|
|
|
|
LEADER |
02283 am a22001813u 4500 |
001 |
51756 |
042 |
|
|
|a dc
|
100 |
1 |
0 |
|a Abu Bakar, Mohamad Hafizi
|e author
|
700 |
1 |
0 |
|a Sarmidi, Mohamad Roji
|e author
|
700 |
1 |
0 |
|a Cheng, Kian Kai
|e author
|
700 |
1 |
0 |
|a Huri, Hasniza Zaman
|e author
|
700 |
1 |
0 |
|a Ya'akob, Harisun
|e author
|
245 |
0 |
0 |
|a Amelioration of mitochondrial dysfunction-induced insulin resistance in differentiated 3T3-L1 adipocytes via inhibition of NF-κB pathways
|
260 |
|
|
|b MDPI AG,
|c 2014.
|
856 |
|
|
|z Get fulltext
|u http://eprints.utm.my/id/eprint/51756/1/MohamadHafiziAbuBakar2014_AMeliorationOfMitochondrialDysfunction.pdf
|
520 |
|
|
|a A growing body of evidence suggests that activation of nuclear factor kappa B (NF-κB) signaling pathways is among the inflammatory mechanism involved in the development of insulin resistance and chronic low-grade inflammation in adipose tissues derived from obese animal and human subjects. Nevertheless, little is known about the roles of NF-κB pathways in regulating mitochondrial function of the adipose tissues. In the present study, we sought to investigate the direct effects of celastrol (potent NF-κB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. Celastrol ameliorates mitochondrial dysfunction by altering mitochondrial fusion and fission in adipocytes. The levels of oxidative DNA damage, protein carbonylation and lipid peroxidation were down-regulated. Further, the morphology and quantification of intracellular lipid droplets revealed the decrease of intracellular lipid accumulation with reduced lipolysis. Moreover, massive production of the pro-inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were markedly depleted. Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. This study signified that the treatments modulated towards knockdown of NF-κB transcription factor may counteract these metabolic insults exacerbated in our model of synergy between mitochondrial dysfunction and inflammation. These results demonstrate for the first time that NF-κB inhibition modulates mitochondrial dysfunction induced insulin resistance in 3T3-L1 adipocytes
|
546 |
|
|
|a en
|
650 |
0 |
4 |
|a QP Physiology
|