Document Detail


The source of leptin, but not leptin depletion in response to food restriction, changes during early pregnancy in mice.
MedLine Citation:
PMID:  22042484     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Maternal food restriction during pregnancy results in adverse consequences for offspring, including obesity and cardiovascular disease. Early pregnancy is a critical period for this programming effect. Leptin is a regulator of energy homeostasis that also affects placental and fetal development. As food restriction results in decreased serum leptin levels, at least in non-pregnant animals, leptin depletion may be one mechanism by which food restriction affects development. The objective of this study was to test whether moderate food restriction affects serum leptin concentrations during the first half of pregnancy. We found that restriction to 50% of ad libitum consumption levels resulted in a significant decrease in serum leptin concentrations in both pregnant and non-pregnant female mice. There was no significant difference in serum leptin concentrations between non-pregnant females and at pregnancy day 11.5 when fed ad libitum. However, there was a difference in the source of leptin during pregnancy, with greater production in visceral fat in pregnant mice, and greater production in subcutaneous fat in non-pregnant mice. Leptin concentrations were dependent on time of day and time of sampling relative to feeding, particularly in restricted mice. There was a significant difference in serum leptin concentrations between fed and restricted mice when they were fed and sampled in afternoon, but not when they were fed and sampled in morning. We conclude that food restriction results in a significant decrease in leptin concentration during the first half of pregnancy in mice, but that detection of this relationship is subject to experimental design considerations.
Authors:
Jessica M Schlitt; Laura C Schulz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-11-01
Journal Detail:
Title:  Endocrine     Volume:  41     ISSN:  1559-0100     ISO Abbreviation:  Endocrine     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-03-12     Completed Date:  2012-07-19     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  9434444     Medline TA:  Endocrine     Country:  United States    
Other Details:
Languages:  eng     Pagination:  227-35     Citation Subset:  IM    
Affiliation:
Department of Obstetrics, Gynecology and Women's Health, University of Missouri, N625 Health Sciences Center, 1 Hospital Drive, Columbia, MO 65212, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / analysis
Caloric Restriction* / adverse effects
Circadian Rhythm
Female
Gene Expression Regulation
Insulin / blood
Intra-Abdominal Fat / metabolism*
Leptin / biosynthesis*,  blood,  genetics
Mice
Mice, Inbred Strains
Organ Specificity
Pregnancy
Prenatal Nutritional Physiological Phenomena*
RNA, Messenger / metabolism
Random Allocation
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Subcutaneous Fat / metabolism
Grant Support
ID/Acronym/Agency:
HD055231/HD/NICHD NIH HHS; R00 HD055231-05/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Leptin; 0/RNA, Messenger
Comments/Corrections

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