切除CTRP13可以改善全身葡萄糖和脂质代谢
Fangluo Chen1, Dylan C Sarver1, Muzna Saqib1
1Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Molecular metabolism
|October 16, 2023
概括
CTRP13缺乏改善了代谢平衡,导致体重降低,更好地处理葡萄糖和脂质. 肥胖症中CTRP13水平降低可能是对胰岛素抵抗的补偿反应.
科学领域:
- 内分泌学 在内分泌学.
- 代谢调节 代谢调节 代谢调节
- 分子生物学分子生物学
背景情况:
- 分泌的荷尔蒙介导组织交叉交叉,以实现综合的代谢控制.
- CTRP13 (C1q家族) 在体外改善葡萄糖代谢和胰岛素作用,并减少小鼠的体重和食物摄入量.
- 以前的研究表明,CTRP13调节胰岛素分泌,但其在代谢平衡中的生理作用尚不清楚.
研究的目的:
- 使用功能丧失的小鼠模型,研究CTRP13在代谢平衡中的生理功能.
- 为了确定CTRP13是否对维持代谢平衡至关重要.
- 探索CTRP13缺乏对葡萄糖和脂质代谢以及系统代谢概况的影响.
主要方法:
- 在标准食和高脂肪饮食条件下生成和研究Ctrp13淘汰赛 (KO) 老鼠.
- 进行了全面的代谢表型化,包括葡萄糖耐受性和胰岛素敏感性测试.
- 对关键代谢组织 (脂肪,肝脏,肌肉) 进行了转录组分析,并与人类队列数据 (METSIM) 整合了数据.
主要成果:
- 不管饮食如何,Ctrp13-KO小鼠表现出增加的体力活动,减少的体重和改善的脂质处理.
- 失去CTRP13可以提高葡萄糖耐受性,胰岛素敏感性和甘油三清除,性别差异显著.
- 转录组数据显示,KO小鼠的炎症和肝硬化减少,抑制脂质合成和增强代谢.
结论:
- CTRP13作为代谢的负调节剂;其缺乏改善了全身代谢概况.
- 在人类肥胖和糖尿病中,循环中CTRP13水平降低可能代表抗胰岛素抵抗的补偿机制.
- 缺乏CTRP13显著影响脂肪组织中的基因表达,这表明它在人类代谢综合征中起因作用.
相关概念视频
Hormones Regulating Blood Glucose
3.4K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
3.4K
Glucose Homeostasis: Regulation of Blood Glucose
1.7K
Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
1.7K
Glucagon-like Receptor Agonists
334
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
334
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
1.3K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
Insulin and C-peptide are...
1.3K


