Tomomi Harazaki1, Seiya Inoue1, Chihiro Imai1, Kazuki Mochizuki2, Toshinao Goda3. 1. Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan. 2. Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan; Research Branch of Food and Nutritional Sciences, Department of Local Produce and Food Sciences, Faculty of Life and Environmental Sciences, University of Yamanashi, Yamanashi, Japan. 3. Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan. Electronic address: gouda@u-shizuoka-ken.ac.jp.
Abstract
OBJECTIVE: CD11s/CD18 dimers induce monocyte/macrophage infiltration into many tissues, including adipose tissues. In particular, it was reported that β2-integrin CD11c-positive macrophages in adipose tissues are closely associated with the development of insulin resistance. The aim of this study was to determine whether intake of resistant starch (RS) reduces macrophage accumulation in adipose tissues and inhibits the development of insulin resistance at an early stage in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: Twenty-two-wk-old male OLETF rats were fed a control diet (55% α-corn starch) or an RS diet (55% RS) for 5 wk. An oral glucose tolerance test was performed after 4 wk of feeding; tissues (mesenteric and epididymal adipose tissues, and liver) and tail vein blood were collected after 5 wk of feeding the test diets. RESULTS: Feeding the RS diet to OLETF rats for 5 wk improved insulin resistance, reduced the mesenteric adipose tissue weight, and enhanced the number of small adipocytes. CD68 expression, a macrophage infiltration marker, was not changed by the RS diet, whereas the gene expression levels of integrins such as CD11c, CD11d, and CD18, but not CD11a, and CD11b, were significantly reduced. CD11c protein expression was reduced by the RS diet. CONCLUSION: These findings suggest that part of the mechanism for the improved insulin resistance by the RS diet involves a reduction of CD11c expression in adipose tissues.
OBJECTIVE: CD11s/CD18 dimers induce monocyte/macrophage infiltration into many tissues, including adipose tissues. In particular, it was reported that β2-integrin CD11c-positive macrophages in adipose tissues are closely associated with the development of insulin resistance. The aim of this study was to determine whether intake of resistant starch (RS) reduces macrophage accumulation in adipose tissues and inhibits the development of insulin resistance at an early stage in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: Twenty-two-wk-old male OLETF rats were fed a control diet (55% α-cornstarch) or an RS diet (55% RS) for 5 wk. An oral glucose tolerance test was performed after 4 wk of feeding; tissues (mesenteric and epididymal adipose tissues, and liver) and tail vein blood were collected after 5 wk of feeding the test diets. RESULTS: Feeding the RS diet to OLETF rats for 5 wk improved insulin resistance, reduced the mesenteric adipose tissue weight, and enhanced the number of small adipocytes. CD68 expression, a macrophage infiltration marker, was not changed by the RS diet, whereas the gene expression levels of integrins such as CD11c, CD11d, and CD18, but not CD11a, and CD11b, were significantly reduced. CD11c protein expression was reduced by the RS diet. CONCLUSION: These findings suggest that part of the mechanism for the improved insulin resistance by the RS diet involves a reduction of CD11c expression in adipose tissues.
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