Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-5-21
pubmed:abstractText
Leptin, the 16-kDa peptide hormone product of the ob gene, regulates body weight via the hypothalamus but also influences several aspects of reproductive function. Results of previous studies have suggested that pregnancy is a state of leptin resistance, because food consumption remains stable or increases despite a progressive rise in plasma leptin across most of gestation. In the present study, we assessed whether this apparent leptin resistance during rat pregnancy was due to either increased plasma leptin-binding activity and/or reduced expression of hypothalamic leptin receptor. Plasma leptin increased from 2.2 +/- 0.4 ng/ml before pregnancy to a maximum at midgestation (4.2 +/- 0.8 ng/ml on Day 12) and then fell by Day 22 and remained low throughout lactation. Despite the higher plasma leptin levels in pregnancy, food consumption increased from a minimum of 13.6 +/- 0.5 g/day before pregnancy to a peak of 21.9 +/- 0.6 g/day on Day 19, then fell before parturition (11.9 +/- 0.4 g/day on Day 22). At least part of the increase in plasma leptin during pregnancy was attributable to a marked increase (P < 0.001) in plasma leptin-binding activity between diestrus and late pregnancy, which then fell after birth but remained at midpregnancy levels to at least Day 12 of lactation. Hypothalamic expression of mRNA encoding the long form of the leptin receptor (Ob-Rb) was elevated in early pregnancy (Day 7) but returned to prepregnancy levels by midgestation and remained stable thereafter. The results of this study confirm that pregnancy in the rat is a state of relative leptin resistance, which is due primarily to increased plasma leptin-binding activity rather than to changes in hypothalamic Ob-Rb expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-3363
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1762-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12021059-Animals, pubmed-meshheading:12021059-Blood Proteins, pubmed-meshheading:12021059-Drug Resistance, pubmed-meshheading:12021059-Eating, pubmed-meshheading:12021059-Female, pubmed-meshheading:12021059-Gene Expression, pubmed-meshheading:12021059-Gestational Age, pubmed-meshheading:12021059-Hypothalamus, pubmed-meshheading:12021059-Lactation, pubmed-meshheading:12021059-Leptin, pubmed-meshheading:12021059-Pregnancy, pubmed-meshheading:12021059-Pregnancy, Animal, pubmed-meshheading:12021059-Protein Binding, pubmed-meshheading:12021059-RNA, Messenger, pubmed-meshheading:12021059-Rats, pubmed-meshheading:12021059-Rats, Wistar, pubmed-meshheading:12021059-Receptors, Cell Surface, pubmed-meshheading:12021059-Receptors, Leptin, pubmed-meshheading:12021059-Reference Values
pubmed:year
2002
pubmed:articleTitle
Plasma leptin-binding activity and hypothalamic leptin receptor expression during pregnancy and lactation in the rat.
pubmed:affiliation
School of Anatomy and Human Biology and The Western Australian Institute for Medical Research, University of Western Australia, Crawley, Perth, Western Australia 6009, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't