中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2014年
6期
368-374
,共7页
李丽玉%林志健%张冰%吴君德%王红坡%王雪洁%牛红娟%朱春胜
李麗玉%林誌健%張冰%吳君德%王紅坡%王雪潔%牛紅娟%硃春勝
리려옥%림지건%장빙%오군덕%왕홍파%왕설길%우홍연%주춘성
高果糖饮水%大鼠%高尿酸血症%病理机制
高果糖飲水%大鼠%高尿痠血癥%病理機製
고과당음수%대서%고뇨산혈증%병리궤제
High fructose drinking water%Rat%Hyperuricemia%Pathological mechanism
目的 探讨长期高果糖饮水对大鼠尿酸水平的影响及其病理机制.方法 雄性SD大鼠20只,采用随机数字表法分为正常组(n=10)和模型组(n=10),分别给予清水和10％的果糖水,均给予普通饲料,自由饮食饮水,连续58 d.动态检测大鼠血清和尿中的尿酸和肌酐水平,计算尿酸清除率(CUA)和内生肌酐清除率(CCR),检测尿酸代谢相关酶黄嘌呤氧化酶(XOD)、腺苷脱氨酶(ADA)和鸟嘌呤脱氨酶(GuDa)活性,并观察造模结束时大鼠肾脏病理变化.结果 实验第7、22、30、37、44、58天,模型组大鼠血清尿酸水平均显著高于正常组[(81.12 ±31.06) μmol/L比(54.27±23.42)μmol/L,P=0.017; (145.82±29.66) μmol/L比(114.90±28.04) μmol/L,P=0.033; (131.16±61.93) μmol/L比(54.67 ±33.49) μmol/L,P=0.002; (110.01±42.82) μmol/L比(66.43 ±22.50) μmol/L,P=0.007; (211.60±44.31) μmol/L比(171.44±38.72)μ.mol/L,P=0.039;(102.97±45.46) μmol/L比(62.24±20.89) μmol/L,P＝0.025].与正常组比较,模型组大鼠实验第22、37天血清XOD活性显著降低[(48.19±8.04)U/L比(58.71 ±5.18) U/L,P=0.003;(60.07 ±6.53) U/L比(66.74±6.58) U/L,P=0.027];实验第37、44天血清ADA活性显著升高[(60.00±8.22) U/ml比(46.19±14.16) U/ml,P=0.048; (75.00±16.94) U/ml比(59.17±10.27) U/ml,P=0.037];实验第44天血清GuDa活性显著升高[(10.07 ±0.66)U/L比(9.33±0.71) U/L,P＝0.037].实验第44天,模型组的CUA和CCR均显著低于正常组[(0.24±0.15)ml/min比(0.40 ±0.12) ml/min,P=0.021; (0.33 ±0.21) ml/min比(0.57 ±0.27)ml/min,P=0.040].实验第58天,模型组大鼠肾小球数量减少、毛细血管壁增厚、囊腔变窄,未见异物沉积.结论 连续饮用高果糖水可引起大鼠血尿酸水平持续升高,诱发高尿酸血症.该病理现象的发生可能与果糖在体内代谢引起尿酸生成增多及尿酸经由肾脏排泄减少相关.
目的 探討長期高果糖飲水對大鼠尿痠水平的影響及其病理機製.方法 雄性SD大鼠20隻,採用隨機數字錶法分為正常組(n=10)和模型組(n=10),分彆給予清水和10％的果糖水,均給予普通飼料,自由飲食飲水,連續58 d.動態檢測大鼠血清和尿中的尿痠和肌酐水平,計算尿痠清除率(CUA)和內生肌酐清除率(CCR),檢測尿痠代謝相關酶黃嘌呤氧化酶(XOD)、腺苷脫氨酶(ADA)和鳥嘌呤脫氨酶(GuDa)活性,併觀察造模結束時大鼠腎髒病理變化.結果 實驗第7、22、30、37、44、58天,模型組大鼠血清尿痠水平均顯著高于正常組[(81.12 ±31.06) μmol/L比(54.27±23.42)μmol/L,P=0.017; (145.82±29.66) μmol/L比(114.90±28.04) μmol/L,P=0.033; (131.16±61.93) μmol/L比(54.67 ±33.49) μmol/L,P=0.002; (110.01±42.82) μmol/L比(66.43 ±22.50) μmol/L,P=0.007; (211.60±44.31) μmol/L比(171.44±38.72)μ.mol/L,P=0.039;(102.97±45.46) μmol/L比(62.24±20.89) μmol/L,P＝0.025].與正常組比較,模型組大鼠實驗第22、37天血清XOD活性顯著降低[(48.19±8.04)U/L比(58.71 ±5.18) U/L,P=0.003;(60.07 ±6.53) U/L比(66.74±6.58) U/L,P=0.027];實驗第37、44天血清ADA活性顯著升高[(60.00±8.22) U/ml比(46.19±14.16) U/ml,P=0.048; (75.00±16.94) U/ml比(59.17±10.27) U/ml,P=0.037];實驗第44天血清GuDa活性顯著升高[(10.07 ±0.66)U/L比(9.33±0.71) U/L,P＝0.037].實驗第44天,模型組的CUA和CCR均顯著低于正常組[(0.24±0.15)ml/min比(0.40 ±0.12) ml/min,P=0.021; (0.33 ±0.21) ml/min比(0.57 ±0.27)ml/min,P=0.040].實驗第58天,模型組大鼠腎小毬數量減少、毛細血管壁增厚、囊腔變窄,未見異物沉積.結論 連續飲用高果糖水可引起大鼠血尿痠水平持續升高,誘髮高尿痠血癥.該病理現象的髮生可能與果糖在體內代謝引起尿痠生成增多及尿痠經由腎髒排洩減少相關.
목적 탐토장기고과당음수대대서뇨산수평적영향급기병리궤제.방법 웅성SD대서20지,채용수궤수자표법분위정상조(n=10)화모형조(n=10),분별급여청수화10％적과당수,균급여보통사료,자유음식음수,련속58 d.동태검측대서혈청화뇨중적뇨산화기항수평,계산뇨산청제솔(CUA)화내생기항청제솔(CCR),검측뇨산대사상관매황표령양화매(XOD)、선감탈안매(ADA)화조표령탈안매(GuDa)활성,병관찰조모결속시대서신장병리변화.결과 실험제7、22、30、37、44、58천,모형조대서혈청뇨산수평균현저고우정상조[(81.12 ±31.06) μmol/L비(54.27±23.42)μmol/L,P=0.017; (145.82±29.66) μmol/L비(114.90±28.04) μmol/L,P=0.033; (131.16±61.93) μmol/L비(54.67 ±33.49) μmol/L,P=0.002; (110.01±42.82) μmol/L비(66.43 ±22.50) μmol/L,P=0.007; (211.60±44.31) μmol/L비(171.44±38.72)μ.mol/L,P=0.039;(102.97±45.46) μmol/L비(62.24±20.89) μmol/L,P＝0.025].여정상조비교,모형조대서실험제22、37천혈청XOD활성현저강저[(48.19±8.04)U/L비(58.71 ±5.18) U/L,P=0.003;(60.07 ±6.53) U/L비(66.74±6.58) U/L,P=0.027];실험제37、44천혈청ADA활성현저승고[(60.00±8.22) U/ml비(46.19±14.16) U/ml,P=0.048; (75.00±16.94) U/ml비(59.17±10.27) U/ml,P=0.037];실험제44천혈청GuDa활성현저승고[(10.07 ±0.66)U/L비(9.33±0.71) U/L,P＝0.037].실험제44천,모형조적CUA화CCR균현저저우정상조[(0.24±0.15)ml/min비(0.40 ±0.12) ml/min,P=0.021; (0.33 ±0.21) ml/min비(0.57 ±0.27)ml/min,P=0.040].실험제58천,모형조대서신소구수량감소、모세혈관벽증후、낭강변착,미견이물침적.결론 련속음용고과당수가인기대서혈뇨산수평지속승고,유발고뇨산혈증.해병리현상적발생가능여과당재체내대사인기뇨산생성증다급뇨산경유신장배설감소상관.
Objective To investigate the pathological mechanism underlying the effects of high fructose drinking water on the uric acid level in rats.Methods 20 male SD rats were randomly divided with random number table to the control group (n =10,given normal water) and the model group (n =10,given 10％ fructose water),both fed with ordinary food for 58 days.Serum and urinary uric acid (UA) and creatine levels in the rats were monitored to calculate clearance of uric acid (CUA) and endogenous creatinine clearance rate (CCR).The activities of serum xanthine oxidase (XOD),adenosine deaminase (ADA),and guanine deaminase (GuDa) were detected,and pathological changes of the kidney of the rats were observed on the 58th day.Results Compared with the control group,the serum UA level of the model group was significantly higher on the 7th,22th,30th,37th,44th,58th days [(81.12 ±31.06) μmmol/L vs.(54.27 ±23.42) μmmol/L,P =0.017; (145.82±29.66) μmol/Lvs.(114.90±28.04) μmol/L,P=0.033; (131.16±61.93) μ mol/L vs.(54.67 ± 33.49) μ mol/L,P =0.002 ; (110.01 ± 42.82) μmol/L vs.(66.43 ± 22.50) μmol/L,P =0.007; (211.60±44.31) μmol/Lvs.(171.44±38.72) μmol/L,P=0.039; (102.97±45.46) μmol/L vs.(62.24 ± 20.89) μ.mol/L,P =0.025].Compared with the control group,XOD activity in the model group decreased significantly on the 22th and the 37th days [(48.19 ±8.04) U/L vs.(58.71 ±5.18) U/L,P=0.003; (60.07 ±6.53) U/L vs.(66.74 ±6.58) U/L,P=0.027] ; ADA activity in the model group increased significantly on the 37th and the 44th day [(60.00 ±8.22) U/ml vs.(46.19 ± 14.16) U/ml,P =0.048; (75.00 ± 16.94) U/ml vs.(59.17 ± 10.27) U/ml,P=0.037] ; and GuDa activity of the model group increased significantly on the 44th days [(10.07 ±0.66) U/L vs.(9.33 ±0.71) U/L,P =0.037].On the 44th day,both CUA and CCR in the model group were significantly lower than those in the control group [(0.24±0.15) ml/minvs.(0.40±0.12) ml/min,P=0.021; (0.33 ±0.21) ml/min vs.(0.57± 0.27) ml/min,P =0.040].On the 58th day,the kidneys of the rats in the model groups demonstrated decreased number of glomeruli,thickened capillary wall,and narrowed Bowman's capsules,but no trace of foreign substance deposition.Conclusions Continuous consumption of high fructose drinking water can increase the serum UA level and induce hyperuricemia.This pathological condition may be related to increased synthesis and decreased renal excretion of UA caused by fructose metabolilsm.
