TY - JOUR
T1 - Telmisartan improves insulin resistance and modulates adipose tissue macrophage polarization in high-fat-fed mice
AU - Fujisaka, Shiho
AU - Usui, Isao
AU - Kanatani, Yukiko
AU - Ikutani, Masashi
AU - Takasaki, Ichiro
AU - Tsuneyama, Koichi
AU - Tabuchi, Yoshiaki
AU - Bukhari, Agussalim
AU - Yamazaki, Yu
AU - Suzuki, Hikari
AU - Senda, Satoko
AU - Aminuddin, Aminuddin
AU - Nagai, Yoshinori
AU - Takatsu, Kiyoshi
AU - Kobayashi, Masashi
AU - Tobe, Kazuyuki
PY - 2011/5
Y1 - 2011/5
N2 - Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor blocker and a peroxisome proliferator-activated receptor-7 agonist, reportedly has more beneficial effects on insulin sensitivity than other angiotensin II type 1 receptor blockers. In this study, we studied the effects of telmisartan on the adipose tissue macrophage phenotype in high-fat-fed mice. Telmisartan was administered for 5 wk to high-fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in visceral adipose tissues were then examined. An insulin-or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight, and adipocyte size without affecting the amount of energy intake. Telmisartan reduced the mRNA expression of CD11c and TNF-α, M1 macrophage markers, and significantly increased the expressions of M2 markers, such as CD163, CD209, and macrophage galactose N-acetyl-galactosamine specific lectin (Mgl2), in a quantitative RT-PCR analysis. A flow cytometry analysis showed that telmisartan decreased the number of M1 macrophages in visceral adipose tissues. In conclusion, telmisartan improves insulin sensitivity and modulates adipose tissue macrophage polarization to an antiinflammatory M2 state in high-fat-fed mice.
AB - Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor blocker and a peroxisome proliferator-activated receptor-7 agonist, reportedly has more beneficial effects on insulin sensitivity than other angiotensin II type 1 receptor blockers. In this study, we studied the effects of telmisartan on the adipose tissue macrophage phenotype in high-fat-fed mice. Telmisartan was administered for 5 wk to high-fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in visceral adipose tissues were then examined. An insulin-or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight, and adipocyte size without affecting the amount of energy intake. Telmisartan reduced the mRNA expression of CD11c and TNF-α, M1 macrophage markers, and significantly increased the expressions of M2 markers, such as CD163, CD209, and macrophage galactose N-acetyl-galactosamine specific lectin (Mgl2), in a quantitative RT-PCR analysis. A flow cytometry analysis showed that telmisartan decreased the number of M1 macrophages in visceral adipose tissues. In conclusion, telmisartan improves insulin sensitivity and modulates adipose tissue macrophage polarization to an antiinflammatory M2 state in high-fat-fed mice.
UR - http://www.scopus.com/inward/record.url?scp=79955438066&partnerID=8YFLogxK
U2 - 10.1210/en.2010-1312
DO - 10.1210/en.2010-1312
M3 - 学術論文
C2 - 21427223
AN - SCOPUS:79955438066
SN - 0013-7227
VL - 152
SP - 1789
EP - 1799
JO - Endocrinology
JF - Endocrinology
IS - 5
ER -
