Elased K, De Souza J B, Playfair J H
Department of Immunology, UCLMS, London, UK.
Clin Exp Immunol. 1995 Mar;99(3):440-4. doi: 10.1111/j.1365-2249.1995.tb05570.x.
Infection of mice with blood-stage Plasmodium yoelii and P. chabaudi malaria induced hypoglycaemia in normal mice and normalized the hyperglycaemia of mice made moderately diabetic with streptozotocin (STZ). Injection of parasite supernatants induced hypoglycaemia accompanied by hyperinsulinaemia in normal mice, and in STZ-diabetic mice induced a profound drop in blood glucose and restored insulin secretion; however, severely diabetic mice (two injections of STZ) remained hyperglycaemic with no change in insulin levels. We conclude that malaria infection and parasite-derived molecules lower blood glucose concentration, but only in the presence of some residual pancreatic function. Diabetic mice were less anaemic, exerted a significant control of parasitaemia, and showed enhanced phagocytic activity compared with normal mice.
用血液期约氏疟原虫和查巴迪疟原虫感染小鼠,可导致正常小鼠出现低血糖,并使链脲佐菌素(STZ)诱导的中度糖尿病小鼠的高血糖恢复正常。注射寄生虫上清液可使正常小鼠出现低血糖并伴有高胰岛素血症,而在STZ糖尿病小鼠中可导致血糖大幅下降并恢复胰岛素分泌;然而,重度糖尿病小鼠(注射两次STZ)仍保持高血糖,胰岛素水平无变化。我们得出结论,疟疾感染和寄生虫衍生分子可降低血糖浓度,但这仅在存在一些残余胰腺功能的情况下发生。与正常小鼠相比,糖尿病小鼠贫血程度较轻,对寄生虫血症有显著控制作用,且吞噬活性增强。