Witek-Janusek L, Filkins J P
Circ Shock. 1983;11(1):23-34.
Various endotoxin preparations were used to determine which portion of endotoxin, lipid A, polysaccharide, or lipid-associated protein (LAP), mediates the hypoglycemic and insulinlike action in rats. Salmonella enteriditis Boivin (SEB), complete endotoxin, and S enteriditis Westphal (SEW), lacking LAP, were equally lethal to endotoxin-sensitized rats; however, S minnesota (SM) glycolipid (lipid A plus 16% polysaccharide) was comparatively more toxic. Toxic effects were prevented by alteration of lipid A through alkaline hydrolysis or polymixin B treatment. SM-lipid A (0.02% polysaccharide) was less toxic than SM-glycolipid. Similar hypoglycemic effects were produced by SEB and SEW; however, SM-glycolipid produced a significantly greater hypoglycemia. Although SEB, SEW, and SM-glycolipid all produced significant increases in adipose tissue glucose oxidation a decreasing trend in effectiveness was observed, while the SM-lipid A was without effect. However, adding detoxified hydrolysates of endotoxin to SM-lipid A produced a significant increase in glucose oxidation. In conclusion, lipid A is the primary endotoxin moiety mediating both the lethal effects of endotoxin and its hypoglycemic action. However, maximal expression of insulinlike action requires the presence of all three portions of endotoxin.
使用了各种内毒素制剂来确定内毒素的哪一部分，即脂多糖A、多糖或脂相关蛋白（LAP），介导大鼠的降血糖和胰岛素样作用。肠炎沙门氏菌Boivin（SEB），完整内毒素，以及缺乏LAP的肠炎沙门氏菌Westphal（SEW），对内毒素致敏的大鼠具有同等的致死性；然而，明尼苏达沙门氏菌（SM）糖脂（脂多糖A加16%多糖）毒性相对更大。通过碱水解或多粘菌素B处理改变脂多糖A可预防毒性作用。SM - 脂多糖A（0.02%多糖）的毒性低于SM - 糖脂。SEB和SEW产生了类似的降血糖作用；然而，SM - 糖脂产生的低血糖作用明显更强。尽管SEB、SEW和SM - 糖脂均使脂肪组织葡萄糖氧化显著增加，但观察到有效性呈下降趋势，而SM - 脂多糖A则无作用。然而，向内毒素解毒水解产物中添加SM - 脂多糖A可使葡萄糖氧化显著增加。总之，脂多糖A是介导内毒素致死作用及其降血糖作用的主要内毒素部分。然而，胰岛素样作用的最大表达需要内毒素的所有三个部分都存在。
