中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
1期
24-27
,共4页
朱其荣%秦波%黄涛%刘汉屈
硃其榮%秦波%黃濤%劉漢屈
주기영%진파%황도%류한굴
肝炎,乙型%受体,胰岛素%胰岛素受体底物2%胰岛素抵抗%酪氨酸磷酸化
肝炎,乙型%受體,胰島素%胰島素受體底物2%胰島素牴抗%酪氨痠燐痠化
간염,을형%수체,이도소%이도소수체저물2%이도소저항%락안산린산화
Hepatitis B,Receptors,insulin%Insulin receptor substrate-2%Insulin resistance%Tyrosine phosphorylation
目的 观察慢性乙型肝炎(CHB)患者肝组织胰岛素受体底物2(IRS-2)的mRNA和蛋白表达及其酪氨酸磷酸化程度,探讨IRS-2在CHB患者胰岛素抵抗(IR)发生中的作用.方法 选择6例肝功能正常者(对照组)及18例CHB患者,CHB患者再按HOMA模型计算的胰岛素抵抗指数分为CHB非IR(＜2.69)组(10例)和CHB合并IR(＞2.69)组(8例).所有患者于术中及肝穿刺后留取肝组织,采用逆转录-聚合酶链反应检测IRS-2 mRNA表达;采用蛋白质免疫印迹法检测IRS-2蛋白表达;采用免疫沉淀及增强化学发光法检测IRS-2酪氨酸磷酸化程度.结果 CHB非IR组肝组织IRS-2 mRNA(0.38±0.06)、蛋白(0.94±0.18)表达及酪氨酸磷酸化程度(0.78±0.09)较对照组(分别为0.45±0.11、0.99±0.20、1.00±0.23)有所降低,但差异无统计学意义(均P＞0.05);CHB合并IR组IRS-2mRNA(0.26±0.08)、蛋白(0.67±0.11)表达及酪氨酸磷酸化程度(0.63±0.14)均较对照组明显降低,差异有统计学意义(P＜0.05或P＜0.01).结论 CHB合并IR患者肝组织IRS-2的mRNA和蛋白表达及酪氨酸磷酸化程度的降低可能是产生IR的机制之一.
目的 觀察慢性乙型肝炎(CHB)患者肝組織胰島素受體底物2(IRS-2)的mRNA和蛋白錶達及其酪氨痠燐痠化程度,探討IRS-2在CHB患者胰島素牴抗(IR)髮生中的作用.方法 選擇6例肝功能正常者(對照組)及18例CHB患者,CHB患者再按HOMA模型計算的胰島素牴抗指數分為CHB非IR(＜2.69)組(10例)和CHB閤併IR(＞2.69)組(8例).所有患者于術中及肝穿刺後留取肝組織,採用逆轉錄-聚閤酶鏈反應檢測IRS-2 mRNA錶達;採用蛋白質免疫印跡法檢測IRS-2蛋白錶達;採用免疫沉澱及增彊化學髮光法檢測IRS-2酪氨痠燐痠化程度.結果 CHB非IR組肝組織IRS-2 mRNA(0.38±0.06)、蛋白(0.94±0.18)錶達及酪氨痠燐痠化程度(0.78±0.09)較對照組(分彆為0.45±0.11、0.99±0.20、1.00±0.23)有所降低,但差異無統計學意義(均P＞0.05);CHB閤併IR組IRS-2mRNA(0.26±0.08)、蛋白(0.67±0.11)錶達及酪氨痠燐痠化程度(0.63±0.14)均較對照組明顯降低,差異有統計學意義(P＜0.05或P＜0.01).結論 CHB閤併IR患者肝組織IRS-2的mRNA和蛋白錶達及酪氨痠燐痠化程度的降低可能是產生IR的機製之一.
목적 관찰만성을형간염(CHB)환자간조직이도소수체저물2(IRS-2)적mRNA화단백표체급기락안산린산화정도,탐토IRS-2재CHB환자이도소저항(IR)발생중적작용.방법 선택6례간공능정상자(대조조)급18례CHB환자,CHB환자재안HOMA모형계산적이도소저항지수분위CHB비IR(＜2.69)조(10례)화CHB합병IR(＞2.69)조(8례).소유환자우술중급간천자후류취간조직,채용역전록-취합매련반응검측IRS-2 mRNA표체;채용단백질면역인적법검측IRS-2단백표체;채용면역침정급증강화학발광법검측IRS-2락안산린산화정도.결과 CHB비IR조간조직IRS-2 mRNA(0.38±0.06)、단백(0.94±0.18)표체급락안산린산화정도(0.78±0.09)교대조조(분별위0.45±0.11、0.99±0.20、1.00±0.23)유소강저,단차이무통계학의의(균P＞0.05);CHB합병IR조IRS-2mRNA(0.26±0.08)、단백(0.67±0.11)표체급락안산린산화정도(0.63±0.14)균교대조조명현강저,차이유통계학의의(P＜0.05혹P＜0.01).결론 CHB합병IR환자간조직IRS-2적mRNA화단백표체급락안산린산화정도적강저가능시산생IR적궤제지일.
Objective To observe the expression of insulin receptor substrate-2(IRS-2)mRNA and protein,and its tyrosine phosphorylation in hepatic tissue of chronic hepatitis B(CHB)patients,and to explore the role of IRS-2 on insulin resistance in CHB patients.Methods Eighteen patients with CFIB were included,and 6 individuals with normal liver function were enrolled as control.Based on the insulin resistance index determined by homeostasis model assessment(HOMA),CHB patients were further divided into CHB without insulin resistance group(＜2.69,n=10)and CHB with insulin resistance group(＞2.69,n=8).Hepatic tissues were harvested from all patients during operation or with liver biopsy.The mRNA expression of IRS-2 in liver tissue was assessed by reverse transcription-polymerase chain reaction (RT-PCR),and the protein expression of IRS-2 was detected by Western blotting.Immunoprecipitation and enhanced chemiluminescent technique were used to measure the tyrosine phosphorylation of IRS-2.Results In CHB without insulin resistance group,the mRNA expression(0.38±0.06),the protein expression (0.94±0.18)and the tyrosine phosphorylation(0.78±0.09)of IRS-2 in hepatic tissue were decreased,but without statistically significant difference(all P＞0.05).as compared to those in control group(0.45±0.11,0.99±0.20,1.00±0.23,respectively).In CHB with insulin resistance group,the mRNA expression (0.26±0.08),the protein expression(0.67±0.11)and the tyrosine phosphorylation(0.63±0.14)of IRS-2 in hepatic tissue were significantly decreased compared with those of the control group with statistically significant difference(P＜0.05 or P＜0.01).Conclusion The decreased expression of mRNA and protein and the reduced tyrosine phosphorylation Of IRS-2 in CHB patients with insulin resistance inducing impairment of the insulin signal pathway may be one of the mechanisms underlying insulin resistance.
