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.
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
小宝爸爸完成签到 ,获得积分10
1秒前
研友_LMBAXn完成签到,获得积分20
1秒前
爆米花完成签到,获得积分10
1秒前
加菲丰丰应助zhuo采纳,获得20
2秒前
勤劳的马里奥完成签到 ,获得积分10
3秒前
冰销雪释完成签到,获得积分10
3秒前
kemal完成签到,获得积分10
3秒前
4秒前
7秒前
青辞198完成签到 ,获得积分10
9秒前
9秒前
小太阳完成签到,获得积分10
9秒前
louis完成签到,获得积分10
9秒前
10秒前
六氟合铂酸氙完成签到,获得积分10
11秒前
左丘幼旋1发布了新的文献求助10
12秒前
和谐的敏完成签到,获得积分10
13秒前
Dsivan发布了新的文献求助10
14秒前
14秒前
izumi完成签到,获得积分10
15秒前
天马行空完成签到,获得积分10
15秒前
Dsivan完成签到,获得积分10
20秒前
慕青应助izumi采纳,获得10
21秒前
冷傲机器猫完成签到,获得积分10
21秒前
果小镁完成签到,获得积分10
23秒前
认真的水香完成签到,获得积分20
25秒前
小黄不慌完成签到,获得积分10
25秒前
天降紫微星完成签到,获得积分10
27秒前
要减肥的chao完成签到,获得积分10
28秒前
jscr完成签到,获得积分10
29秒前
Amy完成签到,获得积分10
30秒前
方兴未艾完成签到 ,获得积分10
32秒前
哇咔咔完成签到 ,获得积分10
33秒前
OnionJJ完成签到,获得积分10
35秒前
silin完成签到,获得积分10
38秒前
念与惜完成签到,获得积分10
38秒前
S飞完成签到 ,获得积分10
41秒前
文献文献完成签到 ,获得积分10
44秒前
SXYYY完成签到,获得积分10
45秒前
田田完成签到,获得积分10
45秒前
高分求助中
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Chen Hansheng: China’s Last Romantic Revolutionary 500
宽禁带半导体紫外光电探测器 388
Case Research: The Case Writing Process 300
Global Geological Record of Lake Basins 300
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 3142849
求助须知:如何正确求助?哪些是违规求助? 2793786
关于积分的说明 7807358
捐赠科研通 2450052
什么是DOI,文献DOI怎么找? 1303590
科研通“疑难数据库(出版商)”最低求助积分说明 627016
版权声明 601350