Placental restriction increases adipose leptin gene expression and plasma leptin and alters their relationship to feeding activity in the young lamb

Simple item page
dc.contributor.authorDe Blasio, M.
dc.contributor.authorBlache, D.
dc.contributor.authorGatford, K.
dc.contributor.authorRobinson, J.
dc.contributor.authorOwens, J.
dc.date.issued2010
dc.description.abstractLow birth weight and catch-up growth predict increased adiposity in children and adults. This may be due in part to leptin resistance, as adults who were born small exhibit increased plasma leptin concentration relative to adiposity. Placental restriction (PR), a major cause of intrauterine growth restriction, reduces size at birth and increases feeding activity and adiposity by 6 wk in sheep. We hypothesized that PR would increase plasma leptin concentration and alter its relationship with feeding activity and adiposity in young lambs. Body size, plasma leptin, feeding activity, adiposity, leptin, and leptin receptor gene expression in adipose tissue were measured (12 control, 12 PR). PR reduced size at birth and increased adiposity. Plasma leptin concentration decreased with age, but to a lesser extent after PR and correlated positively with adiposity similarly in control and PR. PR increased plasma leptin concentration and perirenal adipose tissue leptin expression. Feeding activity correlated negatively with plasma leptin concentration in controls, but positively after PR. PR increases adipose tissue leptin expression and plasma leptin concentration, however, this increased abundance of peripheral leptin does not inhibit feeding activity (suckling event frequency), suggesting PR programs resistance to appetite and energy balance regulation by leptin, leading to early onset obesity.
dc.description.statementofresponsibilityMiles J. De Blasio, Dominique Blache, Kathryn L. Gatford, Jeffrey S. Robinson and Julie A. Owens
dc.identifier.citationPediatric Research, 2010; 67(6):603-608
dc.identifier.doi10.1203/PDR.0b013e3181dbc471
dc.identifier.issn0031-3998
dc.identifier.issn1530-0447
dc.identifier.orcidGatford, K. [0000-0002-2823-3004]
dc.identifier.orcidRobinson, J. [0000-0002-4515-6039]
dc.identifier.orcidOwens, J. [0000-0002-7498-1353]
dc.identifier.urihttp://hdl.handle.net/2440/59973
dc.language.isoen
dc.publisherInt Pediatric Research Foundation Inc
dc.rightsCopyright: © International Pediatrics Research Foundation, Inc. 2010. All Rights Reserved.
dc.source.urihttps://doi.org/10.1203/pdr.0b013e3181dbc471
dc.subjectAdipose Tissue
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectAnimals, Suckling
dc.subjectSheep
dc.subjectFetal Growth Retardation
dc.subjectPlacental Insufficiency
dc.subjectDisease Models, Animal
dc.subjectBirth Weight
dc.subjectHyperphagia
dc.subjectInsulin
dc.subjectLeptin
dc.subjectBlood Glucose
dc.subjectFatty Acids, Nonesterified
dc.subjectFeeding Behavior
dc.subjectAge Factors
dc.subjectUp-Regulation
dc.subjectLactation
dc.subjectPregnancy
dc.subjectFemale
dc.subjectMale
dc.subjectAdiposity
dc.subjectReceptors, Leptin
dc.titlePlacental restriction increases adipose leptin gene expression and plasma leptin and alters their relationship to feeding activity in the young lamb
dc.typeJournal article
pubs.publication-statusPublished

Files

Collections

Paediatrics publications