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Adiponectin deletion impairs insulin signaling in insulin-sensitive but not insulin-resistant 3T3-L1 adipocytes

Title
Adiponectin deletion impairs insulin signaling in insulin-sensitive but not insulin-resistant 3T3-L1 adipocytes
Authors
Chang, EugeneChoi, Jung MookPark, Se EunRhee, Eun-JungLee, Won-YoungOh, Ki-WonPark, Sung-WooPark, Cheol-Young
Ewha Authors
장유진
SCOPUS Author ID
장유진scopus
Issue Date
2015
Journal Title
LIFE SCIENCES
ISSN
0024-3205JCR Link1879-0631JCR Link
Citation
vol. 132, pp. 93 - 100
Keywords
AdipocytesAdiponectinInsulin signalingInsulin resistance
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Aims: Previous reports have demonstrated that the adipocyte-derived peptide adiponectin is closely associated with insulin resistance due to its insulin-sensitizing and anti-inflammatory properties in peripheral tissues; however the autocrine effects of adiponectin remain elusive. This study investigated regulatory effects of adiponectin on glucose transport and insulin signaling in insulin-sensitive or insulin-resistant 3T3-L1 adipocytes. Main methods: 3T3-L1 fibroblasts were transfected with non-target or adiponectin (ADN) siRNA and differentiated. Chronic treatment with insulin (24 h, 100 nM) was employed to induce insulin resistance in differentiated adipocytes. Insulin-stimulated glucose transport was measured and protein and mRNA levels were assessed by Western blot and RT-PCR. Key findings: Prolonged incubation with insulin significantly reduced insulin-stimulated glucose uptake, suggesting the development of insulin resistance and adiponectin mRNA expression. In this insulin-resistant condition, adiponectin deletion did not alter insulin-stimulated glucose uptake. In insulin-sensitive adipocytes, adiponectin ablation reduced insulin-stimulated glucose uptake, expression of IRS-1 and GLUT4, and GLUT4 translocation to the membrane. Adiponectin knockdown did not affect the activation of Ala and p38MAPK (phosphorylation form/total form), but significantly decreased the activation of AMPK in insulin-responsive adipocytes. Significance: Adiponectin deficiency suppresses insulin-induced glucose uptake, insulin signaling, and the AMPK pathway only in insulin-responsive 3T3-L1 adipocytes. (C) 2015 Elsevier Inc. All rights reserved.
DOI
10.1016/j.lfs.2015.02.013
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신산업융합대학 > 식품영양학과 > Journal papers
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