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与雏鸡脂肪肝和肾综合征发生相关的代谢变化。

Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks.

作者信息

Whitehead C C, Bannister D W, Cleland M E

出版信息

Br J Nutr. 1978 Sep;40(2):221-34. doi: 10.1079/bjn19780117.

DOI:10.1079/bjn19780117
PMID:698161
Abstract
  1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks. 2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity. 3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (L-lactate: NAD oxidoreductase; EC 1.1.1.27) activitvities and values for C16:1 : C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity. 4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1 : C18:0 values were the most likely to develop FLKS when fasted. 5. There was no evidence that increased liver weight was associated with increase activities of certain other liver enzymes. 6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome in probably associated with the inhibition of other pathways of gluconeogenesis.
摘要
  1. 研究了在健康的4周龄肉鸡雏鸡中,低生物素饮食导致脂肪肝和肾综合征(FLKS)高发病率和低发病率时一些代谢指标的变化。2. 喂食导致FLKS高发病率饮食的鸡肝脏丙酮酸羧化酶(丙酮酸:二氧化碳连接酶(ADP);EC 6.4.1.1)活性较低,但在该饮食中添加脂肪或蛋白质以降低FLKS发病率时,酶活性增加。3. 喂食高FLKS饮食的鸡肝脏重量、血乳酸浓度、血浆乳酸脱氢酶(L-乳酸:NAD氧化还原酶;EC 1.1.1.27)活性以及肝脏、脂肪组织和血浆甘油三酯中C16:1:C18:0脂肪酸的值最高,所有测量值均与丙酮酸羧化酶活性呈负相关。4. 血浆乳酸脱氢酶活性或甘油三酯C16:1:C18:0值高的鸡在禁食时最有可能发生FLKS。5. 没有证据表明肝脏重量增加与某些其他肝脏酶活性增加有关。6. 得出的结论是,由于生物素饮食不足,FLKS发生在肝脏通过丙酮酸羧化酶进行糖异生能力很少或没有的鸡中,但该综合征的起始可能与糖异生其他途径的抑制有关。

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