中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2010年
8期
625-627
,共3页
孙涛%曲巍%段东明%赵立娜%彭晓琳%郝丽萍%孙秀发
孫濤%麯巍%段東明%趙立娜%彭曉琳%郝麗萍%孫秀髮
손도%곡외%단동명%조립나%팽효림%학려평%손수발
酒精%胰岛素抵抗%肿瘤坏死因子α%瘦素
酒精%胰島素牴抗%腫瘤壞死因子α%瘦素
주정%이도소저항%종류배사인자α%수소
Ethanol%Insulin resistance% TNF-α% Leptin
目的 研究长期酒精摄入对大鼠脂肪组织肿瘤坏死因子α(TNF-α)及瘦素(Leptin)mRNA表达水平的影响,探讨酒精导致胰岛素抵抗的机制.方法 根据给予酒精的剂量0, 0.8, 1.6, 2.4 g·kg-1·bw-1.将Wistar大鼠40只分为对照组(Con)和低剂量酒精(LA)、中剂量酒精(MA)、高剂量酒精(HA)组,测血糖、胰岛素、血TNF-α和Leptin浓度,计算胰岛素抵抗指数,RT-PCR方法测定TNF-α, Leptin mRNA表达水平.结果 与Con组相比,各剂量组血糖呈酒精剂量依赖性升高(r=0.499,P<0.01),各剂量组HOMA-IR增加且差异均具有统计学意义(P<0.05);各剂量组血清中TNF-α浓度及脂肪组织中TNF-α mRNA表达水平增加,HA组差异有统计学意义(P<0.05);各剂量组血清Leptin浓度及脂肪组织Leptin mRNA表达水平均无改变.结论 脂肪组织TNF-α mRNA表达水平升高可能是酒精导致胰岛素抵抗分子机制之一.
目的 研究長期酒精攝入對大鼠脂肪組織腫瘤壞死因子α(TNF-α)及瘦素(Leptin)mRNA錶達水平的影響,探討酒精導緻胰島素牴抗的機製.方法 根據給予酒精的劑量0, 0.8, 1.6, 2.4 g·kg-1·bw-1.將Wistar大鼠40隻分為對照組(Con)和低劑量酒精(LA)、中劑量酒精(MA)、高劑量酒精(HA)組,測血糖、胰島素、血TNF-α和Leptin濃度,計算胰島素牴抗指數,RT-PCR方法測定TNF-α, Leptin mRNA錶達水平.結果 與Con組相比,各劑量組血糖呈酒精劑量依賴性升高(r=0.499,P<0.01),各劑量組HOMA-IR增加且差異均具有統計學意義(P<0.05);各劑量組血清中TNF-α濃度及脂肪組織中TNF-α mRNA錶達水平增加,HA組差異有統計學意義(P<0.05);各劑量組血清Leptin濃度及脂肪組織Leptin mRNA錶達水平均無改變.結論 脂肪組織TNF-α mRNA錶達水平升高可能是酒精導緻胰島素牴抗分子機製之一.
목적 연구장기주정섭입대대서지방조직종류배사인자α(TNF-α)급수소(Leptin)mRNA표체수평적영향,탐토주정도치이도소저항적궤제.방법 근거급여주정적제량0, 0.8, 1.6, 2.4 g·kg-1·bw-1.장Wistar대서40지분위대조조(Con)화저제량주정(LA)、중제량주정(MA)、고제량주정(HA)조,측혈당、이도소、혈TNF-α화Leptin농도,계산이도소저항지수,RT-PCR방법측정TNF-α, Leptin mRNA표체수평.결과 여Con조상비,각제량조혈당정주정제량의뢰성승고(r=0.499,P<0.01),각제량조HOMA-IR증가차차이균구유통계학의의(P<0.05);각제량조혈청중TNF-α농도급지방조직중TNF-α mRNA표체수평증가,HA조차이유통계학의의(P<0.05);각제량조혈청Leptin농도급지방조직Leptin mRNA표체수평균무개변.결론 지방조직TNF-α mRNA표체수평승고가능시주정도치이도소저항분자궤제지일.
Objective To investigate the effect of chronic alcohol intake on TNF-α and leptin mRNA expression in rat adipose tissue and to explore the possible mechanism of the effect of alcohol on insulin sensitivity. Methods 40 Wistar rats were randomly divided into four groups:ethanol dose of 0(contro1 group)，0.8(1ow dose group),1.6(middle dose group)and 2.4 g/(kg BW) (high dose group)daily. Fasting levels of glucose, insulin,TNF-α and leptin were measured. HOMAIR index was calculated. The expressions of TNF-α and leptin mRNA in adipose tissue were detected by RTPCR. Results Compared with control group， the fasting plasma glucose of high dose group， fasting plasma insulin of low and middle dose group and HOMAIR index of all alcoholloading group were significantly increased （all P<0.05）. The serum TNF-α and expression of TNF-α mRNA in adipose tissue were significantly increased in high dose group.There was no significant change of leptin in both serum and adipose tissue in all ethanolloading group. Conclusions The changes of TNF-α mRNA expression in rat adipose tissue are likely to be the molecular mechanisms for alcohol induced insulin resistance.
