Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan.
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.
Nutrition. 2014 May;30(5):590-5. doi: 10.1016/j.nut.2013.10.020. Epub 2013 Oct 31.
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.
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.
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.
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.
CD11s/CD18 二聚体诱导单核细胞/巨噬细胞浸润到许多组织中,包括脂肪组织。特别是,据报道,脂肪组织中β2 整合素 CD11c 阳性的巨噬细胞与胰岛素抵抗的发展密切相关。本研究旨在确定抗性淀粉(RS)的摄入是否能减少脂肪组织中巨噬细胞的积累,并抑制 Otsuka Long-Evans Tokushima Fatty(OLETF)大鼠早期胰岛素抵抗的发展。
22 周龄雄性 OLETF 大鼠喂食对照饮食(55%α-玉米淀粉)或 RS 饮食(55%RS)5 周。在喂食测试饮食 4 周后进行口服葡萄糖耐量试验;在喂食测试饮食 5 周后采集组织(肠系膜和附睾脂肪组织以及肝脏)和尾静脉血。
RS 饮食喂养 OLETF 大鼠 5 周可改善胰岛素抵抗,减少肠系膜脂肪组织重量,并增加小脂肪细胞数量。CD68 表达(一种巨噬细胞浸润标志物)不受 RS 饮食影响,但 CD11c、CD11d 和 CD18 等整合素的基因表达水平,而不是 CD11a 和 CD11b,则显著降低。RS 饮食还降低了 CD11c 蛋白的表达。
这些发现表明,RS 饮食改善胰岛素抵抗的部分机制涉及脂肪组织中 CD11c 表达的减少。