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#校园新闻# Is plastic making us fat?
发布时间:2018-09-05 丨 阅读次数:378

Is plastic making us fat?

塑料会使人变胖吗?


Today, nearly 40 percent of U.S. adults and 21 percent of youth are obese.

今天,美国有近40%的成年人和21%的年轻人肥胖。

 

This trend is on the upswing and the worldwide population is becoming more obese — which is increasing the risk of other conditions like Type 2 diabetes and cardiovascular disease whose prevalence has doubled globally in the last 30 years. But you may be surprised to learn that it’s not just food that is making us fat.

这一趋势正在上升,全球肥胖人口越来越多-这无疑增加了患2型糖尿病和心血管病等疾病的风险。在过去30年里,在全球范围内这些疾病的发病率翻了一番。但你可能会惊讶地发现,我们变胖的原因不仅仅是食物。

 

Experiments using animal models have shown that exposure to chemicals used in industry and found in plastics, preservatives, pesticides and flame retardants, just to name a few, may be important contributors to the growing number of metabolic disorders — including obesity.

利用动物模型进行的实验表明,工业中使用的化学品以及塑料、防腐剂、杀虫剂和阻燃剂中发现的化学品(仅举几个例子)都可能是导致当前越来越多代谢紊乱问题的重要因素,其中也包括肥胖。

 

One of the research goals in my lab is to identify environmental chemicals that may contribute to these increased rates of metabolic diseases and to decipher the mechanisms through which they act. This line of work began with the unexpected discovery that a chemical (tributyltin, or TBT) we were studying for other reasons could activate a hormone receptor linked to the development of fat. We went on to show that TBT could make mice exposed during prenatal life fatter and that this trait could be transmitted to future generations.

我实验室的研究目标之一是找出环境中可能导致代谢疾病发病率增加的化学物质,并破译它们的作用机制。这项工作始于一个意想不到的发现,即我们正在研究的一种化学物质三丁基锡(TBT),它可以激活一种与脂肪的发育相关的激素受体。随后,我们又发现,TBT可以使小鼠在产前长得更胖,并且这一特性可以遗传给后代。

 

Our recent study reveals that dibutyltin, a chemical used in the manufacture of a type of plastic called polyvinyl chloride, or PVC, alters glucose metabolism and increases fat storage in mice.

我们最近的研究表明,二丁基锡,这种用于制造聚氯乙烯(PVC)塑料的化学物质,能够改变小鼠的葡萄糖代谢,并增加它们的脂肪储存量。

 

Obesity and Type 2 diabetes

肥胖与2型糖尿病


In healthy individuals, the pancreas secretes a hormone called insulin into the bloodstream after a meal when the blood sugar levels rise. Insulin stimulates tissues, such as muscle, fat cells and the brain to absorb glucose from the blood and store it as fat. If the pancreas secretes insulin but tissues are not able to detect it, glucose levels remain unchanged leading to “insulin resistance.”

在健康个体中,当血糖水平升高时,进餐后胰腺会分泌一种叫做胰岛素的激素进入血液。胰岛素刺激组织,如肌肉、脂肪细胞和大脑,从血液中吸收葡萄糖,并将其储存为脂肪。如果胰腺分泌胰岛素,但组织不能检测到它,葡萄糖水平保持不变,就会导致“胰岛素抵抗”。

 

As an individual becomes overweight, there is an increase in free fatty acids in the blood stream which may contribute to reduced insulin sensitivity in the tissues, leading to increased glucose levels in blood. At early stages, when sugar levels are higher than normal, but not too high, the individual is considered prediabetic. At that stage, prediabetics can make lifestyle changes — lose weight and exercise more — to lower their glucose levels and reduce the risk to develop diabetes.

当一个人超重时,血液中增加的游离脂肪酸可能会导致组织中胰岛素敏感性的降低,从而致使血液中葡萄糖水平升高。在早期阶段,当人体血糖水平略高于正常水平时,就会被认为是糖尿病前期。在这一阶段,糖尿病前期患者可以改变生活方式-减肥和多运动-以降低血糖水平,降低患糖尿病的风险。

 

However, there is evidence in rodents showing that exposure to certain environmental chemicals hampers fat mobilization during periods of fasting and when animals are exposed to a low-fat diet, suggesting that losing weight may be tougher than curbing calories.

然而,有证据表明,啮齿类动物在禁食期间或动物处于低脂饮食时,一旦接触某些化学物质便会阻碍它们的脂肪动员,减肥可能比控制卡路里更难。

 

Chemicals in plastics associated with obesity

塑料中与肥胖有关的化学物质

 

The most common explanation for obesity is overeating calorie-rich foods and sedentary lifestyle. However, in the last 10 years, a subset of endocrine-disrupting chemicals (EDCs) called obesogens has been shown to cause obesity in animals and were associated with more fat mass in humans. EDCs are chemicals from outside of the body that interfere with the action of natural hormones present in living organisms. Hormones are secreted by the endocrine glands, such as the pancreas and thyroid, which regulate critical biological functions in the body including reproduction and glucose metabolism. Therefore, altering hormone levels or action can contribute to disease.

肥胖最常见的原因是过量摄入高热量的食物和久坐不动的生活方式。然而,在过去的10年里,一种叫做致胖因子内分泌干扰化学物质(EDCs)已经被证明能引起动物的肥胖,并且与人类的脂肪量有关。EDCs是来自身体外的化学物质,有干扰生物体中天然激素的作用。激素由内分泌腺体分泌,如胰腺和甲状腺,调节体内的重要生物功能,包括生殖和葡萄糖代谢。因此,改变激素水平或作用可能会导致疾病。

 

Obesogens act by inappropriately stimulating fat storage in the organism by altering fat tissue biology, energy balance and/or the regulation of metabolic needs.

致胖因子通过改变脂肪组织、打破能量平衡和/或干扰代谢调节,从而不适当地刺激了机体中的脂肪储存量。

 

Dibutyltin (DBT) salts are used in the manufacture of PVC (vinyl) plastics that are extensively utilized in many applications including construction materials (e.g., window frames and vinyl flooring), and medical devices (e.g., tubing and packaging). DBT has been found in seafood and house dust, suggesting that DBT exposure may be widespread. However, there is little information available about DBT levels in humans.

二丁基锡(DBT)盐用于制造PVC(乙烯基)塑料,广泛应用于建筑材料(如窗框和乙烯基地板)和医疗设备(如管材和包装)。我们在海鲜和家庭灰尘中发现了DBT,这表明DBT接触可能是广泛存在的。然而,几乎没有关于人体DBT水平的信息。

 

Exposure to DBT in mice

接触过DBT的小鼠

 

We used cells in culture to show that DBT activated two proteins that promote fat cell precursors to become mature fat cells, leading to more fat cells and increased fat in each. Therefore, chemicals that activate these receptors promote the development of fat tissue, making them obesogens.

通过细胞培养发现,DBT激活了两种蛋白质,促使脂肪细胞前体发展成为成熟的脂肪细胞,进而导致脂肪细胞增多,脂肪增加。因此,激活这些受体的化学物质促进脂肪组织的发育,使其成为致胖基因。

 

In our study, cells exposed to concentrations of DBT that are in the realm of what humans are predicted to be exposed to show increased fat storage, as seen under the microscope, as well as increased activity of genes involved in fat tissue development.

在我们的研究中,可在显微镜下看到那些接触了一定浓度DBT的细胞:在人类预测的接触范围内显示有更多的脂肪储存量,以及参与脂肪组织发育的基因活性会增加。

 

Additionally, we gave DBT to pregnant mice via their drinking water and extended the exposure through lactation. Male offspring, which were exposed during development in the womb and through maternal breast milk, accumulated more fat when their diet was changed from a low-fat to a slightly higher fat diet than did unexposed animals. This indicates that DBT exposure during development and early in life predisposed these DBT exposed animals to become obese. Interestingly, we did not find this response to diet in females.

此外,我们还通过给怀孕小鼠饮用含DBT的水,以及用哺乳延长DBT接触时间。在子宫发育阶段和母乳喂养过程中接触过DBT的雄性后代,当他们的饮食从低脂转变为略高脂时,将比未接触过的动物积累更多的脂肪。这表明在发育阶段和生命早期接触的DBT会使动物变得肥胖。有趣的是,我们却没有发现女性有这种反应。

 

In these mice we noted that insulin production in the pancreas was altered.

在这些小鼠中,我们注意到胰腺中的胰岛素生成发生了改变。

 

Interestingly, they also had increased higher levels of leptin, a hormone secreted by the fat tissue involved in the regulation of appetite and blood glucose levels. Higher fasting glucose levels were found in both genders, but only males showed increased leptin levels and glucose intolerance. The results of our study indicate early exposure to obesogen DBT and increased dietary fat induces prediabetes in male mice.

有趣的是,他们还提高了瘦素的水平,瘦素是由参与调节食欲和血糖水平的脂肪组织分泌的一种激素。当不同性别的空腹血糖水平都较高时,只有男性的瘦素水平和葡萄糖耐受性增高。我们的研究结果表明,早期接触过致胖因子DBT以及不断增加饮食脂肪量的雄性小鼠易得糖尿病前期。

 

Since the sources of human exposure to obesogens are numerous, monitoring obesogen levels, including DBT, in human tissues will help understand and prevent the increasing rates of metabolic disorders such as obesity and T2D in human populations. Reducing the use of plastics that contain obesogens will not only improve our health but will be good for the environment as well, considering the huge plastic garbage patches in the world’s oceans.

由于人类接触致胖因子的来源很多,监测人体组织中包括DBT在内的致胖因子将有助于了解和防止患肥胖症和T2D等代谢紊乱人数增加问题。考虑到世界海洋中巨大的塑料垃圾块,减少使用含有致胖因子的塑料不仅会改善我们的健康,而且对环境也会有好处。