ID 110183
Title Transcription
Cbl-b ケッソン ニ ヨル マクロファージ ノ カッセイカ オ カイシタ タイトウノウ イジョウ
Title Alternative
Deficiency of Cbl-b gene enhances infiltration and activation of macrophages in adipose tissue and causes peripheral insulin resistance in mice
Author
Hirasaka, Katsuya Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School KAKEN Search Researchers
Kohno, Shohei Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School
Kagawa, Sachiko Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School
Nakao, Reiko Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Furochi, Harumi Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School
Kishi, Kyoichi Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Nikawa, Takeshi Department of Nutritional Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
Cbl-b-deficient mice
macrophage
cytokine
white adipose tissue
insulin resistance
Content Type
Journal Article
Description
Obesity is a major cause of insulin resistance and is considered a chronic low-grade inflammatory disease. Substantial evidence has accumulated in recent years that chronic infiltration and activation of macrophages in white adipose tissue underlie the obesity-related component of these insulin resistant states. In the present study, we examined the role of Cbl-b, ubiquitin ligase, in insulin action. Elderly Cbl-b-deficient mice(Cbl-b-/-mice)developed glucose intolerance and peripheral insulin resistance. Deficiency of Cbl-b gene was associated with infiltration of macrophages into the WAT and expression of cytokines, such as tumor necrosis factor-α, interleukin-6 and monocyte chemoattractant protein-1. Furthermore, Vav1, a key factor in macrophage activation, was highly phosphorylated in peritoneal Cbl-b-/-macrophages, compared with wild type macrophages, suggesting that Cbl-b deficiency induces macrophage activation. Our results suggest that Cbl-b is a negative regulator of macrophage activation, and that macrophage activation by Cbl-b deficiency, at least in part, contributes to the peripheral insulin resistance and glucose intolerance.
Journal Title
四国医学雑誌
ISSN
00373699
NCID
AN00102041
Publisher
徳島医学会
Volume
63
Issue
3-4
Start Page
111
End Page
115
Sort Key
111
Published Date
2007-08-25
EDB ID
FullText File
language
jpn
TextVersion
Publisher
departments
Medical Sciences