Activity of Group 2 Innate Lymphoid Cells is Associated with Chronic Inflammation and Dysregulated Metabolic Homoeostasis in Type 2 Diabetic Nephropathy

糖尿病肾病 医学 内科学 内分泌学 糖尿病 肾病 2型糖尿病 代谢综合征 先天性淋巴细胞 血压 2型糖尿病 免疫学 先天免疫系统 受体
作者
Ping Lü,Xiaoyun Ji,Jie Wan,Huaxi Xu
出处
期刊:Scandinavian Journal of Immunology [Wiley]
卷期号:87 (2): 99-107 被引量:16
标识
DOI:10.1111/sji.12637
摘要

The metabolic syndrome (MS) is an independent risk factor for type 2 diabetic nephropathy and accompanied by subclinical inflammation which involves immune-deriving factors. Emerging studies indicate that group 2 innate lymphoid cells (ILC2s) can regulate adipose metabolism, but much less is known about the activity of ILC2s in metabolic imbalance in obesity and diabetes. This study explored the effect of ILC2s-related molecules on the occurrence of MS in type 2 diabetic nephropathy. Thirty patients with type 2 diabetic nephropathy were included in the study; the mRNA expression of ILC2s-associated molecules from peripheral blood mononuclear cell and the correlation of the ILC2s activity and the MS-related indicators were analysed. The results indicated that the waist circumference, fasting blood glucose, systolic blood pressure, diastolic blood pressure and triglyceride in patients with simple diabetes and diabetic nephropathy were increased, and the incidence of MS was 46.67% and 86.67%, respectively. The ILC2s-associated factors RORα, T1/ST2 and IL-5/IL-13 mRNA were increased in diabetic nephropathy. There was a positive correlation between the expression level of IL-13 or T1/ST2 mRNA and some MS indexes. In addition, the levels of plasma sTNFR, eotaxin-2 and I-309 were also increased in patients with type 2 diabetic nephropathy. It suggested that the patients with type 2 diabetic nephropathy were more likely to have multiple components of MS than those with simple type 2 diabetes mellitus, and enhanced ILC2s activity might be involved in the formation of MS in diabetic nephropathy via influencing blood pressure and lipid metabolism.

科研通智能强力驱动
Strongly Powered by AbleSci AI
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
刚刚
奋斗平卉发布了新的文献求助10
刚刚
涯欤完成签到,获得积分10
1秒前
1秒前
2秒前
愉快的忆丹完成签到,获得积分20
2秒前
2秒前
liao应助清脆海雪采纳,获得20
2秒前
绿野仙踪发布了新的文献求助30
3秒前
min完成签到,获得积分20
3秒前
3秒前
Bian发布了新的文献求助10
3秒前
3秒前
4秒前
搞怪哑铃发布了新的文献求助10
4秒前
4秒前
小二郎应助MM采纳,获得10
4秒前
Owen应助个性思真采纳,获得10
4秒前
支安白发布了新的文献求助10
5秒前
5秒前
科研通AI2S应助科研通管家采纳,获得10
5秒前
SMLW完成签到,获得积分10
5秒前
bkagyin应助科研通管家采纳,获得10
5秒前
5秒前
赘婿应助科研通管家采纳,获得10
5秒前
小蘑菇应助科研通管家采纳,获得10
5秒前
乐乐应助科研通管家采纳,获得10
5秒前
科目三应助鲤鱼诗桃采纳,获得10
5秒前
NexusExplorer应助科研通管家采纳,获得10
5秒前
5秒前
MHB应助科研通管家采纳,获得10
6秒前
6秒前
Ava应助科研通管家采纳,获得10
6秒前
FashionBoy应助科研通管家采纳,获得10
6秒前
FashionBoy应助科研通管家采纳,获得10
6秒前
tiptip应助科研通管家采纳,获得10
6秒前
爆米花应助科研通管家采纳,获得10
6秒前
研友_VZG7GZ应助科研通管家采纳,获得10
6秒前
研友_VZG7GZ应助科研通管家采纳,获得10
6秒前
田様应助科研通管家采纳,获得10
6秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Handbook of pharmaceutical excipients, Ninth edition 5000
Aerospace Standards Index - 2026 ASIN2026 3000
Signals, Systems, and Signal Processing 610
Discrete-Time Signals and Systems 610
Principles of town planning : translating concepts to applications 500
Modified letrozole versus GnRH antagonist protocols in ovarian aging women for IVF: An Open-Label, Multicenter, Randomized Controlled Trial 360
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6062856
求助须知:如何正确求助?哪些是违规求助? 7895107
关于积分的说明 16312191
捐赠科研通 5206081
什么是DOI,文献DOI怎么找? 2785179
邀请新用户注册赠送积分活动 1767848
关于科研通互助平台的介绍 1647431