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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #152898
Title: INSULIN / INSULIN-LIKE GROWTH FACTOR-I (IGF-I) HYBRID RECEPTOR ABUNDANCE DECREASES WITH DEVELOPMENT IN NEONATAL PIGS

Author
item SURYAWAN, AGUS - BAYLOR COLLEGE MED
item NGUYEN, HANH - BAYLOR COLLEGE MED
item ORELLANA, RENAN - BAYLOR COLLEGE MED
item BUSH, JILL - BAYLOR COLLEGE MED
item LIU, CHUN - BAYLOR COLLEGE MED
item Davis, Teresa

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/17/2003
Publication Date: 3/17/2003
Citation: Suryawan, A., Nguyen, H.V., Orellana, R.A., Bush, J.A., Liu, C.W., Davis, T.A. 2003. Insulin-insulin-like growth factor-I (IGF-I) hybrid receptor abundance decreases with development in neonatal pigs [abstract]. Federation of American Societies for Experimental Biology Conference. Part II, 17(5):A1158.

Interpretive Summary: Not needed for an Abstract

Technical Abstract: The activation of the insulin signaling pathway that leads to translation initiation is enhanced in skeletal muscle of neonates and decreases with development in parallel with the developmental decline in muscle protein synthesis. Because the elevated expression of insulin receptor (IR)/IGF-I-R hybrids has been associated with insulin resistance in some studies, we hypothesized that IR/IGF-I-R hybrid abundance and binding affinity increase with development. The abundances and binding affinities of the IR, IGF-I-R, and hybrid receptor were determined in muscle of 7- and 26-day-old pigs. The abundances of IR, IGF-I-R, and hybrid receptor were higher in muscle of 7- than 26-day-old pigs. However, the relative proportion of hybrid receptor abundance compared to IR abundance and to IGF-I-R abundance was similar in both ages. The binding affinities of the IR, IGF-I-R, and hybrid receptor also were similar in both ages. Overall, the results suggest that insulin/IGF-I hybrid receptor abundance and activation does not contribute to the developmental decline in the activation of the insulin signaling pathway.