Potential Role of TNF-α in the Pathogenesis of Insulin Resistance and Type 2 Diabetes

胰岛素抵抗 内分泌学 内科学 脂肪组织 2型糖尿病 胰岛素 肿瘤坏死因子α 下调和上调 脂解 胰岛素受体 医学 生物 糖尿病 生物化学 基因
作者
David E. Moller
出处
期刊:Trends in Endocrinology and Metabolism [Elsevier]
卷期号:11 (6): 212-217 被引量:692
标识
DOI:10.1016/s1043-2760(00)00272-1
摘要

Abstract

Tumor necrosis factor α (TNF-α) has well-described effects on lipid metabolism in the context of acute inflammation, as in sepsis. Recently, increased TNF-α production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-α has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. Thus, current evidence suggests that administration of exogenous TNF-α to animals can induce insulin resistance, whereas neutralization of TNF-α can improve insulin sensitivity. Importantly, results from knockout mice deficient in TNF-α or its receptors have suggested that TNF-α has a role in regulating in vivo insulin sensitivity. However, the absence of TNF-α action might only partially protect against obesity-induced insulin resistance in mice. Multiple mechanisms have been suggested to account for these metabolic effects of TNF-α. These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPARγ, an important insulin-sensitizing nuclear receptor. Although current evidence suggests that neutralizing TNF-α in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-α is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
搜集达人应助ju龙哥采纳,获得10
1秒前
YK发布了新的文献求助10
1秒前
科研通AI2S应助yaoyh_gc采纳,获得10
1秒前
tgww完成签到,获得积分10
2秒前
XXXX完成签到,获得积分10
2秒前
3秒前
整化学发布了新的文献求助10
3秒前
3秒前
劲秉应助Andy采纳,获得10
4秒前
稳稳稳完成签到,获得积分10
4秒前
江小农发布了新的文献求助10
6秒前
完美世界应助cccc采纳,获得10
6秒前
7秒前
7秒前
7秒前
8秒前
8秒前
好好完成签到,获得积分10
8秒前
标致贞完成签到 ,获得积分10
8秒前
陶火桃完成签到,获得积分10
9秒前
maomaolaile2完成签到,获得积分10
9秒前
整化学完成签到,获得积分10
9秒前
Owen应助小陆采纳,获得10
9秒前
zz完成签到,获得积分10
12秒前
园yuan完成签到,获得积分10
12秒前
FashionBoy应助科研通管家采纳,获得10
12秒前
Billy应助科研通管家采纳,获得10
12秒前
领导范儿应助科研通管家采纳,获得10
12秒前
xiaoxiao应助科研通管家采纳,获得50
12秒前
华仔应助科研通管家采纳,获得10
12秒前
FashionBoy应助科研通管家采纳,获得10
12秒前
ding应助科研通管家采纳,获得10
13秒前
顾矜应助科研通管家采纳,获得10
13秒前
Billy应助科研通管家采纳,获得10
13秒前
赘婿应助科研通管家采纳,获得10
13秒前
嗯哼应助科研通管家采纳,获得20
13秒前
李爱国应助科研通管家采纳,获得10
13秒前
科目三应助科研通管家采纳,获得10
13秒前
斯文败类应助科研通管家采纳,获得10
13秒前
FashionBoy应助科研通管家采纳,获得10
13秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
Evolution 3rd edition 1500
保险藏宝图 1000
Lire en communiste 1000
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 700
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 700
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3185378
求助须知:如何正确求助?哪些是违规求助? 2835713
关于积分的说明 8006076
捐赠科研通 2498150
什么是DOI,文献DOI怎么找? 1333296
科研通“疑难数据库(出版商)”最低求助积分说明 636828
邀请新用户注册赠送积分活动 604451