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蛋白质合成受抑制期间的脂肪吸收:淋巴乳糜微粒研究

Fat absorption during inhibition of protein synthesis: studies of lymph chylomicrons.

作者信息

Glickman R M, Kirsch K, Isselbacher K J

出版信息

J Clin Invest. 1972 Feb;51(2):356-63. doi: 10.1172/JCI106821.

Abstract

The effect of protein synthesis inhibition on the absorption of oleic acid from micellar solution was studied in mesenteric lymph fistula rats. A micellar solution of oleic acid labeled with tracer doses of oleic acid-(14)C was administered by intraduodenal infusion to rats with indwelling mesenteric lymph cannulas. Protein synthesis was inhibited by intraperitoneal acetoxycycloheximide (ACH), 0.25 mg/kg, 1 hr before lipid infusion. Lymph chylomicrons labeled with oleic acid-(14)C were collected from control and protein inhibited animals at various times after lipid infusion and subjected to sucrose density gradient centrifugation to determine changes in size. In control animals there was a transient increase in chylomicron size during maximal triglyceride absorption; however, in protein-inhibited animals there was a marked and sustained increase in chylomicron size as late as 4 hr after lipid infusion. Triglyceride and phospholipid determinations on washed chylomicrons from both groups indicated a greater triglyceride/phospholipid ratio after protein synthesis inhibition supporting a greater chylomicron size. Electron microscopy of lymph from both groups further confirmed a markedly increased chylomicron size after protein synthesis inhibition. It is proposed that an increase in size conserves chylomicron surface components, i.e. apoprotein, during conditions of inhibition of protein synthesis. These studies clearly demonstrate that the intestinal inhibition of protein synthesis is associated with an increase in the size of intestinal lymph chylomicrons and support the concept that protein synthesis is important in the formation and transport of chylomicrons from the mucosal cell into the lymph.

摘要

在肠系膜淋巴瘘大鼠中研究了蛋白质合成抑制对油酸从胶束溶液中吸收的影响。用示踪剂量的油酸 -(14)C标记的油酸胶束溶液通过十二指肠内输注给予留置肠系膜淋巴插管的大鼠。在脂质输注前1小时,腹腔注射乙酰氧基环己酰亚胺(ACH)0.25mg/kg抑制蛋白质合成。在脂质输注后的不同时间,从对照动物和蛋白质合成受抑制的动物中收集用油酸 -(14)C标记的淋巴乳糜微粒,并进行蔗糖密度梯度离心以确定大小的变化。在对照动物中,在最大甘油三酯吸收期间乳糜微粒大小有短暂增加;然而,在蛋白质合成受抑制的动物中,直到脂质输注后4小时,乳糜微粒大小仍有明显且持续的增加。对两组洗涤后的乳糜微粒进行甘油三酯和磷脂测定表明,蛋白质合成抑制后甘油三酯/磷脂比值更高,这支持了乳糜微粒更大的大小。两组淋巴的电子显微镜检查进一步证实了蛋白质合成抑制后乳糜微粒大小明显增加。有人提出,在蛋白质合成受抑制的情况下,大小增加可保留乳糜微粒的表面成分,即载脂蛋白。这些研究清楚地表明,肠道蛋白质合成抑制与肠道淋巴乳糜微粒大小增加有关,并支持蛋白质合成在乳糜微粒从粘膜细胞形成并转运到淋巴中起重要作用这一概念。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69bc/302134/5b630b612be6/jcinvest00174-0176-a.jpg

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