Insulin-Like Growth Factor I Resistance in Peripheral Tissue but not in Liver in Streptozotocin-Induced Diabetic Rats

Endocrine Journal

AKIRA SEKIKAWA¹  KEIICHI YAMATANI¹  MAKOTO TOMINAGA¹  HIDEYUKI EGUCHI¹  MASAHIKO IGARASHI¹  MAKOTO DAIMON¹  HIDEO SASAKI¹ 

[1] Third Department of Internal Medicine, Yamagata University School of Medicine

关键词: IGF-I;    Streptozotocin;    Insulin resistance;    IGF-I resistance;    Glucose clamp;   

DOI  :  10.1507/endocrj.42.397

学科分类：内分泌与代谢学

来源: Japan Endocrine Society

【 摘 要 】

References(27)Cited-By(2)The metabolic effect of recombinant human insulin-like growth factor I (IGF-I) was investigated by the glucose clamp technique in normal rats and streptozotocin-induced diabetic rats, a model of insulin-dependent diabetes mellitus (IDDM), and compared with that of insulin. Glucose uptake by peripheral tissues was stimulated by intravenous administration of IGF-I at rates of from 0.369 to 3.690nmol/kg/min in a dose dependent manner, with a potency of 1/52 that of insulin estimated on the basis of the ED50 molar ratio in normal rats. In streptozotocin-induced diabetic rats, the maximum effects of IGF-I and insulin were reduced to 72% and 70% of those in normal rats, respectively, indicating the presence of both IGF-I and insulin resistance. Hepatic glucose output in normal rats was suppressed by IGF-I in a dose dependent manner with a weaker potency of 1/99 that of insulin assessed on the basis of the ED50 values. In streptozotocin-induced diabetic rats, a dose-response curve of the suppressive effect of insulin on hepatic glucose output shifted to the right, indicating the presence of hepatic insulin resistance, but a leftward shifting of the suppressive effect of IGF-I on hepatic glucose output was observed. We concluded that the IGF-I effect on peripheral tissue was decreased but that on the liver was rather increased in streptozotocin-induced diabetic rats, in contrast to the resistance of both peripheral tissues and liver to insulin.

【 授权许可】

Unknown