相关实验视频
Updated: Mar 18, 2026

08:58
Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
17.1K
缺乏TTC39B可以稳定LXR,减少动脉样硬化和脂肪肝
Joanne Hsieh1, Masahiro Koseki1,2, Matthew M Molusky1
1Division of Molecular Medicine, Department of Medicine, Columbia University, New York, New York 10032, USA.
Nature
|July 8, 2016
概括
甲基重复域蛋白39B (T39) 促进肝脏X受体 (LXR) 的降解. 通过保持LXR活性,抑制T39可以预防脂肪肝炎和动脉样硬化.
科学领域:
- 代谢疾病
- 分子生物学
- 遗传学
背景情况:
- 脂肪肝炎是一种常见的肝病,目前尚无治疗方法.
- 肝X受体 (LXR) 有有益的胆固醇去除和抗炎性质,但其激动剂可以诱导脂肪肝.
- 了解脂肪肝炎的细胞机制对于开发治疗至关重要.
研究的目的:
- 在调节肝X受体 (LXR) 中研究四基重复域蛋白39B (Ttc39b,T39).
- 确定针对脂肪肝炎和动脉样硬化的治疗潜力.
主要方法:
- 使用了绝杀性小鼠模型 (T39-),肝细胞特异性T39缺乏,Ldlr-/-) T39-/-)
- 包括高脂肪/高胆固醇/胆盐和西式饮食在内的各种饮食.
- 分析了高密度脂蛋白 (HDL) 胆固醇,LXR蛋白和mRNA水平,肝脏基因表达和动脉样硬化标志物.
主要成果:
- 在小鼠中,T39缺乏增加了HDL胆固醇,并防止了饮食引起的脂肪肝炎和死亡.
- 在Ldlr-/ -T39-/ -小鼠中,T39缺乏减少脂肪肝,降低低密度脂蛋白 (LDL) 和改善动脉样硬化.
- 缺少T39会保留肝脏LXR蛋白,导致胆固醇的去除增加和脂质生成的减少.
结论:
- 三重复域蛋白39B (T39) 促进了LXR的泛化和降解.
- 抑制T39可保持LXR活性,为脂肪肝炎和动脉样硬化提供潜在的治疗策略.
- 向T39可以同时解决代谢和心血管并发症.
相关概念视频
Liver Regeneration
4.7K
The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are...
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are...
4.7K
Atherosclerosis III: Management
567
Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
567
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow
324
Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug...
324

