Regulation of the insulin-like growth factors and their binding proteins by glucocorticoid and growth hormone in nonislet cell XXXX .

@entity1 @entity19518 @entity2301 @entity5 @entity442 @entity10513 @entity10116 @entity5100 @entity4053 @entity2777 @entity413 @entity617
@entity4053 in @entity1 with nonislet cell @entity5 is often secondary to overexpression of @entity5 @entity5100 . In these @entity1 the formation of serum complexes between IGFs, @entity2301 ( @entity2301 ), and the @entity2777 ( @entity2777 ) is impaired. An 87-yr-old @entity1 with nonislet cell @entity5 resulting from a localized fibrous @entity5 was treated for 97 days with graded doses of @entity617 (30, 10, and 5 mg/day) followed by GH (1, 4, 8, 4, and 2 U/day). Both @entity617 and GH alleviated the @entity4053 , concomitantly with increases in @entity442 , @entity2301 , and @entity2777 levels. Pretreatment serum @entity10513 and @entity19518 levels were greatly elevated, but as @entity413 normalized with treatment, only @entity10513 decreased, showing an inverse correlation with @entity413 (r = 0.716). @entity10116 gave a variable pattern not clearly related to blood @entity413 . Both treatments caused a redistribution of serum @entity2301 from binary- to ternary-complexed forms. However, only @entity617 improved the ability of @entity2301 to bind @entity2777 in vitro. @entity617 also suppressed @entity5100 , the effect being confined to pro- @entity5100 forms. Compared with normal @entity5100 , pro- @entity5100 inhibited @entity2777 binding to @entity2301 in vitro. Although @entity617 and GH reverse @entity4053 by different mechanisms, with only @entity617 suppressing @entity5 @entity5100 secretion, both increase the formation of ternary IGF- @entity2301 complexes. We conclude that the failure of serum @entity2301 and @entity5 @entity5100 to complex with @entity2777 is a primary cause of @entity4053 in nonislet cell @entity5 .
