scholarly journals The Role of the Bisphenol A in Diabetes and Obesity

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 666
Author(s):  
Marcelino Pérez-Bermejo ◽  
Irene Mas-Pérez ◽  
Maria Teresa Murillo-Llorente

Bisphenol A is a compound commonly found in products meant for daily use. It was one of the first compounds to be identified as an endocrine disruptor that was capable of disrupting the endocrine system and producing very similar effects to those of metabolic syndrome. It has recently gained popularity in the scientific arena as a risk factor for obesity and diabetes due to its ability to imitate natural oestrogens and bind to their receptors. The aim was to study the possible relationship between the Bisphenol A endocrine disruptor with diabetes and obesity. The analysis of the articles allows us to conclude that Bisphenol A is an additional risk factor to consider in the development of diabetes and obesity, since it is capable of stimulating the hypertrophy of adipocytes and altering the endocrine system by mimicking the effects of the oestrogen molecule, since epidemiological studies carried out have suggested that the same disruptions seen in experimental studies on animals can be found in humans; however, despite many countries having developed policies to limit exposure to this disruptor in their populations, there is a lack of international agreement. Understanding its relationship with obesity and diabetes will help to raise awareness in the population and adopt public health campaigns to prevent exposure—especially among young people—to these substances.

Biomedicines ◽  
2020 ◽  
Vol 8 (6) ◽  
pp. 137 ◽  
Author(s):  
Eleonora Rotondo ◽  
Francesco Chiarelli

The purpose of this article is to review the evidence linking background exposure to endocrine-disrupting chemicals (EDCs) with insulin resistance in children. Although evidence in children is scarce since very few prospective studies exist even in adults, evidence that EDCs might be involved in the development of insulin resistance and related diseases such as obesity and diabetes is accumulating. We reviewed the literature on both cross-sectional and prospective studies in humans and experimental studies. Epidemiological studies show a statistical link between exposure to pesticides, polychlorinated bisphenyls, bisphenol A, phthalates, aromatic polycyclic hydrocarbides, or dioxins and insulin resistance.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
M. Migliaccio ◽  
T. Chioccarelli ◽  
C. Ambrosino ◽  
A. Suglia ◽  
F. Manfrevola ◽  
...  

Bisphenol A is an industrial chemical compound, pervasively polluting the environment and diet, classified as an endocrine disruptor because of its interference effects on the endocrine system. In zebrafish, BPA exposure induces follicular atresia. To acquire knowledge on this atretic effect, using a qualitative and quantitative histomorphological approach, we studied zebrafish ovarian follicular stage development in response to low BPA concentrations. Results show that BPA interferes with follicular progression by affecting the previtellogenic and vitellogenic phases. In particular, BPA exposure (i) increases follicular recruitment by acting on primary stage follicles, (ii) forces the follicular transition from stage III to stage IV producing enlarged stage IV follicles, and (iii) induces atresia by producing atretic follicles that are peculiarly enlarged (i.e., big atretic follicles). We suggest that BPA induces atresia by the primary effect on recruitment of stage I follicles. This forces follicular progression and produces stage IV follicles that are peculiarly enlarged that undertake the atretic development.


2021 ◽  
Vol 12 ◽  
Author(s):  
Eduardo Rivera-Mancilla ◽  
Linda Al-Hassany ◽  
Carlos M. Villalón ◽  
Antoinette MaassenVanDenBrink

Migraine is a disabling neurovascular disorder, characterized by moderate to severe unilateral headaches, nausea, photophobia, and/or phonophobia, with a higher prevalence in women than in men, which can drastically affect the quality of life of migraine patients. In addition, this chronic disorder is related with metabolic comorbidities associated with the patient's lifestyle, including obesity and diabetes mellitus (DM). Beyond the personal and socioeconomic impact caused by migraine, obesity and DM, it has been suggested that these metabolic disorders seem to be related to migraine since: (i) they are a risk factor for developing cardiovascular disorders or chronic diseases; (ii) they can be influenced by genetic and environmental risk factors; and (iii) while clinical and epidemiological studies suggest that obesity is a risk factor for migraine, DM (i.e., type 1 and type 2 DM) have been reported to be either a protective or a risk factor in migraine. On this basis, and given the high worldwide prevalence of migraine, obesity, and DM, this article provides a narrative review of the current literature related to the association between the etiology and pathophysiology of migraine and these metabolic disorders, considering lifestyle aspects, as well as the possible involvement of neurotransmitters, neuropeptides, and/or sex hormones. While a link between migraine and metabolic disorders has been suggested, many studies are contradictory and the mechanisms involved in this association are not yet sufficiently established. Therefore, further research should be focused on understanding the possible mechanisms involved.


Diabetes ◽  
1990 ◽  
Vol 39 (7) ◽  
pp. 855-857 ◽  
Author(s):  
S. Easteal ◽  
M. R. Kohonen-Corish ◽  
P. Zimmet ◽  
S. W. Serjeantson

2018 ◽  
Vol 24 (3) ◽  
pp. 341-358 ◽  
Author(s):  
Xiaotong Ji ◽  
Yingying Zhang ◽  
Guangke Li ◽  
Nan Sang

Recently, numerous studies have found that particulate matter (PM) exposure is correlated with increased hospitalization and mortality from heart failure (HF). In addition to problems with circulation, HF patients often display high expression of cytokines in the failing heart. Thus, as a recurring heart problem, HF is thought to be a disorder characterized in part by the inflammatory response. In this review, we intend to discuss the relationship between PM exposure and HF that is based on inflammatory mechanism and to provide a comprehensive, updated evaluation of the related studies. Epidemiological studies on PM-induced heart diseases are focused on high concentrations of PM, high pollutant load exposure in winter, or susceptible groups with heart diseases, etc. Furthermore, it appears that the relationship between fine or ultrafine PM and HF is stronger than that between HF and coarse PM. However, fewer studies paid attention to PM components. As for experimental studies, it is worth noting that coarse PM may indirectly promote the inflammatory response in the heart through systematic circulation of cytokines produced primarily in the lungs, while ultrafine PM and its components can enter circulation and further induce inflammation directly in the heart. In terms of PM exposure and enhanced inflammation during the pathogenesis of HF, this article reviews the following mechanisms: hemodynamics, oxidative stress, Toll-like receptors (TLRs) and epigenetic regulation. However, many problems are still unsolved, and future work will be needed to clarify the complex biologic mechanisms and to identify the specific components of PM responsible for adverse effects on heart health.


2019 ◽  
Vol 17 (6) ◽  
pp. 591-594 ◽  
Author(s):  
John C. Stevenson ◽  
Sophia Tsiligiannis ◽  
Nick Panay

Cardiovascular disease, and particularly coronary heart disease (CHD), has a low incidence in premenopausal women. Loss of ovarian hormones during the perimenopause and menopause leads to a sharp increase in incidence. Although most CHD risk factors are common to both men and women, the menopause is a unique additional risk factor for women. Sex steroids have profound effects on many CHD risk factors. Their loss leads to adverse changes in lipids and lipoproteins, with increases being seen in low density lipoprotein (LDL) cholesterol and triglycerides, and decreases in high density lipoprotein (HDL) cholesterol. There is a reduction in insulin secretion and elimination, but increases in insulin resistance eventually result in increasing circulating insulin levels. There are changes in body fat distribution with accumulation in central and visceral fat which links to the other adverse metabolic changes. There is an increase in the incidence of hypertension and of type 2 diabetes mellitus, both major risk factors for CHD. Oestrogens have potent effects on blood vessels and their loss leads to dysfunction of the vascular endothelium. All of these changes result from loss of ovarian function contributing to the increased development of CHD. Risk factor assessment in perimenopausal women is recommended, thereby permitting the timely introduction of lifestyle, hormonal and therapeutic interventions to modify or reverse these adverse changes.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T.J Jernberg ◽  
E.O Omerovic ◽  
E.H Hamilton ◽  
K.L Lindmark ◽  
L.D Desta ◽  
...  

Abstract Background Left ventricular dysfunction after an acute myocardial infarction (MI) is associated with poor outcome. The PARADISE-MI trial is examining whether an angiotensin receptor-neprilysin inhibitor reduces the risk of cardiovascular death or worsening heart failure (HF) in this population. The aim of this study was to examine the prevalence and prognosis of different subsets of post-MI patients in a real-world setting. Additionally, the prognostic importance of some common risk factors used as risk enrichment criteria in the PARADISE-MI trial were specifically examined. Methods In a nationwide myocardial infarction registry (SWEDEHEART), including 87 177 patients with type 1 MI between 2011–2018, 3 subsets of patients were identified in the overall MI cohort (where patients with previous HF were excluded); population 1 (n=27 568 (32%)) with signs of acute HF or an ejection fraction (EF) <50%, population 2 (n=13 038 (15%)) with signs of acute HF or an EF <40%, and population 3 (PARADISE-MI like) (n=11 175 (13%)) with signs of acute HF or an EF <40% and at least one risk factor (Age ≥70, eGFR <60, diabetes mellitus, prior MI, atrial fibrillation, EF <30%, Killip III-IV and STEMI without reperfusion therapy). Results When all MIs, population 1 (HF or EF <50%), 2 (HF or EF <40%) and 3 (HF or EF <40% + additional risk factor (PARADISE-MI like)) were compared, the median (IQR) age increased from 70 (61–79) to 77 (70–84). Also, the proportion of diabetes (22% to 33%), STEMI (38% to 50%), atrial fibrillation (10% to 24%) and Killip-class >2 (1% to 7%) increased. After 3 years of follow-up, the cumulative probability of death or readmission because of heart failure in the overall MI population and in population 1 to 3 was 17.4%, 26.9%, 37.6% and 41.8%, respectively. In population 2, all risk factors were independently associated with death or readmission because of HF (Age ≥70 (HR (95% CI): 1.80 (1.66–1.95)), eGFR <60 (1.62 (1.52–1.74)), diabetes mellitus (1.35 (1.26–1.44)), prior MI (1.16 (1.07–1.25)), atrial fibrillation (1.35 (1.26–1.45)), EF <30% (1.69 (1.58–1.81)), Killip III-IV (1.34 (1.19–1.51)) and STEMI without reperfusion therapy (1.34 (1.21–1.48))) in a multivariable Cox regression analysis. The risk increased with increasing number of risk factors (Figure 1). Conclusion Depending on definition, post MI HF is present in 13–32% of all MI patients and is associated with a high risk of subsequent death or readmission because of HF. The risk increases significantly with every additional risk factor. There is a need to optimize management and improve outcomes for this high risk population. Figure 1 Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Novartis


Author(s):  
Judit Biosca-Brull ◽  
Cristian Pérez-Fernández ◽  
Santiago Mora ◽  
Beatriz Carrillo ◽  
Helena Pinos ◽  
...  

Autism spectrum disorder (ASD) is a complex set of neurodevelopmental pathologies characterized by impoverished social and communicative abilities and stereotyped behaviors. Although its genetic basis is unquestionable, the involvement of environmental factors such as exposure to pesticides has also been proposed. Despite the systematic analyses of this relationship in humans, there are no specific reviews including both human and preclinical models. The present systematic review summarizes, analyzes, and discusses recent advances in preclinical and epidemiological studies. We included 45 human and 16 preclinical studies. These studies focused on Organophosphates (OP), Organochlorine (OC), Pyrethroid (PT), Neonicotinoid (NN), Carbamate (CM), and mixed exposures. Preclinical studies, where the OP Chlorpyrifos (CPF) compound is the one most studied, pointed to an association between gestational exposure and increased ASD-like behaviors, although the data are inconclusive with regard to other ages or pesticides. Studies in humans focused on prenatal exposure to OP and OC agents, and report cognitive and behavioral alterations related to ASD symptomatology. The results of both suggest that gestational exposure to certain OP agents could be linked to the clinical signs of ASD. Future experimental studies should focus on extending the analysis of ASD-like behaviors in preclinical models and include exposure patterns similar to those observed in human studies.


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