Denko C W
J Rheumatol. 1976 Jun;3(2):205-11.
The effects of essential fatty acid (EFA) deficiency on connective tissue metabolism were studied in rats deficient in EFA and prostaglandins (PG). In chronic EFA deficiency, 3H-proline fixation, a measure of protein synthesis, was markedly reduced in the stomach, liver, adrenal, kidney, spleen, heart, and small intestine. Collagen rich tissues, such as lung, aorta, and cartilage also demonstrated reduced 3H-proline incorporation. 35S uptake, a measure of glycosaminoglycan synthesis, was inhibited in the lung, kidney, spleen, aorta, small intestine, and cartilage. Shorter periods of EFA deficiency resulted in similar diminished 35S incorporation. However, corn oil supplements largely corrected these metabolic defects. PGE1 injections stimulated 35S uptake in the mucus secreting tissues of the stomach and intestine. Comments are presented suggesting that the anti-PG actions of steroids and non-steroidal anti-inflammatory drugs contribute to ulcer formation during drug therapy.
在缺乏必需脂肪酸(EFA)和前列腺素(PG)的大鼠中,研究了必需脂肪酸缺乏对结缔组织代谢的影响。在慢性必需脂肪酸缺乏状态下,作为蛋白质合成指标的3H-脯氨酸固定在胃、肝脏、肾上腺、肾脏、脾脏、心脏和小肠中显著减少。富含胶原蛋白的组织,如肺、主动脉和软骨,也显示出3H-脯氨酸掺入减少。作为糖胺聚糖合成指标的35S摄取在肺、肾脏、脾脏、主动脉、小肠和软骨中受到抑制。较短时间的必需脂肪酸缺乏也导致类似的35S掺入减少。然而,补充玉米油在很大程度上纠正了这些代谢缺陷。注射前列腺素E1刺激了胃和肠道黏液分泌组织中的35S摄取。文中提出的观点表明,类固醇和非甾体抗炎药的抗前列腺素作用在药物治疗期间促成溃疡形成。