Please use this identifier to cite or link to this item: http://localhost:8080/xmlui/handle/123456789/3244
Title: Development of Insulin Resistance Through Sprouting of Inflammatory Markers During Hypoxia in 3T3-L1 Adipocytes and Amelioration with Curcumin
Authors: Priyanka, A
Shyni, G L
Anupama, N
Salin Raj, P
Anusree, S S
Raghu, K G
Keywords: Hypoxia
Inflammation
Insulin resistance
3T3-L1 adipocytes
Curcumin
Issue Date: 5-Oct-2017
Publisher: Elsevier
Citation: European Journal of Pharmacology, 812:73-81
Abstract: 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 24 h 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.
URI: http://10.10.100.66:8080/xmlui/handle/123456789/3244
Appears in Collections:2017

Files in This Item:
File Description SizeFormat 
Development of insulin - Priyanka A - European Journal Pharmocology.pdf
  Restricted Access
847.62 kBAdobe PDFView/Open Request a copy


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.