Fujimoto K, Sakaguchi T, Ui M
Horm Metab Res. 1981 Jul;13(7):368-70. doi: 10.1055/s-2007-1019272.
Metabolic rate constants for blood glucose turnover were estimated based on the decay of [U-14C, 6-3H]glucose injected intravenously in genetically diabetic KK mice. Comparison was made with the rate constants similarly obtained with non-diabetic and streptozotocin-induced diabetic ICR mice. Recycling of blood glucose via the Cori cycle, as estimated from the difference in the decay rate between 14C and 3H, was more active in KK mice than in non-diabetic and diabetic ICR mice. The Cori cycle activity was reduced by beta-adrenergic blockade in KK mice and was enhanced by alpha-blockade in ICR mice. It is concluded that predominance of beta-adrenergic functions in KK mice is responsible for activation of the Cori cycle as one of the mechanisms for metabolic resistance to endogenous insulin.
基于静脉注射[U-14C, 6-3H]葡萄糖后在遗传性糖尿病KK小鼠体内的衰减情况，估算了血糖周转的代谢率常数。并与非糖尿病以及链脲佐菌素诱导的糖尿病ICR小鼠以同样方式获得的速率常数进行了比较。根据14C和3H衰减率的差异估算，通过科里循环进行的血糖再循环在KK小鼠中比在非糖尿病和糖尿病ICR小鼠中更为活跃。β-肾上腺素能阻断降低了KK小鼠的科里循环活性，而α-阻断增强了ICR小鼠的科里循环活性。得出的结论是，KK小鼠中β-肾上腺素能功能占主导地位是激活科里循环的原因，这是对内源性胰岛素产生代谢抵抗的机制之一。
