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链脲佐菌素诱导糖尿病大鼠肠道中的谷氨酰胺和酮体代谢

Glutamine and ketone-body metabolism in the gut of streptozotocin-diabetic rats.

作者信息

Ardawi M S

机构信息

Department of Clinical Biochemistry, College of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.

出版信息

Biochem J. 1988 Jan 15;249(2):565-72. doi: 10.1042/bj2490565.

Abstract
  1. In short- and long-term diabetic rats there is a marked increase in size of both the small intestine and colon, which was accompanied by marked decreases (P less than 0.001) and increases (P less than 0.001) in the arterial concentrations of glutamine and ketone bodies respectively. 2. Portal-drained viscera blood flow increased by approx. 14-37% when expressed as ml/100 g body wt., but was approximately unchanged when expressed as ml/g of small intestine of diabetic rats. 3. Arteriovenous-difference measurements for ketone bodies across the gut were markedly increased in diabetic rats, and the gut extracted ketone bodies at approx. 7 and 60 nmol/min per g of small intestine in control and 42-day-diabetic rats respectively. 4. Glutamine was extracted by the gut of control rats at a rate of 49 nmol/min per g of small intestine, which was diminished by 45, 76 and 86% in 7-, 21- and 42-day-diabetic rats respectively. 5. Colonocytes isolated from 7- or 42-day-diabetic rats showed increased and decreased rates of ketone-body and glutamine metabolism respectively, whereas enterocytes of the same animals showed no apparent differences in the rates of acetoacetate utilization as compared with control animals. 6. Prolonged diabetes had no effects on the maximal activities of either glutaminase or ketone-body-utilizing enzymes of colonic tissue preparations. 7. It is concluded that, although the epithelial cells of the small intestine and the colon during streptozotocin-induced diabetes exhibit decreased rates of metabolism of glutamine, such decreases were partially compensated for by enhanced ketone-body utilization by the gut mucosa of diabetic rats.
摘要
  1. 在短期和长期糖尿病大鼠中,小肠和结肠的大小均显著增加,同时动脉血中谷氨酰胺浓度显著降低(P<0.001),酮体浓度显著升高(P<0.001)。2. 以毫升/100克体重表示时,门脉引流内脏血流量增加约14 - 37%,但以毫升/克糖尿病大鼠小肠表示时,血流量大致不变。3. 糖尿病大鼠肠道酮体的动静脉差值测量值显著增加,对照大鼠和42天糖尿病大鼠小肠每克提取酮体的速率分别约为7和60纳摩尔/分钟。4. 对照大鼠小肠每克提取谷氨酰胺的速率为49纳摩尔/分钟,在7天、21天和42天糖尿病大鼠中分别降低了45%、76%和86%。5. 从7天或42天糖尿病大鼠分离的结肠细胞分别显示酮体和谷氨酰胺代谢速率增加和降低,而同一动物的肠细胞与对照动物相比,乙酰乙酸利用速率无明显差异。6. 长期糖尿病对结肠组织制剂中谷氨酰胺酶或酮体利用酶的最大活性无影响。7. 得出的结论是,虽然链脲佐菌素诱导的糖尿病期间小肠和结肠的上皮细胞谷氨酰胺代谢速率降低,但糖尿病大鼠肠道黏膜对酮体利用的增强部分补偿了这种降低。

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本文引用的文献

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Glycolysis, glutaminolysis and cell proliferation.糖酵解、谷氨酰胺分解与细胞增殖。
Cell Biol Int Rep. 1982 Jul;6(7):635-50. doi: 10.1016/0309-1651(82)90125-4.

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