Milk protein intake, the metabolic-endocrine response, and growth in infancy: data from a randomized clinical trial1234567

https://doi.org/10.3945/ajcn.110.000596Get rights and content
Under an Elsevier user license
open archive

Background: Protein intake in early infancy has been suggested to be an important risk factor for later obesity, but information on potential mechanisms is very limited.

Objective: This study examined the influence of protein intake in infancy on serum amino acids, insulin, and the insulin-like growth factor I (IGF-I) axis and its possible relation to growth in the first 2 y of life.

Design: In a multicenter European study, 1138 healthy, formula-fed infants were randomly assigned to receive cow-milk–based infant and follow-on formulas with lower protein (LP; 1.77 and 2.2 g protein/100 kcal) or higher protein (HP; 2.9 and 4.4 g protein/100 kcal) contents for the first year. Biochemical variables were measured at age 6 mo in 339 infants receiving LP formula and 333 infants receiving HP formula and in 237 breastfed infants.

Results: Essential amino acids, especially branched-chain amino acids, IGF-I, and urinary C-peptide:creatinine ratio, were significantly (P < 0.001) higher in the HP group than in the LP group, whereas IGF–binding protein (IGF-BP) 2 was lower and IGF-BP3 did not differ significantly. The median IGF-I total serum concentration was 48.4 ng/mL (25th, 75th percentile: 27.2, 81.8 ng/mL) in the HP group and 34.7 ng/mL (17.7, 57.5 ng/mL) in the LP group; the urine C-peptide:creatinine ratios were 140.6 ng/mg (80.0, 203.8 ng/mg) and 107.3 ng/mg (65.2, 194.7 ng/mg), respectively. Most essential amino acids, IGF-I, C-peptide, and urea increased significantly in both the LP and HP groups compared with the breastfed group. Total IGF-I was significantly associated with growth until 6 mo but not thereafter.

Conclusions: HP intake stimulates the IGF-I axis and insulin release in infancy. IGF-I enhances growth during the first 6 mo of life. This trial was registered at clinicaltrials.gov as NCT00338689.

Cited by (0)

1

From the Children’s Memorial Health Institute, Warsaw, Poland (PS, DG, and RJ); Dr von Hauner Children’s Hospital, University of Munich Medical Centre, Munich, Germany (VG, HD, and BK); the Institute of Social Pediatrics and Adolescent Medicine, University of Munich, Munich, Germany (VG); Universitad Rovira i Virgili, IISPV, Tarragona, Spain (RC-M and JES); the Department of Pediatrics, University of Milano, Milan, Italy (SS and EV); the Department of Pediatrics, Université Libre de Bruxelles, Brussels, Belgium (ED); CHC St Vincent, Liège-Rocourt, Belgium (J-PL); and the Danone Research Centre for Specialized Nutrition, Schiphol, Netherlands (EP).

2

Presented at the conference “The Power of Programming: Developmental Origins of Health and Disease,” held in Munich, Germany, 6–8 May 2010.

3

PS and VG contributed equally to this manuscript.

4

Members of the European Childhood Obesity Trial Study Group are listed before the References.

5

This manuscript does not necessarily reflect the views of the Commission of the European Community–specific Research and Technological Development Programme and in no way anticipates the future policy in this area.

6

Supported in part by the Commission of the European Community–specific RTD Programme, “Quality of Life and Management of Living Resources,” within the 5th Framework Programme (research grants QLRT–2001–00389 and QLK1-CT-2002-30582) and the 6th Framework Programme (contract 007036). The formula for the study was produced by Bledina (Villefranche-sur-Saône Cédex, France, part of Danone Baby Nutrition), which operated as a partner of this European Union project and received a grant from the European Union Commission for this task.

7

Address correspondence to P Socha, Al. Dzieci Polskich 20, 04-730 Warszawa, Poland. E-mail: [email protected].