Christian J S, Rege R V
Department of Surgery, Lakeside Veteran's Administration Medical Center, Chicago, Illinois 60611, USA.
J Surg Res. 1996 Feb 15;61(1):275-81. doi: 10.1006/jsre.1996.0116.
Dogs fed a marginal protein, high carbohydrate diet containing borderline amounts of methionine consistently develop pigment gallstones, marked taurine deficiency, and abnormal secretion of unconjugated bile salts. Since taurine is essential for normal secretion of bile salts in the dog, a species that cannot use glycine for bile salt conjugation, we hypothesized that taurine deficiency plays an important role in the pathogenesis of canine pigment gallstones. The rates of formation of pigment gallstones at 6 weeks were compared in dogs fed normal dog chow, lithogenic diet alone, and lithogenic diet supplemented with either taurine or methionine (45-55 mg/kg/day). No dog fed normal dog chow, but 11 of 12 dogs fed lithogenic diet, formed pigment gallstones and sludge. Supplementation of the lithogenic diet with taurine did not protect against pigment gallstones; five of six dogs developed gallstones and sludge. However, supplementation with methionine was protective, only one of six dogs was found to have a few flecks of pigmented material in its gallbladder. Interestingly, neither taurine nor methionine protected against previously observed increases in the concentrations of biliary calcium and bile salt profile indicating that at least some of the abnormalities previously observed in this model are not related to methionine/taurine deficiency. These results disprove our initial hypothesis that taurine deficiency plays an important role in the pathogenesis of pigment gallstones, but did show that a lack of methionine is linked to the formation and growth of canine pigment gallstones. The mechanism(s) leading to the formation of gallstones in dogs that are methionine deficient are is not clear from these studies.
给狗喂食含边缘量蛋氨酸的低蛋白、高碳水化合物饮食，它们会持续形成色素性胆结石、出现明显的牛磺酸缺乏以及未结合胆汁盐的异常分泌。由于狗无法利用甘氨酸进行胆汁盐结合，牛磺酸对狗胆汁盐的正常分泌至关重要，因此我们推测牛磺酸缺乏在犬色素性胆结石的发病机制中起重要作用。比较了喂食正常狗粮、仅喂食致石性饮食以及喂食添加了牛磺酸或蛋氨酸（45 - 55毫克/千克/天）的致石性饮食的狗在6周时色素性胆结石的形成率。喂食正常狗粮的狗没有形成色素性胆结石，但喂食致石性饮食的12只狗中有11只形成了色素性胆结石和胆泥。在致石性饮食中添加牛磺酸并不能预防色素性胆结石；6只狗中有5只形成了胆结石和胆泥。然而，添加蛋氨酸具有保护作用，6只狗中只有1只在其胆囊中发现有少量色素沉着物质。有趣的是，牛磺酸和蛋氨酸都不能预防之前观察到的胆汁钙浓度升高和胆汁盐谱异常，这表明在此模型中之前观察到的至少一些异常与蛋氨酸/牛磺酸缺乏无关。这些结果反驳了我们最初的假设，即牛磺酸缺乏在色素性胆结石的发病机制中起重要作用，但确实表明蛋氨酸缺乏与犬色素性胆结石的形成和生长有关。这些研究尚不清楚蛋氨酸缺乏的狗形成胆结石的机制。
