Telmisartan Improves Insulin Resistance and Modulates Adipose Tissue Macrophage Polarization in High-Fat-Fed Mice
Epididymis
0301 basic medicine
Gene Expression Profiling
Body Weight
Antigens, Differentiation, Myelomonocytic
Flow Cytometry
Benzoates
Dietary Fats
CD11c Antigen
3. Good health
03 medical and health sciences
Glucose
Adipose Tissue
Gene Expression Regulation
Antigens, CD
Adipocytes
Animals
Benzimidazoles
Lectins, C-Type
Insulin Resistance
Angiotensin II Type 1 Receptor Blockers
Cell Adhesion Molecules
Cell Size
DOI:
10.1210/en.2010-1312
Publication Date:
2011-03-23T02:33:08Z
AUTHORS (16)
ABSTRACT
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-γ 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.
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