中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2013年
6期
515-519
,共5页
谷雪梅%沈飞霞%潘伟%叶菁%顾雪疆%倪连松%李卫平%林迪妮
穀雪梅%瀋飛霞%潘偉%葉菁%顧雪疆%倪連鬆%李衛平%林迪妮
곡설매%침비하%반위%협정%고설강%예련송%리위평%림적니
水通道蛋白7%胰岛素抵抗%蛋白激酶B
水通道蛋白7%胰島素牴抗%蛋白激酶B
수통도단백7%이도소저항%단백격매B
Aquaglyceroporin 7%Insulin resistance%Protein kinase B
目的 探讨脂肪细胞中水通道蛋白7(AQP7)表达与胰岛素抵抗的关系.方法 培养3T3-L1前体脂肪细胞,诱导分化为成熟的脂肪细胞,并用地塞米松(DXM)处理建立胰岛素抵抗模型.构建Ad-AQP7重组腺病毒,转染胰岛素抵抗的脂肪细胞,检测AQP7表达水平的改变与脂肪细胞甘油释放水平、葡萄糖代谢能力以及磷酸化PKB表达改变的关系,从而阐明AQP7改善胰岛素抵抗的可能机制.结果 100 nmol/L DXM作用分化成熟的脂肪细胞诱导胰岛素抵抗,48 h后p-PKB水平和葡萄糖消耗量明显减少(P＜0.01),为胰岛素抵抗的最佳状态.胰岛素抵抗状态下AQP7 mRNA和蛋白水平明显减少(均P＜0.01).Ad-AQP7腺病毒转染胰岛素抵抗的脂肪细胞72h,随着AQP7表达增加,培养基中甘油释放浓度增加,胰岛素刺激下的p-PKB水平呈现同样上升趋势,并且葡萄糖代谢能力得到明显改善.结论 AQP7可能参与胰岛素抵抗的分子机制;高表达AQP7可改善胰岛素抵抗,其机制可能与PKB信号通路改善有关.
目的 探討脂肪細胞中水通道蛋白7(AQP7)錶達與胰島素牴抗的關繫.方法 培養3T3-L1前體脂肪細胞,誘導分化為成熟的脂肪細胞,併用地塞米鬆(DXM)處理建立胰島素牴抗模型.構建Ad-AQP7重組腺病毒,轉染胰島素牴抗的脂肪細胞,檢測AQP7錶達水平的改變與脂肪細胞甘油釋放水平、葡萄糖代謝能力以及燐痠化PKB錶達改變的關繫,從而闡明AQP7改善胰島素牴抗的可能機製.結果 100 nmol/L DXM作用分化成熟的脂肪細胞誘導胰島素牴抗,48 h後p-PKB水平和葡萄糖消耗量明顯減少(P＜0.01),為胰島素牴抗的最佳狀態.胰島素牴抗狀態下AQP7 mRNA和蛋白水平明顯減少(均P＜0.01).Ad-AQP7腺病毒轉染胰島素牴抗的脂肪細胞72h,隨著AQP7錶達增加,培養基中甘油釋放濃度增加,胰島素刺激下的p-PKB水平呈現同樣上升趨勢,併且葡萄糖代謝能力得到明顯改善.結論 AQP7可能參與胰島素牴抗的分子機製;高錶達AQP7可改善胰島素牴抗,其機製可能與PKB信號通路改善有關.
목적 탐토지방세포중수통도단백7(AQP7)표체여이도소저항적관계.방법 배양3T3-L1전체지방세포,유도분화위성숙적지방세포,병용지새미송(DXM)처리건립이도소저항모형.구건Ad-AQP7중조선병독,전염이도소저항적지방세포,검측AQP7표체수평적개변여지방세포감유석방수평、포도당대사능력이급린산화PKB표체개변적관계,종이천명AQP7개선이도소저항적가능궤제.결과 100 nmol/L DXM작용분화성숙적지방세포유도이도소저항,48 h후p-PKB수평화포도당소모량명현감소(P＜0.01),위이도소저항적최가상태.이도소저항상태하AQP7 mRNA화단백수평명현감소(균P＜0.01).Ad-AQP7선병독전염이도소저항적지방세포72h,수착AQP7표체증가,배양기중감유석방농도증가,이도소자격하적p-PKB수평정현동양상승추세,병차포도당대사능력득도명현개선.결론 AQP7가능삼여이도소저항적분자궤제;고표체AQP7가개선이도소저항,기궤제가능여PKB신호통로개선유관.
Objective To investigate the role of aquaglyceroporin 7 (AQP7) played in insulin resistance of adipocytes.Methods 3T3-L1 preadipocyte cells were induced to be fully differentiated adipocytes and then insulin resistance was induced by dexamethasone (DXM).Adenovirus vector over-expressing AQP7 (Ad-AQP7) was constructed and transfected into adipocytes.Expression levels of AQP7,glycerol release from adipocytes,changes in glucose consumption,and phosphorylated protein kinase B (p-PKB) were measured.Results 48 h-treatment of dexamethasone significantly inhibited the expression level of p-PKB (P＜0.01) and decreased glucose utilization,as well as down-regulation of AQP7 (P＜0.01).Over-expression of AQP7 by transfecting Ad-AQP7 to dexamethasone (DXM)-induced insulin resistant adipocytes could improve glycerol secretion of adipocytes,being consistent with the restoration of p-PKB expression levels and glucose consumption.Conclusions AQP7 may improve in molecular mechanism of insulin resistance in adipocytes.Overexpression of AQP7 may contribute to the improvement of insulin resistance in adipocytes and might be correlated with better phosphorylation of PKB.
