Development of insulin resistance through sprouting of inflammatory markers during hypoxia in 3T3-L1 adipocytes and amelioration with curcumin. Eur J Pharmacol 2017 Oct 05;812:73-81
Date
07/08/2017Pubmed ID
28684236DOI
10.1016/j.ejphar.2017.07.005Scopus ID
2-s2.0-85021958665 (requires institutional sign-in at Scopus site) 20 CitationsAbstract
The role of phytochemicals in general well-being has been recognized. Curcumin is an ideal example. Hypoxia in adipose tissue is a major cause of inflammation and insulin resistance in obesity. Herein we mainly explored inflammation, insulin resistance and angiogenesis in 3T3-L1 adipocytes and possible reversal with the curcumin during hypoxia. Hypoxia for 24h significantly increased (P ≤ 0.05) the secretion of monocyte chemotactic protein-1 (4.59 fold), leptin (2.96 fold) and reduced adiponectin (2.93 fold). mRNA level of resistin (6.8 fold) and toll-like receptor-4 (TLR-4) (8.8 fold) was upregulated. Increased serine phosphorylation of insulin receptor substrate 1 (IRS-1) (1.9 fold) and decreased expression of insulin receptor substrate 2 (IRS-2) (0.53 fold) in hypoxic group were observed. Hypoxia significantly increased (P ≤ 0.05) basal glucose uptake (3.3 fold), GLUT-1 expression and angiogenic factors but down regulated GLUT-4. Curcumin protected adipocytes from hypoxia induced inflammation and insulin resistance via reducing inflammatory adipokine, nuclear factor-κB (NF-κB)/c-jun N-terminal kinase (JNK) and serine phosphorylation of IRS-1 receptors and improving adiponectin secretion.
Author List
Priyanka A, Shyni GL, Anupama N, Raj PS, Anusree SS, Raghu KGAuthor
Anupama Nair PhD Postdoctoral Researcher 3 in the Obstetrics and Gynecology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
3T3-L1 CellsActive Transport, Cell Nucleus
Adipocytes
Animals
Biomarkers
Cell Hypoxia
Cell Nucleus
Curcumin
Cytokines
Enzyme Activation
Gene Expression Regulation
Glucose Transporter Type 1
Insulin Resistance
JNK Mitogen-Activated Protein Kinases
Mice
Toll-Like Receptor 4
Transcription Factor RelA
