Open AccessNormal Serum Indices of Bone Collagen Biosynthesis and Degradation in Small for Gestational Age Infants
Author(s) -
Ran Namgung,
Reginald C. Tsang,
Rosa I. Sierra,
Mona Ho
Publication year - 1996
Publication title -
journal of pediatric gastroenterology and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 131
eISSN - 1536-4801
pISSN - 0277-2116
DOI - 10.1097/00005176-199610000-00004
Subject(s) - n terminal telopeptide , small for gestational age , medicine , osteocalcin , endocrinology , type i collagen , bone remodeling , fetus , procollagen peptidase , pregnancy , biochemistry , chemistry , alkaline phosphatase , biology , enzyme , genetics
Serum carboxyterminal propeptide of type I procollagen (PICP) and cross-linked carboxyterminal telopeptide of type I collagen (ICTP), new markers of bone collagen type I biosynthesis and degradation, have not been studied in small for gestational age (SGA) infants. In an earlier study, we found a lower bone mineral content (BMC) and decreased serum osteocalcin in SGA than in appropriate for gestational age (AGA) infants, supporting the thesis that decreased fetal bone formation is a cause of lower BMC in SGA. In view of the role of insulin-like growth factor-I (IGF-I) in the regulation of collagen type I synthesis and degradation, and low serum IGF-I concentrations in SGA infants, we hypothesized that serum PICP would be lower and serum ICTP would be higher in SGA than in AGA infants, reflecting decreased bone collagen type I biosynthesis or enhancement of bone collagen type I degradation in SGA. We studied 19 term SGA and 38 term AGA infants that were matched specifically 1:2 by gestation and birth month. There were no differences between SGA and AGA infants in serum PICP nor ICTP concentrations. Serum ICTP was correlated with osteocalcin and with PICP in SGA infants but not in AGA infants. Thus, serum biochemical indices of bone collagen type I biosynthesis and degradation in term SGA infants are similar to those in term AGA infants. These findings are not consistent with the thesis of altered fetal bone collagen type I biosynthesis or degradation in SGA. We suggest that the reduced bone mineral content in SGA infants is predominantly related to a lower supply of minerals rather than defective regulation of bone collagen type I metabolism.