title: Insulin resistance without obesity induced by cotton pellet granuloma in mice.
abstract: 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-gamma 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.
authors.affiliation: Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
authors.forename: Hung-Tsung
authors.initials: HT
authors.lastname: Wu
authors.forename: Cheng Kuei
authors.initials: CK
authors.lastname: Chang
authors.forename: Chiung-Wen
authors.initials: CW
authors.lastname: Tsao
authors.forename: Ya-Ju
authors.initials: YJ
authors.lastname: Wen
authors.forename: Sheng-Ming
authors.initials: SM
authors.lastname: Ling
authors.forename: Kai-Chun
authors.initials: KC
authors.lastname: Cheng
authors.forename: Chi-Jean
authors.initials: CJ
authors.lastname: Chang
authors.forename: Juei-Tang
authors.initials: JT
authors.lastname: Cheng
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism* / Q000473:pathology; D052436:Adipose Tissue, White / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D018925:Chemokines / Q000378:metabolism; D032561:Cotton Fiber; D004195:Disease Models, Animal; D004822:Epididymis / Q000473:pathology; D005951:Glucose Tolerance Test; D006099:Granuloma / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007333:Insulin Resistance; D007958:Leukocyte Count; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018482:Muscle, Skeletal / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000502:physiology; D009765:Obesity; D047495:PPAR gamma / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism; D014044:Tolbutamide / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D018925:Chemokines; D007004:Hypoglycemic Agents; D047495:PPAR gamma; D014044:Tolbutamide; D011972:Receptor, Insulin; D051057:Proto-Oncogene Proteins c-akt