钙对用克山病病区粮喂养大鼠甲状旁腺激素降钙素以及生长…

用模仿克山病病区易感人群膳食组成的病区粮偏食喂养大鼠，观察在该饲料中补充不同浓度的钙对大鼠内分泌及生长代谢的影响。结果表明：病区粮偏食明显低钙，仅为常规食的１／３２；用该饲料喂养的大鼠体重增长缓慢；血清总钙及血浆钙离子水平明显降低，仅约为常规食组动物的一半左右，血Ｐ升高；血清甲状旁腺激素（ＰＴＨ），降钙素（ＣＴ）和生长激素（ＧＨ）水平均明显降低，与常规食组比，均为Ｐ〈０．０１。补Ｃａ后随血清Ｃａ增     

钙对模拟克山病偏食喂养大鼠甲状腺素代谢的影响

本文研究了克山病偏食饲料及在这种饲料中补充钙和硒、ＶｉｔＥ对大鼠甲状腺素代谢的影响。结果表明，用偏食饲料喂养大鼠的血清钙水平仅及常规食组一半，Ｔ３↓、Ｔ４↑，ＴＳＨ↓；饲料补钙后Ｔ３↓，Ｔ４↑，ＴＳＨ↓；补硒、ＶｉｔＥ后Ｔ３↑，Ｔ４↑，ＴＳＨ↓，表明钙在病区粮偏食喂养大鼠的甲状腺素代谢中起重要作用，补充钙同时补充硒和ＶｉｔＥ效果更好。     

钙硒对模拟克山病偏食喂养大鼠生长激素分泌的影响

模拟克山病偏食饲料及在这种饲料中补充钙和硒对大鼠生长和生长激素的影响。结果表明，这种克山病偏食饲料中除低硒外低钙特别突出，所饲大鼠血清钙水平及全血ＧＳＨ－Ｐｘ活性、血清总蛋白、生长激素明显低于常规食组。在克山病偏食饲料中单纯补钙或硒可明显改善大鼠生长状态及生长激素增多。表明钙和硒在病区粮偏食喂养大鼠所致生长迟缓方面及生长激素的释放中起重要作用。补充钙同时补充硒效果更好。     

钙对模拟克山病偏食喂养大鼠自由基代谢的影响

本文研究了克山病偏食饲料及在这种饲料中补育钙和硒对大鼠自由基代谢的影响。结果表明，这种克山病偏食饲料中除低硒外低钙特别突出，所饲大鼠血清钙水平、全血及心肌谷城肽过氧化物酶活性，过氧化氢酶、超氧化物歧化酶等自由基清除酶明显低于常规食组；心肌及血清中脂质过氧化物水平明显升高。在克山病偏食饲料中单饲料中单纯补钙可明显改善大鼠生长状态和降低心肌及血清中脂质过氧化物含量，但ＧＳＨ－ＰＸ水平无增高，血清ＣＡＴ     

膳食低钙对饲克山病病区粮大鼠肝脏Ⅰ型T_45′－脱碘酶活性的影响

用克山病病区玉米、黄豆为主组成偏食低钙及补钙饲料喂养大鼠８周。结果表明病区粮所饲大鼠生长迟缓，肝脏Ⅰ型Ｔ４５′—脱碘酶（ＩＤ—Ⅰ）活性、血清Ｔ３浓度及全血和肝脏谷胱甘肽过氧化物酶（ＧＳＨ—Ｐｘ）活性显著低于非病区粮及常规食组，血清和肝脏脂质过氧化物（ＬＰＯ），血清ＧＰＴ及ＡＬＰ浓度增加。病区粮单纯补钙使上述指标显著改善。提示钙可能参与了ＩＤ—Ⅰ活性及甲状腺激素代谢的调节过程，其机制可能与低钙使脂质过氧化加重，清除自由基能力下降而损害肝脏脱碘过程有关。     

钙硒与维生素E对饲予克山病病区粮大鼠心肌细胞抗氧化能力…

用克山病病区粮组成偏食低钙基础饲料及在饲料中补一定剂量钙、硒与维生素Ｅ（ＶＥ），观察其对大鼠心肌细胞抗氧化酶系活性及在一过性缺氧条件下心肌酶活性的影响。结果表明病区粮组成的偏食低钙饲料引起大鼠心肌组织ＧＳＨ－Ｐｘ，ＳＯＤ及Ｃａｔ活性明显降低，ＬＰＯ含量升高。在ＮａＮＯ２引起的缺氧条件下，心肌多种酶活性下降，而血清酶活性升高。联合补充钙，硒与ＶＥ可显著提高心肌细胞抗氧化酶系活性及增强心肌细胞抵抗缺氧     

膳食低钼对饲克山病病区粮大鼠肝脏Ⅰ型T45‘—脱碘酶活性的影响

用克山病病区玉米，黄豆为主组成偏食低钙及补钙饲料喂养大鼠８周。结果表明病区粮所饲大鼠生长迟缓，肝脏Ⅰ型Ｔ４５－脱碘酶活性，血清Ｔ３浓度及全血和肝脏谷胱甘这氧化物酶活性显著低于非病区粮及常规食组，血清和肝脏脂质过氧化物，血清ＧＰＴ及ＡＬＰ浓度增加。     

钙硒与维生素E对饲予克山病病区粮大鼠心肌细胞抗氧化能力的影响

用克山病病区粮组成偏食低钙基础饲料及在饲料中补一定剂量钙、硒与维生素Ｅ（ＶＥ），观察其对大鼠心肌细胞抗氧化酶系活性及在一过性缺氧条件下心肌酶活性的影响。结果表明病区粮组成的偏食低钙饲料引起大鼠心肌组织ＧＳＨ－Ｐｘ、ＳＯＤ及Ｃａｔ活性明显降低．ＬＰＯ含量升高。在ＮａＮＯ２引起的缺氧条件下，心肌多种酶活性下降，而血清酶活性升高．联合补充钙、硒与ＶＥ可显著提高心肌细胞抗氧化酶系活性及增强心肌细胞抵抗缺氧性损害的能力，提示偏食低钙可加重硒和ＶＥ缺乏条件下心肌细胞总抗氧化能力的减退，对缺血缺氧性因素的敏感性增加。     

钙缺乏对克山病病区粮养大鼠肾脏I型T4T‘—脱碘酶活性的…

以克山病病区玉米和黄豆为主，组成偏食低钙及补钙饲料喂养大鼠８周，结果病区粮所饲大鼠生长缓慢，血清总钙含量、肾脏Ｉ型Ｔ４５＇－脱碘酶（ＩＤ－Ｉ）活性、血清Ｔ３浓度及全血和肾脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力显著降低，血清和肾脏脂质过氧化物（ＬＰＯ）浓度增加。补钙使上述指标显著改善，恢复至常规饲料组水平。提示膳食低钙本身即可抑制ＩＤ－Ｉ活性，使甲状腺激素（ＴＨ）代谢发生障碍，机体抗氧化能力减退。     

钙,硒对膳食低钙大鼠红细胞钠／钾ATP酶及钙／镁ATP酶活性的影响

实验通过向模拟克山病偏食饲料中补充一定量的钙和硒／维生素Ｅ（Ｓｅ／ＶＥ）来观察大鼠红细胞钠／钾ＡＴＰ酶及钙／镁ＡＴＰ酶（Ｎａ－Ｋ－ＡＴＰａｓｅ,Ｃａ－Ｍｇ－ＡＴＰａｓｅ）活性的变化。探讨钙和硒对大鼠ＲＢＣ膜的变化规律。结果表明,病区粮组血钙水平最低,仅及常规食（ｓｔｏｃｋ）组一半,血清硒（Ｓｅ）,α－ＶＥ水平低于ｓｔｏｃｋ组,红细胞Ｎａ－Ｋ－ＡＴＰａｓｅ,Ｃａ－Ｍｇ－ＡＴＰａｓｅ,活性降低,血清过     

膳食低钙对饲克山病区粮大鼠胰岛素分泌的影响

本实验通过对模拟克山病偏食饲料中补充一定量的钙和硒来观察Wistar大鼠胰岛素(Ins)的变化。结果表明,病区粮组血钙水平最低,仅及常规食(stock)组一半;血清硒(Se),α-VE水平低于Stock组;Ins减少;血清过氧化脂质水平明显高于Stock组;血清GSH-Px活性低,有显著差异。补钙后钙水平升高,Se、α-VE水平变化不大;Ins显著升高。补Se/VE组Se、α-VE水平明显高于EM组。联合补Se/VE和Ca组Se、α-VE水平高于单纯补Se/VE组,有显著差异,Ins升高。补Se/VE、Ca各组可使过氧化脂质水平下降,有显著差异。综合分析结果表明,补Ca各组与EM组比较差异显著,表明膳食钙量对胰岛素影响极大。     

钙缺乏对克山病病区粮养大鼠肾脏Ⅰ型T_45′—脱碘酶活性的影响

以克山病病区玉米和黄豆为主,组成偏食低钙及补钙饲料喂养大鼠8周,结果病区粮所饲大鼠生长缓慢,血清总钙含量、肾脏Ⅰ型T_45′—脱碘酶(ID—I)活性、血清T_3浓度及全血和肾脏谷胱甘肽过氧化物酶(GSH—Px)活力显著降低,血清和肾脏脂质过氧化物(LPO)浓度增加。补钙使上述指标显著改善,恢复至常规饲料组水平。提示膳食低钙本身即可抑制ID—I活性,使甲状腺激素(TH)代谢发生障碍,机体抗氧化能力减退。膳食低钙可能参与了克山病发病中的TH代谢障碍过程。     

Lack of insulin-like growth factor I exaggerates the effect of calcium deficiency on bone accretion in mice

Recent studies provide evidence that the GH/IGF-I axis plays a critical role in the regulation of bone accretion that occurs during puberty and that the peak bone mineral density (BMD) is dependent on the amount of dietary calcium intake during the active growth phases. To evaluate whether IGF-I deficiency exaggerates the effect of calcium deficiency on bone accretion during active growth phases, IGF-I knockout (KO) and wild-type (WT) mice were fed with low calcium (0.01%) or normal calcium (0.6%) for 2 wk during the pubertal growth phase and were labeled with tetracycline. The low calcium diet caused significant decreases in endosteal bone formation parameters and a much greater increase in the resorbing surface of both the endosteum and periosteum of the tibia of IGF-I KO mice compared with WT mice. Accordingly, femur BMD measured by dual energy x-ray absorptiometry or peripheral quantitative computed tomography increased significantly in IGF-I WT mice fed the low calcium diet, but not in IGF-I KO mice. IGF-I-deficient mice fed the normal calcium diet showed elevated PTH levels, decreased serum 1,25-dihydroxyvitamin D and serum calcium levels at baseline. Serum calcium changes due to calcium deficiency were greater in IGF-I KO mice compared with WT mice. PTH levels were 7-fold higher in IGF-I KO mice fed normal calcium compared with WT mice, which was further elevated in mice fed the low calcium diet. Treatment of IGF-I-deficient lit/lit mice with GH decreased the serum PTH level by 70% (P < 0.01). Based on these and past findings, we conclude that: 1) IGF-I deficiency exaggerates the negative effects of calcium deficiency on bone accretion; and 2) IGF-I deficiency may lead to 1,25-dihydroxyvitamin D deficiency and elevated PTH levels even under normal calcium diet.     

慢性氟中毒对大鼠胰岛机能与形态的影响

为观察慢性氟中毒对大鼠胰岛的影响，选用ｗｉｓｔａｒ大白鼠饮用１００ｍｇ／Ｌ高氟水一年，复制慢笥氟中毒动物模型。结果显示；氟中毒大鼠血清胰素含量较对照组显著升高，胰高糖素水平略有下降；胰岛组织化学染色的形态学定理分析研究也证实，胰岛面积显著增加，胰岛素样反应阳笥产物面积也有一定程度的增加，同时，胰岛形状因子显著变小。     

硒和维生素E对冷刺激条件下心肌内皮素和心肌营养性血流量的影响

低硒（Ｓｅ）低维生素Ｅ（ＶＥ）饲料喂养大鼠和小鼠１０周，处死前均经两次冰浴刺激。小鼠静脉注射８６Ｒｂ，测定心肌放射性计数，以此代表心肌营养性血流量；取大鼠心肌经放免测定内皮素（ＥＴ）含量。结果显示：低Ｓｅ低ＶＥ饮食小鼠心肌营养性血流量明显降低，同样饮食大鼠心肌ＥＴ含量明显增加，通过补充Ｓｅ和ＶＥ，可使心肌营养性血流量和心肌ＥＴ水平有不同程度的改善，这些结果有助于深入探讨克山病心肌坏死的发生机制。     

钼对克山病病区粮养大鼠红细胞NADH－细胞色素b_5高铁血红蛋白还原酶活力的影响

Ｗｉｓｔａｒ大鼠３０只，雌雄各半分层均匀分为非病区粮组、病区粮组和病区粮补相组（１００ｍｇ／ｋｇ），分别喂以克山病非病区粮和克山病病区粮，实验期为４个月。病区粮养大鼠红细胞还原高铁血红蛋白的能力，ＮＡＤＨ—细胞色素ｂ_５高铁血红蛋白还原酶活力均低于非病区粮组。病区粮补钼可升高此酶活力，提高红细胞还原高铁血红蛋白的能力，在一次性失血的应激情况下，程度达到显著。病区粮补钼（１００ｍｇ／ｋｇ）对红细胞谷胱甘肽过氧化物酶活力无明显影响。     

骨软化性氟骨症发病机理研究

在偏食条件下给大白鼠饮水中加过量氟造成骨软化性氟骨症,引起一系列生化代谢改变。这些变化,在单纯低钙偏食时即已出现,投氟后则进一步加重。本文讨论了骨软化性氟骨症的发病机理,认为食饵低钙是骨软化性氟骨症发生、发展的基本条件;因血钙浓度下降而引发的趋钙激素的变化,使得骨软化愈演愈烈,改善居民钙营养状况,对防治地方性氟中毒具有重要意义。     

Effects of hypophysectomy and growth hormone treatment on renal hydroxylation of 25-hydroxycholecalciferol in rats

Growth hormone stimulates intestinal calcium absorption. This action has been linked to vitamin D metabolism. We have investigated the effects of hypophysectomy and GH treatment on renal metabolism of 25-hydroxycholecalciferol (25-OH-D3). Renal hydroxylation of 25-OH-D3 was measured in vitro using the renal slice technique. Experiments were performed in young F344 rats fed a vitamin D-replete, low calcium diet for 4 weeks. In hypophysectomized rats, renal conversion of 25-OH-D3 to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was markedly reduced compared with sham-operated rats. Renal conversion of 25-OH-D3 to 24,25-(OH)2D3 was markedly increased in hypophysectomized rats compared with sham-operated rats. Treatment of hypophysectomized rats with rat GH (rGH) for 10 days resulted in a significant increase in renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and a significant decrease in conversion to 24,25-(OH)2D3. Rat GH treatment caused no significant changes in serum levels of immunoreactive parathyroid hormone. Serum calcium concentrations were similar in all groups, and serum phosphorus was low in hypophysectomized rats. Treatment of hypophysectomized rats with ovine GH for 6 days caused changes which were much less pronounced than those induced by rGH. Renal conversion of 25-OH-D3 to 1,25-(OH)2D3 and 24,25-(OH)2D3 correlated well with growth rate (weight gain). These results suggest that GH, either directly or indirectly, modulates renal metabolism of 25-OH-D3.