Barron J T, Kopp S J, Tow J P, Parrillo J E
Department of Medicine, Rush Medical College, Rush-Presbyterian St. Luke's Medical Center, Chicago 60612.
Biochim Biophys Acta. 1991 Jul 10;1093(2-3):125-34. doi: 10.1016/0167-4889(91)90113-c.
The effects of fatty acids of different chain lengths on aerobic glycolysis, lactic acid production, glycogen metabolism and contractile function of vascular smooth muscle were investigated. Porcine carotid artery segments were treated with 50 microM iodoacetate and perchloric acid tissue extracts were then analyzed by 31P-NMR spectroscopy to observe the accumulation of phosphorylated glycolytic intermediates so that the activity of the Embden-Myerhof pathway could be tracked under various experimental paradigms. Aerobic glycolysis and lactate production in resting arteries were almost completely inhibited with 0.5 mM octanoate, partially inhibited with 0.5 mM acetate and unaffected by 0.5 mM palmitate. Inhibition of glycolysis by octanoate was not attributable to inhibition of glucose uptake or glucose phosphorylation. Basal glycogen synthesis was unchanged with palmitate and acetate, but was inhibited by 52% with octanoate incubation. The characteristic glycogenolysis which occurs upon isometric contraction with 80 mM KCl in the absence of fatty acid in the medium was not demonstrable in the presence of any of the fatty acids tested. Glycogen sparing was also demonstrable in norepinephrine contractions with octanoate and acetate, but not with palmitate. Additionally, norepinephrine-stimulated isometric contraction was associated with enhanced synthesis of glycogen amounting to 6-times the basal rate in medium containing octanoate. Contractile responses to norepinephrine were attenuated by 20% in media containing fatty acids. Thus, fatty acids significantly alter metabolism and contractility of vascular smooth muscle. Fatty acids of different chain lengths affect smooth muscle differentially; the pattern of substrate utilization during contraction depends on the contractile agonist and the fatty acid present in the medium.
研究了不同链长脂肪酸对血管平滑肌有氧糖酵解、乳酸生成、糖原代谢及收缩功能的影响。用50微摩尔碘乙酸处理猪颈动脉段，然后用31P核磁共振波谱分析高氯酸组织提取物，以观察磷酸化糖酵解中间产物的积累，从而在各种实验范式下追踪糖酵解途径的活性。在静息动脉中，0.5毫摩尔辛酸几乎完全抑制有氧糖酵解和乳酸生成，0.5毫摩尔乙酸部分抑制，而0.5毫摩尔棕榈酸则无影响。辛酸对糖酵解的抑制并非归因于对葡萄糖摄取或葡萄糖磷酸化的抑制。棕榈酸和乙酸对基础糖原合成无影响，但辛酸孵育可使其抑制52%。在培养基中不存在脂肪酸时，80毫摩尔氯化钾等长收缩时发生的典型糖原分解，在任何一种受试脂肪酸存在时均未表现出来。在去甲肾上腺素收缩时，辛酸和乙酸也可显示糖原节省，但棕榈酸则不然。此外，在含辛酸的培养基中，去甲肾上腺素刺激的等长收缩与糖原合成增强有关，合成量达基础速率的6倍。在含脂肪酸的培养基中，对去甲肾上腺素的收缩反应减弱20%。因此，脂肪酸显著改变血管平滑肌的代谢和收缩性。不同链长的脂肪酸对平滑肌的影响不同；收缩过程中底物利用模式取决于收缩激动剂和培养基中存在的脂肪酸。
