatic β-cell apoptosis by inhibiting cyclic adenosine monophosphate pathway: Prevention by pentoxifylline Chronic exposure of pancreatic β-cells to PFOS led to oxidative stress, reduced insulin secretion, and cell death. Elumalai et al. Environ Pollut. Alpha-lipoic acid inhibits sodium arsenite-mediated autophagic death of rat insulinoma cells The antioxidant α-lipoic acid protected insulin-secreting cells from cell death caused by sodium arsenite. Cheng et al. Hum Exp Toxicol. Endocrine adverse effects of mono(2-ethylhexyl) phthalate and monobutyl phthalate in male pubertal rats Male rats exposed to MEHP or MBP had lower pancreas weight, higher glucose and triglyceride levels, and lower insulin levels, but did not have islet autoimmunity. Karabulut and Barlas, Arh Hig Rada Toksikol. Air Pollution Association of walkability and NO2 with metabolic syndrome: A cohort study in China This longitudinal study found that people living in areas with lower walkability and higher concentrations of NO2 had an increased incidence of metabolic syndrome. Zhu et al. Environ Int. Associations of residential green space with incident type 2 diabetes and the role of air pollution: A prospective analysis in UK Biobank More residential green space was associated with lower type 2 diabetes incidence, and air pollution played an important role in this association. Yang et al. Sci Total Environ. Long-term effects of ambient PM2.5 constituents on metabolic syndrome in Chinese children and adolescents Long-term exposure to PM2.5 and PM2.5 constituents, particularly black carbon, was associated with a higher risk of metabolic syndrome in Chinese children and adolescents. Li et al. Environ Res. Effect of long-term exposure to PM2.5 on the risk of type 2 diabetes and arthritis in type 2 diabetes patients: Evidence from a national cohort in China Higher long-term exposure to PM2.5 was associated with an increased risk of developing type 2 diabetes, and with an increased risk of developing arthritis in people who had type 2 diabetes. Liu et al. Environ Int.

To see how these studies relate to existing research, or for more on environmental chemicals and diabetes/obesity, visit www.diabetesandenvironment.org

Collaborative on Health and the Environment in...@healthandenvironment.org | www.healthandenvironment.org

Copyright © 2023 Collaborative on Health and the Environment, All rights reserved. You are receiving this email because you opted in to the Diabetes Obesity Scienceserv Our mailing address is: Collaborative on Health and the Environment PO Box 316 Bolinas, CA 94924 Add us to your address book

[Sarah Howard]

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View this email in your browser CHE Diabetes and Obesity News and Updates

Reviews

Environmental Chemicals: Human Studies Environmental Chemicals: Laboratory Studies Air Pollution

Reviews Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes? "Early-life cadmium exposure can induce hepatic oxidative stress and pancreatic β-cell dysfunction, resulting in insulin resistance and glucose metabolic dyshomeostasis in the offspring." Saedi et al. Life Sci.

Environmental Chemicals: Human Studies

In utero exposure to perfluoroalkyl substances and early childhood BMI trajectories: A mediation analysis with neonatal metabolic profiles Higher in utero PFAS exposure (PFOS, PFNA, and PFDA) was associated with a persistently higher BMI growth trajectory in children to age four (China). Zeng et al. Sci Total Environ.  Environmental Chemicals: Laboratory Studies BPA and its alternatives BPF and BPAF exaggerate hepatic lipid metabolism disorders in male mice fed a high fat diet Exposure to BPA, BPF, and BPAF caused liver damage in mice. Sun et al. Sci Total Environ. Subacute and Low Dose of Tributyltin Exposure Leads to Brown Adipose Abnormalities in Male Rats In adult male rats, low dose chronic TBT exposure lowered body temperature and increased lipid accumulation in brown fat tissue via inflammation and oxidative stress. Merlo et al. Toxicol Lett. Luteolin protects against adipogenic and lipogenic potency induced by human relevant mixtures of persistent organic pollutants (POPs) in the 3T3-L1 model The flavone luteolin reduced fat cell formation and lipid accumulation caused by a mixture of persistent organic pollutants. Xie et al. Food Chem Toxicol. Adult exposure of atrazine alone or in combination with carbohydrate diet hastens the onset/progression of type 2 diabetes in Drosophila In fruit flies, atrazine exposure and a high sugar diet interact synergistically to impair glucose metabolism and lead to the early onset of diabetes and associated complications like cardiomyopathy. Gupta et al. Life Sci. Toxicity Impacts on Human Adipose Mesenchymal Stem/Stromal Cells Acutely Exposed to Aroclor and Non-Aroclor Mixtures of Polychlorinated Biphenyl Exposure to PCB mixtures found in U.S. schools led to impaired adipogenesis and a modest decrease in immunosuppressive capabilities in human adipose mesenchymal stem/stromal cells. Behan-Bush et al. Environ Sci Technol. Air Pollution Long-term air pollution exposure and diabetes risk in American older adults: A national secondary data-based cohort study Exposures to PM2.5 and NO2 are associated with increased diabetes risk in older U.S. adults (all Medicare enrollees), even when the exposure levels are below the EPA's national air quality standards. Sade et al. Environ Pollut.

To see how these studies relate to existing research, or for more on environmental chemicals and diabetes/obesity, visit www.diabetesandenvironment.org

Collaborative on Health and the Environment in...@healthandenvironment.org | www.healthandenvironment.org

Copyright © 2023 Collaborative on Health and the Environment, All rights reserved. You are receiving this email because you opted in to the Diabetes Obesity Scienceserv Our mailing address is: Collaborative on Health and the Environment PO Box 316 Bolinas, CA 94924 Add us to your address book

[Sarah Howard]

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View this email in your browser CHE Diabetes and Obesity News and Updates

Reviews Environmental Chemicals: Human Studies Environmental Chemicals: Laboratory Studies Air Pollution Reviews

The Association between Exposure to Air Pollution and Type 1 Diabetes Mellitus: A Systematic Review and Meta-Analysis. This meta-analysis of the data from six studies found that there was an increased risk of type 1 diabetes with higher levels of O3 and PM2.5 exposures, but not with PM10, SO4, SO3, or NO2. Mozafarian et al. Adv Biomed Res. Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants-A Review Reviews currently available two-dimensional in vitro animal and human cell models for studying the mechanisms of obesogenic action of  food contaminants. Kowalczyk et al. Int J Mol Sci. Partitioning of Persistent Organic Pollutants between Adipose Tissue and Serum in Human Studies All included studies reported high variability in the partitioning of POPs, mainly between adipose tissue and serum. The number of halogen atoms and body mass index were the most important factors. Moriceau et al. Toxics.

Environmental Chemicals: Human Studies

Arsenic metabolism, N6AMT1 and AS3MT single nucleotide polymorphisms, and their interaction on gestational diabetes mellitus in Chinese pregnant women Genetic variants and arsenic metabolism can interact synergistically to influence gestational diabetes occurrence. Liang et al. Environ Res. Concentration of Polycyclic Aromatic Hydrocarbons (PAHs) in Human Serum and Adipose Tissues and Stimulatory Effect of Naphthalene in Adipogenesis in 3T3-L1 Cells In bariatric surgery patients, the concentration of most PAHs was similar in three types of fatty tissue, and it was significantly higher in fat than in blood. Naphthalene levels in adipose tissue were positively associated with BMI; naphthalene also increased cell proliferation of preadipocytes (Poland and France). Mlyczyńska et al. Int J Mol Sci. Association between perfluoroalkyl substances exposure and the prevalence of nonalcoholic fatty liver disease in the different sexes: a study from the National Health and Nutrition Examination Survey 2005-2018 PFAS were associated with NAFLD, and the associations varied by sex, particularly for PFOA and PFNA, which had a positive association with NAFLD in women (U.S.). Limei et al. Environ Sci Pollut Res Int. Prenatal Mercury Exposure and Infant Weight Trajectories in a UK Observational Birth Cohort There was no strong association. Dack et al. Toxics. Environmental endocrine disruptor Bisphenol A induces metabolic derailment and obesity via upregulating IL-17A in adipocytes In a human study, BPA exposure was associated with an increased risk of obesity and inflammation in fat tissue from bariatric surgery. In an animal study, BPA increased inflammation in fat tissue, increased body weight gain and insulin resistance. Hong et al. Environ Int.

Environmental Chemicals: Laboratory Studies

Exploring the Effects of Metabolism-Disrupting Chemicals on Pancreatic α-Cell Viability, Gene Expression and Function: A Screening Testing Approach BPA, BPS, PFOS, DEHP and more all affected pancreatic alpha cells and/or glucagon secretion. Al-Abdulla et al. Int J Mol Sci. Triphenyl phosphate proved more potent than its metabolite diphenyl phosphate in inducing hepatic insulin resistance through endoplasmic reticulum stress The flame retardant TPHP caused insulin resistance in liver cells and in mice. Yue et al. Environ Int. How the Structure of Per- and Polyfluoroalkyl Substances (PFAS) Influences Their Binding Potency to the Peroxisome Proliferator-Activated and Thyroid Hormone Receptors-An In Silico Screening Study Various PFAS bind to PPARα, β, and γ receptors with low or moderate probability, and long-chain PFAS bind to thyroid receptors α and β with a moderately high probability. Kowalska et al. Molecules. Biological effects related to exposure to polychlorinated biphenyl (PCB) and decabromodiphenyl ether (BDE-209) on cats Subcutaneous fat, HDL cholesterol, and triglycerides increased in cats treated with the flame retardant BDE-209. Khidkhan et al. PLoS One. Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress BPA activated ER stress to promote fat accumulation in the liver of mice, and sulforaphane, found in cruciferous vegetables, reversed those effects by alleviating ER stress. Hong et al. Sci Rep. Replacement Flame-Retardant 2-Ethylhexyldiphenyl Phosphate (EHDPP) Disrupts Hepatic Lipidome: Evidence from Human 3D Hepatospheroid Cell Culture This study "brings a novel insight into the metabolic disrupting effects of EHDPP and demonstrates the utility of hepatospheroids as an in vitro cell culture model complemented with omics technology (e.g., lipidomics) for mechanistic toxicity studies." Negi et al. Environ Sci Technol. Air Pollution DNA Damage as a Mechanistic Link between Air Pollution and Obesity? A hypothesis article. Ghanemi et al. Medicines (Basel). Carbohydrate intake quality and gestational diabetes mellitus, and the modifying effect of air pollution Higher air pollution exposure before and during pregnancy was associated with a greater risk of gestational diabetes. Higher exposure to PM2.5, PM10, and SO2 during pregnancy decreased the beneficial effect of a high quality diet (China). Zhang et al. Front Nutr.

To see how these studies relate to existing research, or for more on environmental chemicals and diabetes/obesity, visit www.diabetesandenvironment.org

Collaborative on Health and the Environment in...@healthandenvironment.org | www.healthandenvironment.org

Copyright © 2023 Collaborative on Health and the Environment, All rights reserved. You are receiving this email because you opted in to the Diabetes Obesity Scienceserv Our mailing address is: Collaborative on Health and the Environment PO Box 316 Bolinas, CA 94924 Add us to your address book

[Sarah Howard]

Hi all,

I'm moving this newsletter to a different organization. I can keep forwarding these emails to these lists, but also you can sign up to receive it directly at the link below.

thanks!

Sarah

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View this email in your browser CHE Diabetes and Obesity News and Updates

Important! This newsletter is moving to Healthy Environment and Endocrine Disruptor Strategies (HEEDS), a program of Environmental Health Sciences. To receive it from now on, you will have to sign up for it here. Thank you!   Commentaries Can lipophilic pollutants in adipose tissue explain weight change-related risk in type 2 diabetes mellitus? The release of pollutants from fat tissue during weight loss may explain why there is an increased risk of cardiovascular disease and death in people who lose weight. Lee and Lee, J Diabetes Investig.

Environmental Chemicals: Human Studies

Cross-sectional associations of persistent organic pollutants measured in adipose tissue and metabolic syndrome in clinically diagnosed middle-aged adults In surgery patients from Spain, levels of various POPs in visceral adipose tissue, especially HCB and γ-HCH, were associated with metabolic syndrome and its individual components of (e.g. higher fasting glucose). Reina-Pérez et al. Environ Res. Association between urinary phthalate biomarker concentrations and adiposity among postmenopausal women In U.S. postmenopausal women, exposure to some phthalates was associated with more visceral adipose tissue (measured via DXA scans) three years later. Vieyra et al. Environ Res. Environmental Chemicals: Laboratory Studies Developmental programming: Adipose depot-specific regulation of non-coding RNAs and their relation to coding RNA expression in prenatal testosterone and prenatal bisphenol-A -treated female sheep Changes to non-coding RNA in different fat depots may play a role in the effects of developmental BPA exposure on insulin resistance. Dou et al. Mol Cell Endocrinol.  The potent contraceptive gestodene exerts insulinotropic effects through its a-ring reduced metabolites with intrinsic estrogen-like activity in pancreatic β-cells Long-term use of combined oral contraceptives containing gestodene (GDN), a synthetic progestin, leads to alterations in glucose metabolism in women. These authors found that GDN is converted to metabolites with estrogen-like activities and through this mechanism, GDN may affect β-cell activity. Enríquez et al. J Endocrinol Invest. Paternal phthalate exposure-elicited offspring metabolic disorders are associated with altered sperm small RNAs in mice Paternal exposure to dicyclohexyl phthalate (DCHP) worsened insulin resistance and impaired insulin signaling in offspring (F1) mice without affecting diet-induced obesity. In the subsequent (F2) generation, exposure caused glucose intolerance in females. Liu et al. Environ Int. Air Pollution Exposure to air pollution and gains in body weight and waist circumference among middle-aged and older adults This large longitudinal study from around China found that higher PM2.5, NO2 and O3 exposure was associated with gains in weight and waist circumference. Wang et al. Sci Total Environ.

To see how these studies relate to existing research, or for more on environmental chemicals and diabetes/obesity, visit www.diabetesandenvironment.org

Collaborative on Health and the Environment in...@healthandenvironment.org | www.healthandenvironment.org

Copyright © 2023 Collaborative on Health and the Environment, All rights reserved. You are receiving this email because you opted in to the Diabetes Obesity Scienceserv Our mailing address is: Collaborative on Health and the Environment PO Box 316 Bolinas, CA 94924 Add us to your address book