Renal gluconeogenesis. The effect of diet on the gluconeogenic capacity of rat-kidney-cortex slices.
Renal gluconeogenesis. The effect of diet on the gluconeogenic capacity of rat-kidney-cortex slices.
复制标题
肾糖异生。
作者：
H. Krebs;D. A. Bennett;P. de Gasquet;P. Gasquet;T. Gascoyne;T. Yoshida
已知糖异生不仅发生在肝脏中，而且也发生在肾皮质中。 Benoy & Elliott (1937) 首先在组织切片中观察到来自乳酸、丙酮酸、氨基酸和三羧酸循环中间体的肾糖异生作用，后来由 Weil-Malherbe (1938)、Russell & Wilhehni (1941)、Barron、Lyman、Lipton & Goldinger (1941)、Shipley (1944) 和 Teng (1954a) 证实。 b). Bergman & Drury (1938)、Reinecke (1943)、Reinecke & Roberts (1944)、Roberts & Samuels (1944)、Drury、Wick & MacKay (1950) 和 McCann & Jude (1958) 在去内脏动物身上获得了肾脏原位糖异生的证据。作为研究糖异生的实验材料，肾脏比肝脏具有主要优势。肾脏中预制碳水化合物的含量比肝脏中低得多。喂养良好的大鼠的肝脏可能含有超过 10%（重量/湿重）的糖原和超过 0-5%（重量/湿重）的葡萄糖。大鼠肾脏的相应值是0.0115％的糖原和0.05％的葡萄糖(Marsh&Miller，1953；和我们自己的测量)。因此，很难测量肝脏中孵育 1 或 2 小时后发生的净碳水化合物增加。即使碳水化合物的预先储存因饥饿而减少，也会与前体发生反应。相比之下，孵化时肾脏中碳水化合物的增量相对较大。肾脏中糖异生的最终产物是葡萄糖而不是糖原，因为肾脏中可储存的糖原数量非常少，如 Froesch、Ashmore 和 Renold (1958) 的观察所示。正常大鼠肾脏糖原含量从01xng./g上升。湿重至1*0-1*5毫克/克。湿重持续将葡萄糖输注到血流中后。相同条件下肝糖原值从22 mg./g上升。湿重至 106-137 毫克/克。因此，每单位重量，肝脏储存的糖原大约是肾脏的 100 倍。本文涉及各种前体糖异生速率的测量以及大鼠饮食和培养基成分对速率的影响。切片被用作标准材料，因为其他组织制剂未能给出高比率，其原因在研究过程中变得显而易见。
Gluconeogenesis is known to occur not only in the liver but also in kidney cortex. Renal gluconeogenesis from lactate, pyruvate, amino acids and intermediates of the tricarboxylic acid cycle was first observed in tissue slices by Benoy & Elliott (1937) and later confirmed by Weil-Malherbe (1938), Russell & Wilhehni (1941), Barron, Lyman, Lipton & Goldinger (1941), Shipley (1944), and Teng (1954a, b). Evidence of gluconeogenesis in the kidney in situ was obtained on eviscerated animals by Bergman & Drury (1938), Reinecke (1943), Reinecke & Roberts (1944), Roberts & Samuels (1944), Drury, Wick & MacKay (1950) and McCann & Jude (1958). As an experimental material for the study of gluconeogenesis, the kidney offers major advantages over the liver. The content of preformed carbohydrate is much lower in kidney than in the liver. Liver of well-fed rats may contain more than 10 % (wt./wet wt.) of glycogen and more than 0-5 % (wt./wet wt.) of glucose. The corresponding values for rat kidney are 0.0Il5% of glycogen and 0 05 % of glucose (Marsh & Miller, 1953; and our own measurements). Thus it is difficult to measure in the liver the net carbohydrate increases which *occur after incubation for 1 or 2 hr. with precursors even when the preformed store of carbohydrate has been reduced by starvation. By contrast the increment of carbohydrate in kidney on incubation is relatively large. The end product of gluconeogenesis in kidney is glucose rather than glycogen because the quantities of glycogen which can be stored in the kidney are very small, as shown by the observations of Froesch, Ashmore & Renold (1958). In kidney the glycogen content ofnormal rats rose from 01xng./ g. wet wt. to 1*0-1*5 mg./g. wet wt. after continued glucose infusion into the blood stream. Under the same conditions the liver glycogen value rose from 22 mg./g. wet wt. to 106-137 mg./g. Per unit of weight, liver thus stored about 100 times as much glycogen as kidney. The present paper is concerned with measurements of the rates of gluconeogenesis from various precursors and the effects of the diet of rats and the composition of the medium on the rates. Slices were used as the standard material because other tissue preparations failed to give high rates, for reasons which became obvious during the investigations.