Reduction of mitochondrial 3-oxoacyl-ACP synthase (OXSM) by hyperglycemia is associated with deficiency of α-lipoic acid synthetic pathway in kidney of diabetic mice

内分泌学 发病机制 内科学 糖尿病 硫辛酸 2型糖尿病 医学 生物 化学 生物化学 抗氧化剂
作者
Ting Gao,Shengnan Qian,Shuang Shen,Xiaoying Zhang,Junli Liu,Weiping Jia,Zhong Chen,Jianping Ye
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:512 (1): 106-111 被引量:16
标识
DOI:10.1016/j.bbrc.2019.02.155
摘要

LA (alpha-Lipoic acid) deficiency represents a risk factor in the pathogenesis of diabetic complications as synthetic LA is routinely used in the treatment of the complications in patients. The mechanism underlying LA deficiency remains elusive in the diabetic conditions. In the present study, we investigated the synthetic pathway of LA in both type 1 and 2 diabetic mice. LA deficiency was observed with a reduction in lipoylation of pyruvate dehydrogenase in the kidney of streptozocin-induced diabetic mice. Proteins of three enzymes (MCAT, OXSM and LIAS) in the LA synthetic pathway were examined in the kidney. A reduction was observed in OXSM, but not in the other two. In a 24h study in the cell culture, mRNA and protein of OXSM were transiently reduced by a high concentration of glucose (35 mM), and persistently decreased by TNF-α (20 nM). The high glucose effect was observed with the OXSM reduction in the kidney of db/db mice (type 2 diabetes model). The TNF-α effect was observed with OXSM reduction in the fat tissue of diet-induced obese mice. The result suggest that inhibition of OXSM by hyperglycemia and inflammation may contribute to the LA deficiency in the diabetic complications. The OXSM reduction suggests a new mechanism for the mitochondrial dysfunction in the pathogenesis of diabetic complications.
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
刚刚
1秒前
蔡大胖完成签到,获得积分10
2秒前
2秒前
Timo干物类完成签到,获得积分10
2秒前
3秒前
ESLG应助adgfasdvz采纳,获得10
3秒前
傅傅完成签到,获得积分10
4秒前
4秒前
llx发布了新的文献求助10
4秒前
xuxu完成签到,获得积分10
5秒前
5秒前
怕黑行恶完成签到,获得积分10
5秒前
5秒前
单细胞完成签到 ,获得积分0
5秒前
5秒前
今后应助小熊猫采纳,获得10
5秒前
隐形曼青应助雨淋沐风采纳,获得10
6秒前
赘婿应助淡淡冰薇采纳,获得10
6秒前
聪慧的玉米完成签到,获得积分10
6秒前
6秒前
华仔应助prisfanstein采纳,获得10
6秒前
和谐的阁完成签到,获得积分10
6秒前
7秒前
小青柑发布了新的文献求助10
7秒前
peiqi佩奇发布了新的文献求助10
7秒前
Jeff完成签到,获得积分20
7秒前
joe发布了新的文献求助10
7秒前
薄荷完成签到 ,获得积分10
8秒前
9秒前
Akim应助TsuKe采纳,获得10
9秒前
9秒前
言无间完成签到,获得积分10
9秒前
10秒前
顺心季节发布了新的文献求助10
10秒前
10秒前
kento发布了新的文献求助30
11秒前
司空雨泽发布了新的文献求助10
11秒前
达瓦里氏完成签到 ,获得积分10
12秒前
12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 3185143
求助须知:如何正确求助?哪些是违规求助? 2835525
关于积分的说明 8005128
捐赠科研通 2497954
什么是DOI,文献DOI怎么找? 1333207
科研通“疑难数据库(出版商)”最低求助积分说明 636803
邀请新用户注册赠送积分活动 604389