Rapid responses of adipocytes to iron overload increase serum TG level by decreasing adiponectin

内科学 内分泌学 脂联素 脂肪因子 抵抗素 瘦素 脂肪组织 化学 胰岛素抵抗 胰岛素 医学 肥胖
作者
Yuxiao Tang,Dongyao Wang,Hongwei Zhang,Yinyin Zhang,Jie Wang,Ruirui Qi,Jianxin Yang,Hui Shen,Yan Xu,Min Li
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:236 (11): 7544-7553 被引量:16
标识
DOI:10.1002/jcp.30391
摘要

Iron overload is tightly connected with metabolic disorders. Excess iron in the adipose and its roles in dyslipidemia are of interest to be identified. In acute iron overload mice receiving intraperitoneal injection of 100 mg/kg/day dextran-iron for 5 days, the epididymis adipose showed a remarkable increase in iron. Serum triglyceride and low-density lipoprotein cholesterol (LDL-C) levels were increased and high-density lipoprotein cholesterol (HDL-C) level was decreased, while serum alkaline phosphatase, aspartate aminotransferase, glucose, and insulin were not affected. The serum-cytokine-microarray showed that adipocytokines, including adiponectin, leptin, and resistin were significantly decreased. Other serum cytokines, including pro-insulin cytokines, inflammatory cytokines, chemokines, and growth factors were not changed, except that ghrelin and chemokine RANTES were increased. Iron overload decreased expressions of adiponectin and leptin both in vivo and in vitro. Intraperitoneal injection of recombinant leptin at 1 μg/g in acute iron overload mice had no significant effects on serum levels of TC, TG, HDL-C, and LDL-C, while intraperitoneal injection of recombinant adiponectin at 3 μg/g partially restored serum TG level through improving activities of lipoprotein lipase and hepatic lipase, but abnormal serum LDL-C and HDL-C were not redressed, suggesting other mechanisms also existed. In conclusion, the adipose responds to iron overload at an early stage to interfere with lipid metabolism by secreting adipocytokines, which may further affect glucose metabolism, inflammation, and other iron overload-induced effects on the body.
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
ff完成签到,获得积分10
刚刚
平凡中的限量版完成签到,获得积分10
刚刚
乐乐应助郝宝真采纳,获得10
2秒前
李健的小迷弟应助lxf448采纳,获得10
2秒前
yecheng完成签到,获得积分10
3秒前
问问问完成签到,获得积分10
3秒前
科研通AI2S应助Apple采纳,获得10
3秒前
胖小羊完成签到,获得积分10
3秒前
芈冖完成签到,获得积分10
4秒前
唯美完成签到,获得积分10
5秒前
小二郎应助动人的cc采纳,获得10
5秒前
结实的元灵完成签到,获得积分10
5秒前
爱看文献的七七完成签到,获得积分20
5秒前
小怪兽完成签到,获得积分10
6秒前
7秒前
ntxiaohu完成签到,获得积分10
8秒前
乐观银耳汤完成签到,获得积分10
8秒前
荆月竹完成签到,获得积分10
8秒前
9秒前
研友_8DA7DL完成签到,获得积分10
9秒前
淡定的月半完成签到,获得积分10
10秒前
在我梦里绕完成签到,获得积分10
11秒前
科研通AI2S应助东asdfghjkl采纳,获得10
11秒前
李泽中完成签到,获得积分20
11秒前
小小aa16完成签到,获得积分10
11秒前
小豪号发布了新的文献求助10
12秒前
独摇之完成签到,获得积分10
12秒前
魏106047完成签到,获得积分10
13秒前
tg2024完成签到,获得积分10
13秒前
犹豫梦旋完成签到,获得积分10
13秒前
大侠完成签到,获得积分10
13秒前
所所应助Jason-1024采纳,获得10
13秒前
今后应助平常的仙人掌采纳,获得10
14秒前
15秒前
15秒前
15秒前
巧克力张张包完成签到,获得积分10
16秒前
eternity136应助chen1999采纳,获得10
16秒前
16秒前
Apple完成签到,获得积分10
18秒前
高分求助中
Sustainability in Tides Chemistry 2800
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
Rechtsphilosophie 1000
Bayesian Models of Cognition:Reverse Engineering the Mind 888
Le dégorgement réflexe des Acridiens 800
Defense against predation 800
A Dissection Guide & Atlas to the Rabbit 600
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 3134083
求助须知:如何正确求助?哪些是违规求助? 2784882
关于积分的说明 7769151
捐赠科研通 2440425
什么是DOI,文献DOI怎么找? 1297383
科研通“疑难数据库(出版商)”最低求助积分说明 624959
版权声明 600792