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作 者:William T.Moore Jing Luo Dongmin Liu
机构地区:[1]Department of Human Nutrition,Foods and Exercise,College of Agricultural and Life Sciences,Virginia Tech,Blacksburg 24060,USA [2]Department of Biology and Chemistry,Liberty University,Lynchburg 24515,USA [3]Department of Human Nutrition,Foods and Exercise,Virginia Tech,1981 Kraft Drive,Corporate Research Center,Blacksburg 24061,USA
出 处:《Food Science and Human Wellness》2023年第6期2087-2094,共8页食品科学与人类健康(英文)
基 金:partially supported by grants from Diabetes Action Research and Education Foundation。
摘 要:Insulin resistance is a hallmark of type-2 diabetes(T2D)pathogenesis.Because skeletal muscle(SkM)is the major tissue for insulin-mediated glucose disposal,insulin resistance in SkM is considered a major risk factor for developing T2D.Thus,the identifi cation of compounds that enhance the ability of SkM to take up glucose is a promising strategy for preventing T2D.Our previous work showed that kaempferol,a fl avonol present in many foods,improves insulin sensitivity in obese mice,however,the mechanism underlying this beneficial action remains unclear.Here,we show that kaempferol directly stimulates glucose uptake and prevents lipotoxicity-impaired glucose uptake in primary human SkM.Kaempferol stimulates Akt phosphorylation in a time-dependent manner in human SkM cells.The effect of kaempferol on glucose uptake was blunted by inhibition of glucose transporter 4,phosphoinositide 3-kinase(PI3K),or AMPK.In addition,kaempferol induced AMPK phosphorylation,and inhibition of AMPK prevented kaempferol-stimulated Akt phosphorylation.In vivo,kaempferol administration induced rapid glucose disposal accompanied with increased Akt and AMPK phosphorylation in SkM tissue of the mice.Taken together,these fi ndings suggest that kaempferol stimulates glucose uptake in SkM via an AMPK/Akt dependent mechanism,and it may be a viable therapeutic agent for insulin resistance.
关 键 词:KAEMPFEROL Skeletal muscle AMPK AKT Insulin resistance
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