Stueckemann J, Paretsky D
J Bacteriol. 1971 Jun;106(3):920-4. doi: 10.1128/jb.106.3.920-924.1971.
Liver glycogen is depleted in guinea pigs infected with Coxiella burneti. Syntheses of the glycogen precursors uridine triphosphate and uridine diphosphate glucose are unaffected during Q fever, but glycogen synthetase activity is inhibited. Exogenous cortisol relieves this inhibition in infected animals. Orotate and amino acids are more rapidly incorporated into ribonucleic acid and protein during infection. It is proposed that the biochemical defect in the synthesis of glycogen lies in the inactivation of glycogen synthetase.
感染伯氏考克斯体的豚鼠肝脏糖原会被耗尽。在Q热期间,糖原前体三磷酸尿苷和二磷酸尿苷葡萄糖的合成未受影响,但糖原合成酶活性受到抑制。外源性皮质醇可缓解感染动物的这种抑制作用。在感染期间,乳清酸和氨基酸更快地掺入核糖核酸和蛋白质中。有人提出,糖原合成中的生化缺陷在于糖原合成酶的失活。