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
1秒前
共享精神应助千与千夜采纳,获得10
2秒前
科研通AI2S应助生动的怜菡采纳,获得10
2秒前
科研通AI2S应助生动的怜菡采纳,获得10
2秒前
3秒前
iNk应助路奇k采纳,获得20
3秒前
3秒前
Pomelo发布了新的文献求助10
3秒前
bboo完成签到,获得积分10
3秒前
12完成签到,获得积分10
3秒前
3秒前
医魔完成签到,获得积分20
4秒前
April完成签到,获得积分10
4秒前
5秒前
6秒前
闪闪镜子发布了新的文献求助10
6秒前
夏爷完成签到,获得积分10
7秒前
大个应助化学位移值采纳,获得10
7秒前
调皮飞绿发布了新的文献求助10
7秒前
曾泳钧完成签到,获得积分10
8秒前
劲秉应助直率的从彤采纳,获得10
8秒前
尺八发布了新的文献求助10
8秒前
不安的chen发布了新的文献求助10
10秒前
10秒前
xinyi发布了新的文献求助10
10秒前
NIKE112发布了新的文献求助10
12秒前
白帝关注了科研通微信公众号
12秒前
le完成签到,获得积分10
12秒前
虎虎完成签到,获得积分10
15秒前
领导范儿应助小莹子采纳,获得10
16秒前
zhanghan完成签到,获得积分10
17秒前
orixero应助调皮飞绿采纳,获得10
18秒前
Saluzi完成签到,获得积分20
19秒前
劲秉应助不安的chen采纳,获得30
20秒前
20秒前
麦兜完成签到,获得积分10
21秒前
21秒前
gx完成签到,获得积分10
22秒前
22秒前
由怜雪完成签到,获得积分10
23秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
ALA生合成不全マウスでの糖代謝異常の分子機構解析 520
安全防范技术与工程 500
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
2-Acetyl-1-pyrroline: an important aroma component of cooked rice 500
A real-time energy management strategy based on fuzzy control and ECMS for PHEVs 400
2024 Medicinal Chemistry Reviews 400
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 3191125
求助须知:如何正确求助?哪些是违规求助? 2840488
关于积分的说明 8028591
捐赠科研通 2503810
什么是DOI,文献DOI怎么找? 1337205
科研通“疑难数据库(出版商)”最低求助积分说明 638034
邀请新用户注册赠送积分活动 606497