高蛋白饮食会增加形成动脉阻塞斑块的风险 High-protein diets boost artery-clogging plaque, mouse study shows

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高蛋白饮食可以帮助人们减轻体重并增强肌肉,但是一项对小鼠的新研究表明,它们有不利的一面:它们会导致动脉中更多的斑块。此外,新研究还表明,高蛋白饮食会刺激斑块不稳定,这种斑块最容易破裂并引起动脉阻塞。动脉中更多的斑块堆积,特别是如果不稳定时,会增加心脏病发作的风险。

这项新研究由圣路易斯华盛顿大学医学院的研究人员于1月23日发表在《自然新陈代谢》杂志上。

高级作者医学副教授巴巴克·拉扎尼(Babak Razani)表示:“高蛋白饮食在减肥方面具有明显的好处,这在近几年中日益普及。” “但是动物研究和一些人的大型流行病学研究已将高饮食蛋白与心血管疾病联系在一起。我们决定研究高饮食蛋白与较差的心血管健康之间是否存在真正的因果关系。”

研究人员研究了喂养高脂饮食以故意诱发动脉粥样硬化或动脉斑块堆积的小鼠。据拉扎尼说,老鼠必须吃高脂饮食才能形成动脉斑块。因此,一些小鼠接受了高脂肪饮食,蛋白质含量也很高。其他老鼠则进食高脂,低蛋白饮食以作比较。

拉扎尼说:“在奶昔或冰沙中加入几勺蛋白质粉会增加40克左右的蛋白质-几乎等同于每日推荐的摄入量。” “为了解蛋白质是否对心血管健康有影响,我们将高脂高蛋白质饮食中小鼠摄入的蛋白质量增加了三倍,保持脂肪恒定。蛋白质的热量从15%降至46%。”

高脂,高蛋白饮食的小鼠比高脂,高蛋白饮食的小鼠发生动脉粥样硬化的情况更严重-动脉粥样斑块增加了30%-尽管事实上,进食高蛋白饮食的小鼠不增加体重,这与高脂,普通蛋白质饮食的小鼠不同。

拉扎尼说:“这项研究并不是第一个显示高蛋白饮食能使斑块明显增加的研究,但是通过对斑块的详细分析,它可以使人们对高蛋白的影响有更深入的了解。” “换句话说,我们的研究表明饮食蛋白如何以及为什么导致不稳定斑块的发展。”

斑块包含脂肪,胆固醇,钙沉积物和死细胞的混合物。 Razani小组和其他小组过去的研究表明,称为巨噬细胞的免疫细胞可以清除动脉斑块。但是,斑块内部的环境会使这些细胞不堪重负,当这些细胞死亡时,它们会使问题变得更糟,从而导致斑块积聚和斑块复杂性增加。

拉扎尼说:“在高蛋白饮食的小鼠中,它们的斑块是巨噬细胞的墓地。” “斑块核心中的许多死细胞使其变得极不稳定并易于破裂。当血液流过斑块时,这种作用力(尤其是在高血压的情况下)会对其施加很大压力。这种情况是心脏病发作的秘诀。”

为了了解高膳食蛋白质可能会增加斑块的复杂性,Razani和他的同事研究了蛋白质被消化后所经历的路径-分解成其最初的结构单元,即氨基酸。

Razani和他的团队发现,高蛋白饮食中的过量氨基酸会激活巨噬细胞中称为mTOR的蛋白质,这种蛋白质会告诉细胞生长,而不是执行其清洁房间的任务。来自mTOR的信号关闭了细胞清除噬菌斑的有毒废物的能力,这引发了一系列导致巨噬细胞死亡的事件。研究人员发现,某些氨基酸,特别是亮氨酸和精氨酸,比其他氨基酸在激活mTOR和使巨噬细胞脱离其清理职责,导致细胞死亡方面更有效。

拉扎尼说:“与鱼类或植物中的蛋白质相比,红肉中的亮氨酸含量特别高。” “未来的研究可能会研究具有不同氨基酸含量的高蛋白饮食,以查看是否会对斑块复杂性产生影响。细胞死亡是斑块不稳定的关键特征。如果能够阻止这些细胞死亡,那么可能不会使斑块变小,但可以减少其不稳定性。

他说:“这项工作不仅定义了饮食蛋白质心血管风险的关键过程,而且为靶向这些途径治疗心脏病奠定了基础。”

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NEWS RELEASE 

High-protein diets boost artery-clogging plaque, mouse study shows

Such diets lead to weight loss but could increase heart attack risk

WASHINGTON UNIVERSITY SCHOOL OF MEDICINE

IMAGE
IMAGE: AN UNSTABLE PLAQUE BUILDS UP INSIDE THE AORTA OF A MOUSE ON A HIGH-PROTEIN DIET. A NEW STUDY FROM WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS REVEALS HOW HIGH-PROTEIN… view more 

CREDIT: RAZANI LAB

High-protein diets may help people lose weight and build muscle, but a new study in mice suggests they have a down side: They lead to more plaque in the arteries. Further, the new research shows that high-protein diets spur unstable plaque — the kind most prone to rupturing and causing blocked arteries. More plaque buildup in the arteries, particularly if it’s unstable, increases the risk of heart attack.

The new study, by researchers at Washington University School of Medicine in St. Louis, appears Jan. 23 in the journal Nature Metabolism.

“There are clear weight-loss benefits to high-protein diets, which has boosted their popularity in recent years,” said senior author Babak Razani, MD, PhD, an associate professor of medicine. “But animal studies and some large epidemiological studies in people have linked high dietary protein to cardiovascular problems. We decided to take a look at whether there is truly a causal link between high dietary protein and poorer cardiovascular health.”

The researchers studied mice fed a high-fat diet to deliberately induce atherosclerosis, or plaque buildup in the arteries. According to Razani, mice must eat a high-fat diet to develop arterial plaque. Therefore, some of the mice received a high-fat diet that was also high in protein. And others were fed a high-fat, low-protein diet for comparison.

“A couple of scoops of protein powder in a milkshake or a smoothie adds something like 40 grams of protein — almost equivalent to the daily recommended intake,” Razani said. “To see if protein has an effect on cardiovascular health, we tripled the amount of protein that the mice receive in the high-fat, high-protein diet — keeping the fat constant. Protein went from 15% to 46% of calories for these mice.”

The mice on the high-fat, high-protein diet developed worse atherosclerosis — about 30% more plaque in the arteries — than mice on the high-fat, normal-protein diet, despite the fact that the mice eating more protein did not gain weight, unlike the mice on the high-fat, normal-protein diet.

“This study is not the first to show a telltale increase in plaque with high-protein diets, but it offers a deeper understanding of the impact of high protein with the detailed analysis of the plaques,” Razani said. “In other words, our study shows how and why dietary protein leads to the development of unstable plaques.”

Plaque contains a mix of fat, cholesterol, calcium deposits and dead cells. Past work by Razani’s team and other groups has shown that immune cells called macrophages work to clean up plaque in arteries. But the environment inside plaque can overwhelm these cells, and when such cells die, they make the problem worse, contributing to plaque buildup and increasing plaque complexity.

“In mice on the high-protein diet, their plaques were a macrophage graveyard,” Razani said. “Many dead cells in the core of the plaque make it extremely unstable and prone to rupture. As blood flows past the plaque, that force — especially in the context of high blood pressure — puts a lot of stress on it. This situation is a recipe for a heart attack.”

To understand how high dietary protein might increase plaque complexity, Razani and his colleagues studied the path protein takes after it has been digested — broken down into its original building blocks, called amino acids.

Razani and his team found that excess amino acids from a high-protein diet activate a protein in macrophages called mTOR, which tells the cell to grow rather than go about its housecleaning tasks. The signals from mTOR shut down the cells’ ability to clean up the toxic waste of the plaque, and this sets off a chain of events that results in macrophage death. The researchers found that certain amino acids, especially leucine and arginine, were more potent in activating mTOR — and derailing macrophages from their cleanup duties, leading to cell death — than other amino acids.

“Leucine is particularly high in red meat, compared with, say, fish or plant sources of protein,” Razani said. “A future study might look at high-protein diets with different amino acid contents to see if that could have an effect on plaque complexity. Cell death is the key feature of plaque instability. If you could stop these cells from dying, you might not make the plaque smaller, but you would reduce its instability.

“This work not only defines the critical processes underlying the cardiovascular risks of dietary protein but also lays the groundwork for targeting these pathways in treating heart disease,” he said.

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This work was supported by the National Institutes of Health (NIH), grant number R01 HL125838; VA MERIT, grant number I01 BX0034515; the American Diabetes Association, grant number 1-18-IBS-029; the Washington University Diabetic Cardiovascular Disease Center and Diabetes Research Center, grant number P30 DK020579; the Washington University Mass Spectrometry Core, grant numbers P41GM103422 and P30DK056341; and the Foundation for Barnes-Jewish Hospital.

Zhang X, Sergin I, Evans TD, Jeong S, Rodriguez-Velez A, Kapoor D, Chen S, Song E, Holloway KB, Crowley JR, Epelman S, Weihl CC, Diwan A, Fan D, Mittendorfer B, Stitziel NO, Schilling JD, Lodhi IJ, Razani B. High protein diets increase cardiovascular risk by activating macrophage mTOR to suppress mitophagy. Nature Metabolism. Jan. 23, 2020.

Washington University School of Medicine’s 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

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