小肠在动脉粥样硬化和癌症中调节代谢和炎症的作用。
The role of the small intestine in modulating metabolism and inflammation in atherosclerosis and cancer.
机构信息
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
出版信息
Curr Opin Lipidol. 2019 Oct;30(5):383-387. doi: 10.1097/MOL.0000000000000629.
PURPOSE OF REVIEW
To discuss recent findings on the importance of the small intestine in modulating metabolism and inflammation in atherosclerosis and cancer.
RECENT FINDINGS
Integrin β7 natural gut intraepithelial T cells modulated metabolism and accelerated atherosclerosis in mice. Reducing the generation of lysophospholipids in the small intestine mimicked bariatric surgery and improved diabetes. Enterocyte-specific knockdown of stearoyl-CoA desaturase-1 significantly improved dyslipidemia in LDL receptor null (Ldlr) mice fed a Western diet. Adding a concentrate of tomatoes transgenic for the apolipoprotein A-I mimetic peptide 6F to the chow of wild-type mice altered lipid metabolism in the small intestine, preserved Notch signaling and reduced tumor burden in mouse models. The phospholipid-remodeling enzyme Lpcat3 regulated intestinal stem cells and progenitor cells by stimulating cholesterol biosynthesis; increasing cholesterol in the diet or through genetic manipulation promoted tumorigenesis in Apc mice.
SUMMARY
The small intestine is important for regulating metabolism and inflammation in animal models of both atherosclerosis and cancer.
目的综述
讨论小肠在调节动脉粥样硬化和癌症中代谢和炎症的重要性的最新发现。
最近的发现
整合素β7天然肠道上皮内 T 细胞调节代谢并加速小鼠动脉粥样硬化。减少小肠中溶血磷脂的生成模拟了减重手术并改善了糖尿病。在 LDL 受体缺失（Ldlr）小鼠的西方饮食中，肠细胞特异性敲低硬脂酰辅酶 A 去饱和酶-1 可显著改善血脂异常。在野生型小鼠的饲料中添加富含载脂蛋白 A-I 模拟肽 6F 的转基因番茄浓缩物可改变小肠中的脂质代谢，保留 Notch 信号并减少小鼠模型中的肿瘤负担。磷脂重塑酶 Lpcat3 通过刺激胆固醇生物合成来调节肠道干细胞和祖细胞；增加饮食中的胆固醇或通过遗传操作促进 Apc 小鼠的肿瘤发生。
摘要
小肠在调节动脉粥样硬化和癌症动物模型中的代谢和炎症方面很重要。
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