British Journal of Nutrition

Research Article

Ontogeny and nutritional manipulation of mitochondrial protein abundance in adipose tissue and the lungs of postnatal sheep

A. Mostyna1, V. Wilsona1, J. Dandreaa1, D. P. Yakubua1, H. Budgea1, M. C. Alves-Guerraa2, C. Pecqueura2, B. Mirouxa2, M. E. Symondsa1 c1 and T. Stephensona1

a1 Academic Division of Child Health, School of Human Development, Queen's Medical Centre, University Hospital, Nottingham NG7 2UH, UK

a2 CNRS-CEREMOD, 9 rue Jules Hetzel, 92190 Meudon, France

Abstract

The present study examined the ontogeny of mitochondrial protein abundance in adipose tissue and lungs over the first month of life in the sheep and the extent to which this may be altered by maternal undernutrition during the final month of gestation. The ontogeny of uncoupling protein (UCP), voltage-dependent anion channel (VDAC) and cytochrome c abundance were determined in adipose tissue and lungs sampled from near-term fetuses and young sheep aged 4 h, 1, 7 and 30 d. In adipose tissue, the abundance of UCP1, VDAC and cytochrome c all peaked at 1 d of age and then decreased by 30 d of age, at which stage the brown adipose tissue-specific UCP1 was no longer detectable but UCP2 was clearly abundant. For the lungs, however, UCP2 and VDAC abundance both peaked 7 d after birth and then decreased by 30 d of age. During postnatal development, therefore, a marked change in mitochondrial protein abundance occurs within both adipose tissue and lungs. Maternal nutrient restriction had no effect on lamb growth or tissue weights at 30 d of age but was associated with increased abundance of UCP2 and VDAC but not cytochrome c in both adipose tissue and lungs. These mitochondrial adaptations within both adipose tissue and the lungs of offspring born to previously nutrient-restricted mothers may compromise adipose tissue and lung function during periods of environmental stress.

(Received January 09 2003)

(Revised March 21 2003)

(Accepted April 12 2003)

Correspondence:

c1 *Corresponding author: Dr Michael E. Symonds, fax +44 115 970 9382, email Michael.Symonds@nottingham.ac.uk

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