title: Effect of administration of recombinant human leptin during the neonatal period on the plasma concentration and gene expression of leptin in the piglet.
abstract: Leptin is produced predominantly by white adipocytes and in adults it regulates both appetite and energy expenditure but its role in the neonate remains to be fully established. The aim of this, the first study of leptin administration to Meishan piglets, was to examine the effects of chronic leptin administration to neonatal pigs on their endocrine profile, growth and development. Six Meishan sows gave birth normally at term and 6 pairs of siblings (n = 12), matched by birth weight and gender (male, n = 6; female, n = 6) were randomly allocated to leptin (L: n = 6) or placebo (P: n = 6) administration groups. Piglets remained with their mother throughout the study and from day 3 to 8 of neonatal life each pig received either 4 microg ml(-1) kg(-1) body weight recombinant human leptin or a saline placebo. Plasma concentrations of key hormones and metabolites were determined in conjunction with messenger RNA (mRNA) for leptin, which was assessed by PCR. Recombinant leptin treatment improved growth performance and promoted skeletal growth in favour of adipose tissue accretion. Circulating plasma leptin concentrations were higher on days 4 and 7 in L pigs. Leptin administration altered the endocrine profile of the neonatal pig, although these changes were not maintained. There were no relationships between plasma leptin and body weight or mRNA leptin abundance, irrespective of treatment. Chronic leptin administration appeared to have a beneficial influence on growth rate and body conformation, which may in part be attributed to alterations in metabolism and nutrient partitioning.
authors.affiliation: Department of Agricultural Sciences, Imperial College London, Wye, Ashford, Kent, UK. j.litten@ic.ac.uk
authors.forename: J C
authors.initials: JC
authors.lastname: Litten
authors.forename: A
authors.initials: A
authors.lastname: Mostyn
authors.forename: K S
authors.initials: KS
authors.lastname: Perkins
authors.forename: A M
authors.initials: AM
authors.lastname: Corson
authors.forename: M E
authors.initials: ME
authors.lastname: Symonds
authors.forename: L
authors.initials: L
authors.lastname: Clarke
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn / Q000097:blood* / Q000235:genetics; D001699:Biometry; D001835:Body Weight / Q000187:drug effects; D001846:Bone Development / Q000187:drug effects; D005260:Female; D015870:Gene Expression; D006128:Growth / Q000187:drug effects; D006801:Humans; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D020738:Leptin / Q000008:administration & dosage* / Q000097:blood / Q000235:genetics; D008297:Male; D010919:Placebos; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D011994:Recombinant Proteins / Q000008:administration & dosage; D013552:Swine / Q000097:blood* / Q000235:genetics / Q000254:growth & development*; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D007328:Insulin; D020738:Leptin; D010919:Placebos; D012333:RNA, Messenger; D011994:Recombinant Proteins; D014284:Triiodothyronine; D019344:Lactic Acid; D013974:Thyroxine