Resistant starch improves insulin resistance and reduces adipose tissue weight and CD11c expression in rat OLETF adipose tissue.
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.


CONCLUSIONS
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.
Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan.
Tomomi
T
Harazaki
Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan.
Seiya
S
Inoue
Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences and Global COE Program, University of Shizuoka, Shizuoka, Japan.
Chihiro
C
Imai
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.
Kazuki
K
Mochizuki
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.
Toshinao
T
Goda
D017667:Adipocytes / Q000187:drug effects; D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D039521:CD11c Antigen / Q000378:metabolism*; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology / Q000627:therapeutic use*; D004043:Dietary Fiber / Q000494:pharmacology / Q000627:therapeutic use*; D007333:Insulin Resistance; D008264:Macrophages; D008297:Male; D008643:Mesentery / Q000378:metabolism; D051381:Rats; D020334:Rats, Inbred OLETF; D020318:Rats, Long-Evans; D013213:Starch / Q000494:pharmacology / Q000627:therapeutic use*
D015703:Antigens, CD; D039521:CD11c Antigen; D004040:Dietary Carbohydrates; D004043:Dietary Fiber; D013213:Starch
Adipose tissue; CD11c-positive macrophage; OLETF rat; Resistant starch; β2-integrin