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Lipophilic chemical exposure as a cause of type 2 diabetes (T2D)

机译：亲脂性化学暴露是导致2型糖尿病（T2D）的原因

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The prevalence of type 2 diabetes (T2D) is increasing worldwide in pandemic-like numbers. It is considered, at least in part, to be an environmental illness. Recent research has shown that diabetes can be caused by exposure to persistent organic pollutants (POPs), exudates from common plastics, air pollution, primary and secondary tobacco smoke, and some Pharmaceuticals. These chemicals vary widely in structure, chemical properties, and composition and are not currently believed to induce a similar effect. A unifying explanation for the induction of T2D by this diversified group of chemicals is proposed here. These toxicants have one thing in common. All are lipophilic species that permeate lipophilic body membranes, thereby promoting the absorption of toxic hydrophilic species that would otherwise not penetrate lipophilic membranes. It is further proposed that exposure to the lipophilic and hydrophilic species need not occur simultaneously but can occur sequentially, with the lipophile absorbed first and retained in body serum, followed by a subsequent exposure to the hydrophile. The lipophilic chemical can be one of the POPs (including dioxins, furans, polychlorinated biphenyls, polybrominated biphenyls, poly-brominated diphenyl ethers, or organochlorine pesticides); a more rapidly metabolized or eliminated species including plastic exudates like phthalate esters and bisphenol A; air pollutants and tobacco smoke components including aliphatic, aromatic, or polynuclear aromatic hydrocarbons; or Pharmaceuticals like some statins and second-generation antipsychotic drugs. This hypothesis suggests that the T2D pandemic as well as the rapid increase of other environmental disease prevalence is, at least in part, due to sequential exposure to levels of lipophilic and hydrophilic environmental pollutants that are much lower than those currently believed to be toxic. As a consequence of this hypothesis, the allowable levels of exposure to these pollutants should be dramatically lowered.
机译：2型糖尿病（T2D）的患病率在世界范围内呈大流行状上升。它至少部分被认为是环境疾病。最近的研究表明，糖尿病可能是由于接触持久性有机污染物（POPs），普通塑料的渗出物，空气污染，初级和次级烟草烟雾以及某些药物引起的。这些化学物质在结构，化学性质和组成上差异很大，目前不认为会产生类似的作用。本文提出了由这种多样化的化学物质诱导T2D的统一解释。这些毒物有一个共同点。所有都是渗透亲脂体膜的亲脂性物质，从而促进了有毒亲水性物质的吸收，否则它们将不会渗透亲脂膜。进一步提出，亲脂性和亲水性物质的暴露不必同时发生，而是可以顺序发生，首先将亲脂性物质吸收并保留在人体血清中，然后再暴露于亲水性物质中。亲脂性化学物质可以是持久性有机污染物之一（包括二恶英，呋喃，多氯联苯，多溴联苯，多溴二苯醚或有机氯农药）；代谢或清除速度更快的物种，包括邻苯二甲酸酯和双酚A等塑料渗出液；空气污染物和烟草烟雾成分，包括脂肪族，芳香族或多核芳香族碳氢化合物；或药物，例如某些他汀类药物和第二代抗精神病药。该假设表明，T2D大流行以及其他环境疾病患病率的迅速提高，至少部分是由于相继暴露于亲脂性和亲水性环境污染物的水平，该水平远低于目前认为有毒的污染物。由于这一假设，应大大降低这些污染物的允许暴露水平。

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