PMID- 25575741
OWN - NLM
STAT- MEDLINE
DCOM- 20151208
LR  - 20181113
IS  - 1877-8755 (Electronic)
IS  - 1138-7548 (Linking)
VI  - 71
IP  - 1
DP  - 2015 Mar
TI  - Gene expression profile of high-fat diet-fed C57BL/6J mice: in search of 
      potential role of azelaic acid.
PG  - 29-42
LID - 10.1007/s13105-014-0376-6 [doi]
AB  - High-fat diet (HFD) elevates circulatory fatty acids and influences glucose and 
      fat metabolism. Azelaic acid (AzA), a naturally occurring alpha,omega-dicarboxylic acid 
      in wheat, rye, barley, oat seeds and sorghum, has been reported to exert 
      antidiabetic effects in HFD-induced type 2 diabetes mellitus (T2DM) C57BL/6J 
      mice. The present study was undertaken to identify the genes that are 
      differentially modulated by treatment with AzA in HFD-fed mice. Mice were fed HFD 
      for 10 weeks and subjected to intragastric administration of 80 mg/kg body weight 
      (BW) of AzA daily along with HFD from 11 to 15 weeks. Lipid profile, adipokines 
      and cytokines were examined in the plasma/liver of mice. Whole genome profiling 
      was performed in the liver of mice using microarray and validated by qRT-PCR, 
      Western blot and immunohistochemical analyses. HFD intake resulted in 
      significantly elevated lipids (except high-density lipoproteins), resistin, 
      tumour necrosis factor alpha and interleukin-6 with marked reduction in 
      adiponectin. Administration of AzA to HFD-fed mice significantly restored the 
      lipids, adipokines and cytokines to near normal. Transcript profiling revealed 
      that HFD intake activated the genes involved in stress response, cell cycle 
      regulation and apoptosis. Treatment with AzA caused increased expression of genes 
      involved in reactive oxygen species (ROS) scavenging, receptor-mediated 
      signalling, transcription, protein modification and insulin signal transduction. 
      AzA activates insulin signal molecules leading to insulin sensitivity. The 
      ability of AzA to modulate the expression of these genes supports the notion that 
      AzA is a promising drug candidate for the treatment of insulin resistance 
      associated with T2DM.
FAU - Muthulakshmi, Shanmugam
AU  - Muthulakshmi S
AD  - Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai 
      University, Annamalai Nagar, 608002, Tamil Nadu, India, chaperonein@yahoo.co.in.
FAU - Chakrabarti, Alok K
AU  - Chakrabarti AK
FAU - Mukherjee, Sanjay
AU  - Mukherjee S
LA  - eng
PT  - Journal Article
DEP - 20150111
PL  - Spain
TA  - J Physiol Biochem
JT  - Journal of physiology and biochemistry
JID - 9812509
RN  - 0 (Adipokines)
RN  - 0 (Blood Glucose)
RN  - 0 (Cytokines)
RN  - 0 (DNA Primers)
RN  - 0 (Dicarboxylic Acids)
RN  - 0 (Insulin)
RN  - 0 (Lipids)
RN  - F2VW3D43YT (azelaic acid)
SB  - IM
MH  - Adipokines/blood
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Cytokines/blood
MH  - DNA Primers
MH  - Dicarboxylic Acids/administration & dosage/*pharmacology
MH  - *Diet, High-Fat
MH  - *Gene Expression Profiling
MH  - Insulin/blood
MH  - Lipids/blood
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Real-Time Polymerase Chain Reaction
EDAT- 2015/01/13 06:00
MHDA- 2015/12/15 06:00
CRDT- 2015/01/11 06:00
PHST- 2014/08/19 00:00 [received]
PHST- 2014/12/22 00:00 [accepted]
PHST- 2015/01/11 06:00 [entrez]
PHST- 2015/01/13 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
AID - 10.1007/s13105-014-0376-6 [doi]
PST - ppublish
SO  - J Physiol Biochem. 2015 Mar;71(1):29-42. doi: 10.1007/s13105-014-0376-6. Epub 
      2015 Jan 11.