Document Detail


Prolactin activation of the long form of its cognate receptor causes increased visceral fat and obesity in males as shown in transgenic mice expressing only this receptor subtype.
MedLine Citation:
PMID:  21989556     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To date the best defined function of prolactin (PRL) is its action on the ovary and mammary gland, although it has also been shown to have an effect on lipid metabolism. Using mice engineered to express only the long form of the prolactin receptor (PRL-RL), we demonstrate that PRL acting through PRL-RL alone causes severe adipose accumulation in visceral fat of males at 6 months of age. The increase in visceral fat accumulation is attributed to loss of adipose-derived leptin, which results in diminished lipolysis. The reduction in leptin also corresponds to decreased activation of AMP-activated protein kinase (AMPK), which further results in diminished fatty acid oxidation and increased fatty acid synthesis. Interestingly, the blunted AMPK response was only observed in adipose tissue and not in liver suggesting that this PRL mediated effect is tissue specific. A glucose tolerance study inferred that PRL-RL mice may suffer from insulin resistance or a reduction in insulin production that is not due to aberrant expression of glucose transporter 4 (Glut4). Collectively, our findings demonstrate that PRL signaling through the long form receptor causes reduced fatty acid oxidation, increased lipid storage, glucose intolerance, and obesity. These findings are of great importance towards understanding the etiology of obesity associated with hyperprolactinemia in humans as well as the role of PRL as a metabolic regulator in adipose tissue.
Authors:
J A Le; H M Wilson; A Shehu; Y S Devi; T Aguilar; G Gibori
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-10-11
Journal Detail:
Title:  Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme     Volume:  43     ISSN:  1439-4286     ISO Abbreviation:  Horm. Metab. Res.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-14     Completed Date:  2012-06-07     Revised Date:  2013-10-22    
Medline Journal Info:
Nlm Unique ID:  0177722     Medline TA:  Horm Metab Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  931-7     Citation Subset:  IM    
Copyright Information:
© Georg Thieme Verlag KG Stuttgart · New York.
Affiliation:
Department of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Female
Humans
Insulin / metabolism
Intra-Abdominal Fat / metabolism*
Male
Mice
Mice, Knockout
Mice, Transgenic
Obesity / genetics*,  metabolism
Prolactin / metabolism*
Receptors, Prolactin / genetics,  metabolism*
Signal Transduction
Species Specificity
Up-Regulation
Grant Support
ID/Acronym/Agency:
HD 12356/HD/NICHD NIH HHS; HD11119/HD/NICHD NIH HHS; R01 HD011119/HD/NICHD NIH HHS; R01 HD012356/HD/NICHD NIH HHS; T32 HL007692/HL/NHLBI NIH HHS; T32 HL007692/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Receptors, Prolactin; 9002-62-4/Prolactin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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