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Mechanism of Rh-SAA mediating 3T3-L1 adipocytes insulin resistance

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Title Mechanism of Rh-SAA mediating 3T3-L1 adipocytes insulin resistance
 
Creator Wang, Yanping
Cao, Hong
Hua, WenJin
Dong, QiaoJing
Zhang, Liang
Cao, Min
Xie, Yu
Xue, Jun
 
Subject Diabetes mellitus
Jun N-terminal kinase (JNK) pathway
Obesity
Recombinant SSA
Serum amyloid A proteins
 
Description 818-822
Insulin resistance is a manifestation of both diabetes mellitus and obesity. Insulin signaling and its impairment in obesity and type 2 diabetes continue to excite researchers. Permanent increase in acute-phase serum amyloid A (A-SAA) level has been observed and correlated to both obesity and insulin resistance in humans. In this study, we explored the mechanism of recombinant serum amyloid A (Rh-SAA) mediating insulin resistance and JNK activation of 3T3-L1 adipocytes. We could observe the effect of Rh-SAA on insulin sensitivity of 3T3-LI adipocytes under the intervention of JNK inhibitors. We selected three experimental groups viz. (i) NC Group: Adipocytes without Rh-SAA intervention,;(ii) Rh-SAA Group: A dipocytes with 20μg/mL Rh-SAA intervention; and (iii) JNK Inhibitor Group: Adipocytes pretreated with 50 μmol/L JNK inhibitor SP600125 12 h before 20 μg/mL Rh-SAA intervention. All the three groups were incubated for 48 h, the glucose transport rate of the adipocytes was measured by3H-2-DG, and the level of JNK activation was examined using Western blotting. Compared with the NC group, glucose uptake in the adipocytes treated with 20μg/mL Rh-SAA for 48 h decreased by 26% (P
 
Date 2020-10-29T10:33:00Z
2020-10-29T10:33:00Z
2020-11
 
Type Article
 
Identifier 0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscair.res.in/handle/123456789/55576
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJEB Vol.58(11) [November 2020]