IGF-II産生腫瘍中のIGF-IIの血中存在様式に関する検討

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Extrapancreatic tumor associated with hypoglycemia (non-islet-cell tumor hypoglycemia: NICTH) is one of major causes of fasting hypoglycemia. In some patients with NICTH, insulin-like growth factor II (IGF-II) produced by tumors is thought to be a hypoglycemic agent. However, the mechanisms of hypoglycemia is still unknown, because serum IGF-II levels are not always elevated in patients with NICTH. One of the possible mechanisms of hypoglycemia is an increase of free form of IGF-II in serum. In the present study, we investigated whether free form of IGF-II in serum is increased using gel filtration method. Furthermore, heterogeneity of IGF-II was studied by Western immunoblot. When normal serum was gel filtered at pH 7.4, 150 kDa and 40 kDa complexes of IGF-II with IGF binding proteins (IGFBPs) were found. In patients with NICTH, the 150 kDa and 40 kDa complexes were not found but a peak of IGF-II with IGFBPs eluted as 60～80 kDa was found. In this fraction, four IGFBPs (IGFBP-1, -2, -3, -4) were found by Western ligand blot. A small peak of IGF-II eluted in approximately 17 kDa was found in sera from six of ten patients with NICTH. In the peak fraction (17 kDa), IGFBPs were not found by Western ligand blot and big form of IGF-II (11-18 kDa) was observed by Western immunoblot. These data indicated that free form of big IGF-II was increased in sera from these patients. Furthermore, IGF-II eluted as 60-80 kDa complex in patients with NICTH was mainly big form of IGF-II. These data suggest that big IGF-II binds IGFBPs, and the big IGF-II with IGFBP-3 dose not bind acid labile subunit, resulting in decreased 150 kDa complex formation. An increase of free form of big IGF-II and decreased 150 kDa complex formation in sera from patients with NICTH, might be related to hypoglycemia.
東京女子医科大学の論文
1997-02-25

IGF-II産生腫瘍中のIGF-IIの血中存在様式に関する検討

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