Hypoglycemic Effect of Insulin-like Growth Factor II (IGF-II) Is Mediated Mainly through Insulin and/or IGF-I Receptor but not IGF-II Receptor

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  • Hizuka Naomi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Asakawa-Yasumoto Kumiko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Takano Kazue
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Fukuda Izumi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Okubo Yumiko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Kazama Tomoko
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Demura Hiroshi
    Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
  • Shizume Kazuo
    Department of Medicine, Research Institute, The Foundation for Growth Science
  • Marumoto Yasumasa
    Department of Medicine, Molecular Biology Research Laboratory, Daiichi Pharmaceutical Co., Ltd.
  • Sakano Katsu-ichi
    Department of Medicine, Molecular Biology Research Laboratory, Daiichi Pharmaceutical Co., Ltd.

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Insulin-like growth factor-II (IGF-II) has an insulin-like effect in vitro and in vivo. Recently, mutants of IGF-II have been synthesized by the site-directed mutagenesis technique, and the structure determinants for the function of IGF-II have been studied. With the availability of the biosynthetic IGF-II and IGF-II mutants, we have investigated the hypoglycemic effect of IGF-II in normal rats and insulin resistant mice.<BR>When the IGF-II mutants with markedly decreased affinities for both insulin and IGF-I receptors were injected in normal rats, the blood glucose levels slightly decreased. However, when IGF-II mutant with slightly decreased affinities for both insulin and IGF-I receptors was injected, the blood glucose decreased to the same extent as with IGF-II.<BR>In insulin resistant mice, insulin did not decrease the blood glucose levels, but, the blood glucose levels decreased after IGF-I and IGF-II injection. The hypoglycemic effect of IGF-II was greater than that of IGF-I. The IGF-II mutant without affinity for IGF-II receptor but with affinities for both IGF-I and insulin receptors the same as IGF-II, caused hypoglycemia the same as IGF-I. However, the IGF-II mutant with markedly decreased affinities for both insulin and IGF-I receptors did not decrease blood glucose levels, and the IGF-II mutant with slightly decreased affinities for both insulin and IGF-II receptors slightly decreased blood glucose levels.<BR>These data indicate that the hypoglycemic effect of IGF-II is mediated mainly through insulin and/or IGF-I receptor but not IGF-II receptor. Furthermore, the data suggest that IGF-II might also be useful for the treatment of the insulin resistant status.

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