TY - JOUR
T1 - Natural killer T cells are involved in adipose tissues inflammation and glucose intolerance in diet-induced obese mice
AU - Ohmura, Kazue
AU - Ishimori, Naoki
AU - Ohmura, Yoshinori
AU - Tokuhara, Satoshi
AU - Nozawa, Atsushi
AU - Horii, Shunpei
AU - Andoh, Yasuhiro
AU - Fujii, Satoshi
AU - Iwabuchi, Kazuya
AU - Onoé, Kazunori
AU - Tsutsui, Hiroyuki
PY - 2010/2
Y1 - 2010/2
N2 - BACKGROUND-: Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Natural killer T (NKT) cells, which integrate proinflammatory cytokines, have been demonstrated in the atherosclerotic lesions and in visceral adipose tissue. OBJECTIVE-: To determine whether NKT cells are involved in glucose intolerance and adipose tissue inflammation in diet-induced obese mice. METHODS AND RESULTS-: To determine whether NKT cells are involved in the development of glucose intolerance, male β2-microglobulin knockout (KO) mice lacking NKT cells and C57BL/6J (wild-type) mice were fed with a high-fat diet (HFD) for 13 weeks. Body weight and visceral obesity were comparable between wild-type and KO mice. However, macrophage infiltration was reduced in adipose tissue and glucose intolerance was significantly ameliorated in KO mice. To further confirm that NKT cells are involved in these abnormalities, α-galactosylceramide, 0.1 μg/g body weight, which specifically activates NKT cells, was administered after 13 weeks of HFD feeding. α-Galactosylceramide significantly exacerbated glucose intolerance and macrophage infiltration as well as cytokine gene expression in adipose tissue. CONCLUSION-: NKT cells play a crucial role in the development of adipose tissue inflammation and glucose intolerance in diet-induced obesity.
AB - BACKGROUND-: Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Natural killer T (NKT) cells, which integrate proinflammatory cytokines, have been demonstrated in the atherosclerotic lesions and in visceral adipose tissue. OBJECTIVE-: To determine whether NKT cells are involved in glucose intolerance and adipose tissue inflammation in diet-induced obese mice. METHODS AND RESULTS-: To determine whether NKT cells are involved in the development of glucose intolerance, male β2-microglobulin knockout (KO) mice lacking NKT cells and C57BL/6J (wild-type) mice were fed with a high-fat diet (HFD) for 13 weeks. Body weight and visceral obesity were comparable between wild-type and KO mice. However, macrophage infiltration was reduced in adipose tissue and glucose intolerance was significantly ameliorated in KO mice. To further confirm that NKT cells are involved in these abnormalities, α-galactosylceramide, 0.1 μg/g body weight, which specifically activates NKT cells, was administered after 13 weeks of HFD feeding. α-Galactosylceramide significantly exacerbated glucose intolerance and macrophage infiltration as well as cytokine gene expression in adipose tissue. CONCLUSION-: NKT cells play a crucial role in the development of adipose tissue inflammation and glucose intolerance in diet-induced obesity.
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U2 - 10.1161/ATVBAHA.109.198614
DO - 10.1161/ATVBAHA.109.198614
M3 - Article
C2 - 19910631
AN - SCOPUS:75149169811
VL - 30
SP - 193
EP - 199
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 2
ER -