Persistent organic pollutants and β-cell toxicity: a comprehensive review

Hoyeck, Myriam P; Matteo, Geronimo; MacFarlane, Erin M.; Perera, Ineli; Bruin, Jennifer E.

doi:10.1152/ajpendo.00358.2021

Cited by 31 publications

(23 citation statements)

References 332 publications

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“…Furthermore, dioxins are other group of pollutants generates pancreatic β cell dysfunction ( 96 ). There are several mechanisms involved in pancreatic β cell toxicity produced by dioxins that have been reviewed very recently ( 97 ).…”

Section: Effects Of Toxic Metabolites In β Cell Function and Viabilitymentioning

confidence: 99%

Targeting pancreatic beta cell death in type 2 diabetes by polyphenols

Garcimartín

Guillén

2022

Front. Endocrinol.

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Diabetes is a very complex disease which is characterized by the appearance of insulin resistance that is primarily compensated by an increase in pancreatic beta cell mass, generating hyperinsulinemia. After time, pancreatic beta cells die by apoptosis appearing in the second phase of the disease, and characterized by hypoinsulinemia. There are multiple conditions that can alter pancreatic beta cell homeostasis and viability, being the most relevant ones; ER stress, cytotoxicity by amylin, mTORC1 hyperactivity, oxidative stress, mitochondrial dysfunction, inflammation and alterations in autophagy/mitophagy flux. In addition, the possible effects that different polyphenols could exert in the modulation of these mechanisms and regulating pancreatic beta cell viability are analyzed. It is necessary a profound analysis and understanding of all the possible mechanisms involved in the control and maintenance of pancreatic beta cell viability to develop more accurate and target treatments for controlling beta cell homeostasis and preventing or even reversing type 2 diabetes mellitus.

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Section: Effects Of Toxic Metabolites In β Cell Function and Viabilitymentioning

confidence: 99%

Targeting pancreatic beta cell death in type 2 diabetes by polyphenols

Garcimartín

Guillén

2022

Front. Endocrinol.

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“…Some POPs are diabetogenic because they directly modify β-cell function and/or mass ( 31 ). In contrast, other EDCs are nonpersistent, do not accumulate as readily, and are metabolized and excreted in ∼24 h; such EDCs include phthalates and most bisphenols.…”

Section: Endocrine Disrupting Chemicalsmentioning

confidence: 99%

Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus

Martı́nez-Pinna

Sempere-Navarro

Medina-Gali

et al. 2023

American Journal of Physiology-Endocrinology and Metabolism

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Plastic pollution breaks a planetary boundary threatening wildlife and humans through its physical and chemical effects. Of the latter, the release of endocrine disrupting chemicals (EDCs) has consequences on the prevalence of human diseases related to the endocrine system. Bisphenols (BPs) and phthalates are two groups of EDCs commonly found in plastics that migrate into the environment and make low dose human exposure ubiquitous. Here we review epidemiological, animal, and cellular studies linking exposure to BPs and phthalates to altered glucose regulation, with emphasis on the role of pancreatic β-cells. Epidemiological studies indicate that exposure to BPs and phthalates is associated with diabetes mellitus. Studies in animal models indicate that treatment with doses within the range of human exposure decrease insulin sensitivity and glucose tolerance, induce dyslipidemia, and modify functional β-cell mass and serum levels of insulin, leptin and adiponectin. These studies reveal that disruption of β-cell physiology by EDCs plays a key role in impairing glucose homeostasis by altering the mechanisms used by β-cells to adapt to metabolic stress such as chronic nutrient excess. Studies at the cellular level demonstrate that BPs and phthalates modify the same biochemical pathways involved in adaptation to chronic excess fuel. These include changes in insulin biosynthesis and secretion, electrical activity, expression of key genes, and mitochondrial function. The data summarized here indicate that BPs and phthalates are an important risk factor for diabetes mellitus and support a global effort to decrease plastic pollution and human exposure to EDCs.

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“…Numerous epidemiological studies suggest that POPs exposure may be related to the prevalence of diabetes. − In a meta-analysis of six prospective studies, POPs such as total PCBs and HCB were associated with an increased risk of type 2 diabetes . In a recent review, POPs were suggested as a contributing factor causing altered glucose homeostasis and impaired β-cell function in the pancreas . Demographic characteristics might modify the association between POPs exposure and incident diabetes: In a recent meta-analysis, gender-dependency was suggested for associations between POP exposure and incident diabetes .…”

Section: Introductionmentioning

confidence: 99%

Gender- and Age-Group Specific Association of Persistent Organic Pollutants (POPs) Exposure with Diabetes Mellitus: Korean National Environmental Health Survey (KoNEHS) 2015–2017

Lee,

Kim,

Choi

et al. 2024

Environ. Health

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Exposure to persistent organic pollutants (POPs) has been reported as a potential risk factor for diabetes in adults. However, effect modifications by sex and age, especially among Asian populations, have seldom been investigated. In the present study, we assessed associations of major POPs exposure including organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs), with diabetes in Korean adults (n = 1,295), a subset of the Korean National Environmental Health Survey (KoNEHS) Cycle 3 (2015−2017). In the adult population, serum levels of dichlorodiphenyltrichloroethanes (DDTs) and PCB167 showed an increased odds ratio (OR) for diabetes. When stratified by gender, associations became stronger and more consistent in women: In women, serum levels of OCPs including p,p′-DDT, p,p′dichlorodiphenyldichloroethylene (p,p′-DDE), and ΣOCPs and mono-ortho PCBs, such as PCB118 and PCB157, were significantly associated with diabetes. In the male participants, however, no significant positive associations were detected. When stratified by a cutoff age of 50 years, most studied POPs except PBDEs, i.e., p,p′-DDT, p,p′-DDE, PCB118, PCB157, PCB167, PCB138, and PCB153, showed significant associations with diabetes, in the older adults. In the younger group, however, no measured POPs showed a significant positive association. Effects of endogenous sex hormones or interaction of POPs on aryl hydrocarbon receptors may partly explain the observed differences by gender and age, although further experimental confirmations should follow. Our findings show that POPs exposure at the current levels is associated with diabetes among general Korean adults, and such associations could be modified by gender and age.

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Persistent organic pollutants and β-cell toxicity: a comprehensive review

Cited by 31 publications

References 332 publications

Targeting pancreatic beta cell death in type 2 diabetes by polyphenols

Targeting pancreatic beta cell death in type 2 diabetes by polyphenols

Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus

Gender- and Age-Group Specific Association of Persistent Organic Pollutants (POPs) Exposure with Diabetes Mellitus: Korean National Environmental Health Survey (KoNEHS) 2015–2017

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