Exposure to environmental chemicals and type 1 diabetes: an update

Howard, Sarah

doi:10.1136/jech-2018-210627

Cited by 36 publications

(22 citation statements)

References 34 publications

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“…Lut has a defensive activity contradicted to the damage because of OS in specific organs, for example, the kidney, the heart, and the liver. Past investigations have proven that Lut could prevent hepatotoxicity caused by the administration of BPA, by diminishing OS and inflammation by means of blocking NF‐κB incitement . OS means that tissue damage brings about by BPA administration.…”

Section: Discussionmentioning

confidence: 99%

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

Sita¹,

Gowthami²,

Srikanth³

et al. 2019

IUBMB Life

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For the development of renal diseases, oxidative stress (OS) is reasoned to be one of the risk factors. For the treatment or prevention of the renal disease, the use of antioxidants could be a hopeful therapeutic mediation as they retard or block the oxidative reaction along with the inflammatory process. Luteolin (Lut) is a plant flavonoid, a pharmacologically active component normally found in glycosylated forms in basic perilla leaf, green pepper, celery, seed, honeysuckle bloom, and chamomile blossom; it exhibits antioxidant activity. In this investigation, we explored the nephroprotective activity of Lut on bisphenol A (BPA)‐induced nephron toxicity in rats. Orally administering Lut (100 and 200 mg/kg) diminished BPA‐induced anomalies in the kidney, blood urea nitrogen, creatinine, and serum uric acid levels. Lut therapy reduced the BPA‐influenced generation of inflammatory mediators, inclusive of tumor necrosis factor alpha, interleukin 6, and interleukin 1 beta. This was coupled with significant improvement in kidney histopathologic features. Lut enhanced the nuclear factor‐like 2 (Nrf2) and heme oxygenase 1 (HO‐1) expression, which showed protection against OS induced by BPA. The current outcomes of the study showed that Lut has a strong reactive oxygen species scavenging property and potentially decreases the lipid peroxidation as well as inhibits DNA damage in renal toxicity induced by BPA. In conclusion, the potential antioxidant effect of Lut may be because of its modulatory effect on the Nrf2/antioxidant response element (ARE)/HO‐1 pathway, which means it protects the kidney from BPA‐induced oxidative injury. © 2019 IUBMB Life, 2019

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Section: Discussionmentioning

confidence: 99%

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

Sita¹,

Gowthami²,

Srikanth³

et al. 2019

IUBMB Life

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“…Environmental chemicals have been suggested to influence type 1 diabetes by various mechanisms, but there are few high quality studies of human type 1 diabetes. 142 A few studies have found suggestive evidence for an association between air pollution and risk of type 1 diabetes, but there are methodological difficulties with exposure measurements. Overall, there seem to be no consistent association between environmental toxins and type 1 diabetes, or islet autoimmunity.…”

Section: Toxinsmentioning

confidence: 99%

“…Overall, there seem to be no consistent association between environmental toxins and type 1 diabetes, or islet autoimmunity. 142,143 Although many toxins have been introduced into the environment, many have been banned resulting in decreasing exposure trends. 144 Air pollution is highest in areas with low incidence of type 1 diabetes and has decreased over the past decades in high-income countries.…”

Section: Toxinsmentioning

confidence: 99%

Type 1 diabetes—early life origins and changing epidemiology

Norris

Johnson

Stene

2020

The Lancet Diabetes & Endocrinology

253

171

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Type 1 diabetes is a chronic, immune-mediated disease characterised by the destruction of insulinproducing cells. Standardised registry data show that type 1 diabetes incidence has increased 3-4% over the past three decades, supporting the role of environmental factors. Although several factors have been associated with type 1 diabetes, none of the associations are of a magnitude that could explain the rapid increase in incidence alone. Moreover, evidence of changing prevalence of these exposures over time is insufficient. Multiple factors could simultaneously explain the changing type 1 diabetes incidence, or the magnitude of observed associations could have been underestimated because of exposure measurement error, or the mismodelling of complex exposure-time-response relationships. The identification of environmental factors influencing the risk of type 1 diabetes and increased understanding of the cause at the individual level, regardless of the ability to explain the changing incidence at the population level, is important because of the implications for prevention.

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“…Research on environmental factors involved in the etiology of islet autoimmunity were focused on the role of viruses [20,21], early infant diet [22,23], childhood weight gain [24], vitamin D [25], gut microbiome [26][27][28], and environmental endocrine disrupting chemicals (EDCs) [29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Endocrine Disrupting Chemicals and Type 1 Diabetes

Predieri

Bruzzi

Bigi

et al. 2020

IJMS

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Type 1 diabetes (T1D) is the most common chronic metabolic disease in children and adolescents. The etiology of T1D is not fully understood but it seems multifactorial. The genetic background determines the predisposition to develop T1D, while the autoimmune process against β-cells seems to be also determined by environmental triggers, such as endocrine disrupting chemicals (EDCs). Environmental EDCs may act throughout different temporal windows as single chemical agent or as chemical mixtures. They could affect the development and the function of the immune system or of the β-cells function, promoting autoimmunity and increasing the susceptibility to autoimmune attack. Human studies evaluating the potential role of exposure to EDCs on the pathogenesis of T1D are few and demonstrated contradictory results. The aim of this narrative review is to summarize experimental and epidemiological studies on the potential role of exposure to EDCs in the development of T1D. We highlight what we know by animals about EDCs’ effects on mechanisms leading to T1D development and progression. Studies evaluating the EDC levels in patients with T1D were also reported. Moreover, we discussed why further studies are needed and how they should be designed to better understand the causal mechanisms and the next prevention interventions.

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Exposure to environmental chemicals and type 1 diabetes: an update

Cited by 36 publications

References 34 publications

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

Type 1 diabetes—early life origins and changing epidemiology

Endocrine Disrupting Chemicals and Type 1 Diabetes

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