TY - JOUR
T1 - Insulin resistance without obesity induced by cotton pellet granuloma in mice
AU - Wu, Hung Tsung
AU - Chang, Cheng Kuei
AU - Tsao, Chiung Wen
AU - Wen, Ya Ju
AU - Ling, Sheng Ming
AU - Cheng, Kai Chun
AU - Chang, Chi Jean
AU - Cheng, Juei Tang
N1 - Funding Information:
We appreciate Miss MJ Wang for the research assistance. We thank Professor YS Lin (Department of Microbiology and Immunology, National Cheng Kung University, Tainan City, Taiwan, ROC) for kindly providing us the antibodies. This work was supported in part by Grant NSC 96-2320-B006-010 from the National Science Council, Taiwan. We also thank Bill Franke for editorial assistance.
PY - 2009/3
Y1 - 2009/3
N2 - Obesity leads to insulin resistance because the larger adipocytes in obese persons secrete proinflammatory cytokines that cause chronic inflammation in adipose tissue. This, in turn, leads to the alteration of adipokine secretion, which can induce insulin resistance. However, the development of insulin resistance without obesity is still obscure. We aimed to use an animal inflammation model with cotton pellet granuloma (CPG) in adipose tissue to characterize insulin resistance formation. We found that CPG in epididymal white adipose tissue (WAT), rather than in interscapular brown adipose tissue, impaired insulin sensitivity, and glucose utilization, and that it decreased levels of phosphoinsulin receptor and phospho-Akt in both muscle and liver tissue, but that it did not modify the body weight or food intake in mice. Macrophage infiltration in adipose tissue, leukocyte counts, monocyte chemoattractant protein-1, and interleukin-6 were elevated in CPG-treated mice. However, we found a marked decrease of plasma adiponectin only in the WAT group, which might have been because of the lower level of peroxisome proliferator-activated receptor-γ in WAT. These results show that granuloma formation in WAT by implantation of a cotton pellet may induce insulin resistance under nonobese condition through circulating inflammatory mediators, especially the low level of adiponectin.
AB - Obesity leads to insulin resistance because the larger adipocytes in obese persons secrete proinflammatory cytokines that cause chronic inflammation in adipose tissue. This, in turn, leads to the alteration of adipokine secretion, which can induce insulin resistance. However, the development of insulin resistance without obesity is still obscure. We aimed to use an animal inflammation model with cotton pellet granuloma (CPG) in adipose tissue to characterize insulin resistance formation. We found that CPG in epididymal white adipose tissue (WAT), rather than in interscapular brown adipose tissue, impaired insulin sensitivity, and glucose utilization, and that it decreased levels of phosphoinsulin receptor and phospho-Akt in both muscle and liver tissue, but that it did not modify the body weight or food intake in mice. Macrophage infiltration in adipose tissue, leukocyte counts, monocyte chemoattractant protein-1, and interleukin-6 were elevated in CPG-treated mice. However, we found a marked decrease of plasma adiponectin only in the WAT group, which might have been because of the lower level of peroxisome proliferator-activated receptor-γ in WAT. These results show that granuloma formation in WAT by implantation of a cotton pellet may induce insulin resistance under nonobese condition through circulating inflammatory mediators, especially the low level of adiponectin.
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U2 - 10.1038/labinvest.2008.161
DO - 10.1038/labinvest.2008.161
M3 - Article
C2 - 19139723
AN - SCOPUS:61349188875
SN - 0023-6837
VL - 89
SP - 362
EP - 369
JO - Laboratory Investigation
JF - Laboratory Investigation
IS - 3
ER -