Thyroid hormones regulate key steps in organ development brain, ear, and bone and on the metabolism of carbohydrates, lipids, and proteins, with impact on metabolic rate [64, 65], functions that become impaired upon exposure to EDCs with thyroid hormone- hormone disrupting abilities [56]. The control exerted by the hypothalamic-pituitary-adrenal HPA axis plays a critical role to regulate energy homeostasis.
In addition to systemic adrenal production, localized control over glucocorticoid signalling can be influenced by EDCs in peripheral tissues. The aryl hydrocarbon receptor has roles on the metabolism of endogenous substances mainly hormones and exogenous substances, being a key integrator of detoxification and bioactivation of xenobiotics [66].
It has also been demonstrated that the aryl hydrocarbon receptor may affect cell proliferation, differentiation, apoptosis, and intercellular communication [67, 68], being implicated in tumor promotion upon activation by dioxins [67, 69, 70]. EDCs interaction with receptors such as AhR may compromise the normal cell functions by activating oxidative stress- sensitive signalling pathways and subsequent proinflammatory events.
The coplanar PCBs, as well as other environmental contaminants are AhR agonists, establishing a link between exposure and inflammation [71]. Several other mechanisms such as oxidative stress, mitochondrial dysfunction and epigenetic modifications are possible pathways of EDCs interference in the inflammatory processes [42, 75].
Epigenetic processes are also involved in these endocrine disrupting effects, through modifications of factors that regulate gene expression independently of modifications to the DNA sequence. These effects include changes in DNA methyltransferases, histone acetyltransferases, histone deacetylases, and histone methyltransferases with possible significant and sustained effects on gene transcription [84, 85]. Indeed, epigenetic changes mediated by dietary and environmental factors, rather than genetic changes, are a more plausible explanation for the obesity epidemic in Western countries.
In this sense, the role of epigenetics is being evaluated in CVD development and progression [86]. Showing this increased interest, a recent paper demonstrated distinct disease-specific and remodelling DNA methylation signatures in nonalcoholic fatty liver disease after bariatric surgery [87]. The knowledge regarding the epigenetic mechanisms and DNA methylation signatures related with disease progression and interaction with environmental exposures is still scarce, namely with the obesogenic effect.
Additionally, one of the ultimate goals is to define novel and potentially useful disease biomarkers, namely in the interaction with environmental exposures and disease progression.
Perinatal exposure is an important key factor, as the developing fetus or neonate are extremely sensitive to disturbance. In fact, in order to promote survival, the developing organism responds to cues of environmental quality by selecting an appropriate trajectory of growth, leading to early life metabolic adaptations and preparing the organism for its likely adult environment.
However, these established traits are a poor fit for the modern obesogenic environment. An emerging additional view hypothesizes that metabolic programming of obesity and metabolic risk may be linked to perinatal exposure to EDCs at low environmentally relevant doses [94 - 97]. Indeed, it is well acknowledged that perinatal exposure to these compounds occurs with influence in birth weight and later health outcomes [98 - ].
The hormone like activity of EDCs can disrupt the programming of endocrine signalling pathways that are established during perinatal differentiation, contributing to the development of obesity in adulthood. The specific pathways and mechanisms affected by perinatal exposure may be dependent upon the dose and the precise time of exposure, as well as other factors such as circulating endogenous hormone levels present during exposure [80].
Nevertheless, this concept needs to be supported by relevant mechanisms of action and to date, plausible molecular mechanisms include imprinting of obesity related genes or changes in cell type and number such as adipocytes [93, ].
Epigenetic alterations appear to be the most likely mechanisms that could explain perinatal programming leading to later life obesity and metabolic diseases [], giving rise to the thrifty epigenotype hypothesis.
Among the several environmental exposures, bisphenol-A exposure with influence in later disease risk are becoming increasingly well documented [, ]. Indeed, in utero exposure to environmental relevant doses of bisphenol-A was shown to have a disruption impact on glucose homeostasis and gene expression of adult mice offspring, contributing to the development of metabolic disorders.
The mechanisms by which this perinatal exposure programs the AT and endocrine function are under investigation, but it is known that maternal tobacco smoke predisposes human and rat offspring to visceral obesity in early adulthood, possibly by programming AT dysfunction via alterations in the glucocorticoid pathway and development of leptin and insulin resistance [, ].
Furthermore, in animals, epigenetic effects such as DNA methylation can also be passed to successive generations, promoting a transgenerational inheritance of environmental obesogens [, ]. Evidently, these prenatal effects can primarily occur through changes in the main organ involved in supplying nutrients to the fetus, the placenta, affecting feto-placental development and subsequent adulthood metabolic disease. In addition to changes in placenta size and morphology, the epigenetic regulation of imprinting and transporter gene expression are also important to evaluate placental programming [].
Recent research provides accumulating evidence to hypothesise that EDCs might have an important obesogenic and metabolic dysregulation ability that, to some extent, can also explain the interindividual variability of obesity effects in MetS development or T2D pathogenesis and probably different susceptibility to successful weight loss Fig. Schematic representation of the proposed mechanisms for the obesogenic and dysmetabolic effects of endocrine disrupting chemicals EDCs , depending on timing of exposure.
In order to act and monitor the extent of human contamination with environmental contaminants, even in countries with strict regulations. Therefore, additional research directed at understanding the nature and action of EDCs will illuminate the connection between health and the environment and may also reveal unappreciated new mechanisms regulating AT development, obesity, T2D and MetS.
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There are currently about registered Chinese firms in Nigeria. They are involved in construction, furniture, food and beverages, beauty, and product assembling plants, among others. Between and , for instance, the trade deficit stood at N6. This affirms that China benefits more at the moment. With the crash in the crude oil price and a global economic downturn caused by the new coronavirus, Nigeria needs Chinese investment and loans now more than ever.
China is a major financier of large projects in Nigeria. Many of these are financed by Chinese loans. It will be difficult for a country that relies so much on China to take action against Beijing. Get your free PDF by completing the following form. The latest treatment of Nigerians in China is a dent on Nigeria-China relations. But if relations are to make progress, at least two important issues must be addressed.
First, the Chinese government must do more to educate its people, making ordinary Chinese sensitive to issues of racism. Second, Chinese citizens in China must understand that their actions could have implications for their compatriots in Africa. But these issues concern not just ordinary Chinese citizens. Racism may be a symptom of much bigger problems for the Chinese government.
This could be an opportunity for the Xi Jinping government to learn , and more importantly act. This article is republished from The Conversation under a Creative Commons. Read the original article. We believe that Africa is poorly represented, and badly under-estimated. Most importantly, the level of inputs China is mobilizing is not consistently and smoothly translating into successful technology innovation outputs.
Old-school banks and new-school investment vehicles are all getting in on the action. No longer are funds just being tossed at large-scale white elephants. Commercial competitiveness is now a central part of the decision calculus.
Although this is a definite improvement over the earlier financing system, China may have overcorrected. By avoiding spending on basic research and foundational technologies, income is being generated less as a result of novel technologies and more as a result of new applications or business models.
However, the Chinese state is not entirely withdrawing, but is, in fact, strengthening its role in some regards. Whether one is discussing licensing and royalties, mergers and acquisitions, or dispute settlement, Chinese patents still have little commercial value. Chinese companies are acquiring greater market share in high tech, particularly in the most commodified segments of sectors.
From a more positive perspective, China is achieving incremental progress by benefiting from its strong capacity in manufacturing, the accumulation and diffusion of tacit knowledge, and the opportunities provided by such a large market.
Regardless of the level of support they receive from their government, Chinese companies will face growing challenges in their interactions with multinational businesses and in overseas markets.
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