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Suppression of leptin-induced hypothalamic JAK/STAT signaling and feeding response during pregnancy in the mouse.
MedLine Citation:
PMID:  22580369     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Hyperphagia during pregnancy, despite rising concentrations of the satiety hormone leptin, suggests a state of leptin resistance develops. This study investigated the satiety response and hypothalamic responses to leptin during pregnancy in the mouse. Pregnant (day 13) and nonpregnant mice received an intraperitoneal (i.p.) injection of either leptin or vehicle then 24 hour food intake was measure. Further groups of pregnant and nonpregnant mice were perfused 2 hours after leptin or vehicle injections and brains were processed for pSTAT3 and pSTAT5 immunohistochemistry. Leptin treatment significantly decreased food intake in nonpregnant mice. During pregnancy however, leptin treatment did not suppress food intake indicating a state of leptin resistance. In the arcuate nucleus, leptin treatment increased the number of cells positive for pSTAT3, a marker of leptin activity, to a similar degree in both nonpregnant and pregnant mice. In the ventromedial nucleus (VMN) of pregnant mice, the leptin-induced increase in pSTAT3 positive cell number was significantly reduced compared to the leptin-induced increase in nonpregnant mice. In nonpregnant mice, leptin treatment had no effect on the number of pSTAT5 positive cells, suggesting that in this animal model leptin does not act through STAT5. During pregnancy, basal levels of pSTAT5 were higher than nonpregnant levels, and leptin treatment led to a decrease in the number of pSTAT5 positive cells in the hypothalamus. Overall these results demonstrate that during pregnant in the mouse a state of leptin resistance develops and this is associated with a reduced sensitivity of the VMN to leptin.
Authors:
Sharon R Ladyman; Diana M Fieldwick; Dave R Grattan
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-5-10
Journal Detail:
Title:  Reproduction (Cambridge, England)     Volume:  -     ISSN:  1741-7899     ISO Abbreviation:  -     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-5-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100966036     Medline TA:  Reproduction     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
S Ladyman, Department of Anatomy, and Centre for Neuroendocrinology, University of Otago, Dunedin, New Zealand.
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