Influence of size at birth on the endocrine profiles and expression of uncoupling proteins in subcutaneous adipose tissue, lung, and muscle of neonatal pigs.
Epidemiological studies suggest that infants of low birth weight show poor neonatal growth and increased susceptibility to adult diseases such as diabetes and lung disease. Uncoupling protein 2 and 3 (UCP2 and UCP3) have been implicated in the development of such diseases; pigs provide an ideal model to examine the influence of birth weight due to the natural variance in piglet weight within a litter. This study examined whether birth weight influences the expression of UCP2 and UCP3 in adipose tissue, skeletal muscle, and lung. Piglets from 11 litters were ranked according to birth weight and three from each litter assigned to small (SFD), normal (NFD), or large for dates (LFD) groups. Blood samples and morphometric measurements were taken over the first 14 days of life, and tissue samples were taken on day 7 or 14. Plasma hormone and metabolite concentrations and the expression of UCP2 and UCP3 mRNA in adipose tissue, skeletal muscle, and lung were measured. UCP2 and UCP3 expression in adipose tissue was lower in the SFD compared with the LFD group on day 7. UCP3 expression in skeletal muscle was higher than that of adipose tissue. Lung UCP2 and skeletal muscle UCP3 mRNA expression were unaffected by size at birth. Regression analysis indicated that UCP3 expression was differentially associated with IGF-1, leptin, and insulin. In conclusion, low birth weight is associated with tissue-specific effects on UCP expression. It remains to be established whether these subsequently contribute to pathological conditions such as diabetes.
Mostyn
Alison
A
Centre for Reproduction and Early Life, Institute of Clinical Research, Academic Division of Child Health, School of Human Development, University Hospital, Nottingham, NG7 2UH United Kingdom. alison.mostyn@nottingham.ac.uk
Litten
Jennie C
JC
Perkins
Katharine S
KS
Euden
Philippa J
PJ
Corson
Anne M
AM
Symonds
Michael E
ME
Clarke
Lynne
L
D000273:Adipose Tissue / Q000378:metabolism*; D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001724:Birth Weight / Q000502:physiology*; D001831:Body Temperature / Q000502:physiology; D002352:Carrier Proteins / Q000096:biosynthesis / Q000378:metabolism*; D004553:Electric Conductivity; D004702:Endocrine Glands / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D006128:Growth / Q000502:physiology; D006728:Hormones / Q000097:blood; D007473:Ion Channels; D008168:Lung / Q000378:metabolism*; D026901:Membrane Transport Proteins / Q000096:biosynthesis / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000096:biosynthesis / Q000378:metabolism*; D009132:Muscles / Q000378:metabolism*; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis; D013552:Swine; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3
D002352:Carrier Proteins; D005227:Fatty Acids; D006728:Hormones; D007473:Ion Channels; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; C000604389:UCP2 protein, human; C000604392:UCP3 protein, human; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3