中华医学杂志(英文版)
中華醫學雜誌(英文版)
중화의학잡지(영문판)
CHINESE MEDICAL JOURNAL
2001年
6期
592-595
,共4页
曹筱佩%傅祖植%明文玉%杨荣泽%程桦
曹篠珮%傅祖植%明文玉%楊榮澤%程樺
조소패%부조식%명문옥%양영택%정화
瘦素%糖代谢%肥胖症%肝细胞
瘦素%糖代謝%肥胖癥%肝細胞
수소%당대사%비반증%간세포
leptin%glucose metabolism%obesity%hepatic cell
目的观察不同剂量的瘦素对肝细胞葡萄糖氧化的急性与慢性影响,以及对葡萄糖激酶mRNA表达的影响。
方法正常大鼠肝细胞株BRL分别用不同浓度(10ng/ml-200ng/ml)的瘦素(leptin)作用1小时和24小时,以液体闪烁计数法检测葡萄糖氧化,以半定量逆转录PCR法检测葡萄糖激酶mRNA表达。
结果急性作用1小时,leptin 10ng/ml对基础及胰岛素刺激的葡萄糖氧化无明显影响。但leptin 50ng/ml时,基础及胰岛素刺激的葡萄糖氧化均较未用leptin的对照组显著下降(P<0.05),剂量上升至100ng/ml、200ng/ml时进一步下降。慢性作用24小时,各浓度leptin(10ng/ml-200ng/ml)对基础及胰岛素刺激的葡萄糖氧化均无明显影响。Leptin 100ng/ml处理1小时或24小时,均可明显抑制GK mRNA表达(与空白组比较P<0.05)。
结论瘦素可直接作用于肝细胞并影响肝糖代谢,相当于生理剂量的瘦素对基础状态和胰岛素作用下的肝细胞葡萄糖氧化无明显影响。高浓度瘦素对基础与胰岛素作用下的葡萄糖氧化具有急性可逆性的抑制作用,并可抑制GK mRNA的表达。
目的觀察不同劑量的瘦素對肝細胞葡萄糖氧化的急性與慢性影響,以及對葡萄糖激酶mRNA錶達的影響。
方法正常大鼠肝細胞株BRL分彆用不同濃度(10ng/ml-200ng/ml)的瘦素(leptin)作用1小時和24小時,以液體閃爍計數法檢測葡萄糖氧化,以半定量逆轉錄PCR法檢測葡萄糖激酶mRNA錶達。
結果急性作用1小時,leptin 10ng/ml對基礎及胰島素刺激的葡萄糖氧化無明顯影響。但leptin 50ng/ml時,基礎及胰島素刺激的葡萄糖氧化均較未用leptin的對照組顯著下降(P<0.05),劑量上升至100ng/ml、200ng/ml時進一步下降。慢性作用24小時,各濃度leptin(10ng/ml-200ng/ml)對基礎及胰島素刺激的葡萄糖氧化均無明顯影響。Leptin 100ng/ml處理1小時或24小時,均可明顯抑製GK mRNA錶達(與空白組比較P<0.05)。
結論瘦素可直接作用于肝細胞併影響肝糖代謝,相噹于生理劑量的瘦素對基礎狀態和胰島素作用下的肝細胞葡萄糖氧化無明顯影響。高濃度瘦素對基礎與胰島素作用下的葡萄糖氧化具有急性可逆性的抑製作用,併可抑製GK mRNA的錶達。
목적관찰불동제량적수소대간세포포도당양화적급성여만성영향,이급대포도당격매mRNA표체적영향。
방법정상대서간세포주BRL분별용불동농도(10ng/ml-200ng/ml)적수소(leptin)작용1소시화24소시,이액체섬삭계수법검측포도당양화,이반정량역전록PCR법검측포도당격매mRNA표체。
결과급성작용1소시,leptin 10ng/ml대기출급이도소자격적포도당양화무명현영향。단leptin 50ng/ml시,기출급이도소자격적포도당양화균교미용leptin적대조조현저하강(P<0.05),제량상승지100ng/ml、200ng/ml시진일보하강。만성작용24소시,각농도leptin(10ng/ml-200ng/ml)대기출급이도소자격적포도당양화균무명현영향。Leptin 100ng/ml처리1소시혹24소시,균가명현억제GK mRNA표체(여공백조비교P<0.05)。
결론수소가직접작용우간세포병영향간당대사,상당우생리제량적수소대기출상태화이도소작용하적간세포포도당양화무명현영향。고농도수소대기출여이도소작용하적포도당양화구유급성가역성적억제작용,병가억제GK mRNA적표체。
Objective To observe the short-term and long-term effects of leptin on hepatic glucose oxidation and glucokinase gene expression.
Methods Rat hepatic cell line BRL was incubated with leptin of different doses (range from 10?ng/ml-200?ng/ml) for 1?h or 24?h. Glucose oxidation was determined by liquid scintillation counting. Glucokinase gene expression (corrected by β-actin) was determined by reverse transcription semi-quantitative polymerase chain reaction.
Results Treatment with leptin 10?ng/ml for 1?h had no significant effects on glucose oxidation in hepatic cells. However, at the doses ranging from 50?ng/ml to 200?ng/ml, leptin significantly inhibited glucose oxidation. These effects disappeared when the hepatic cells were exposed to leptin for 24?h. Glucokinase mRNA expression was reduced significantly after both 1?h and 24?h exposure to leptin (100?ng/ml) as compared to that of the control group.
Conclusion A low dose of leptin has no significant effect on glucose oxidation in hepatic cells. A relatively high dose of leptin has an acute inhibitory effect on the glucose oxidation in hepatic cells. This effect may likely involve the inhibition of glucokinase gene expression. The inhibitory effect on glucose oxidation is transient and disappears with prolonged exposure time.