| Maternal obesity during pregnancy and lactation programs the development of offspring non-alcoholic fatty liver disease in mice. | |
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MedLine Citation:
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PMID: 20413174 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND & AIMS: Obesity induced, non-alcoholic fatty liver disease (NAFLD), is now the major cause in affluent countries, of the spectrum of steatosis-to-cirrhosis. Obesity and NAFLD rates in reproductive age women, and adolescents, are rising worldwide. Our hypothesis was that maternal obesity and lactation transmit to the offspring a pre-disposition to dysmetabolism, obesity and NAFLD. METHODS: Female mice were fed standard or obesogenic chow, before, throughout pregnancy, and during lactation. The critical developmental period was studied by cross-fostering offspring of lean and obese dams. Offspring were then weaned onto standard chow and studied at 3months. Read-outs included markers of metabolic dysfunction, biochemical and histological indicators of NAFLD, induction of liver fibrogenesis, and activation of pro-fibrotic pathways. Mechanisms involved in programming a dysmetabolic and NAFLD phenotype were investigated by assaying breast milk components. RESULTS: Offspring of obese dams had a dysmetabolic, insulin resistant and NAFLD phenotype compared to offspring of lean dams. Offspring of lean dams that were suckled by obese dams showed an exaggerated dysmetabolic and NAFLD phenotype, with increased body weight, as well as increased levels of insulin, leptin, aspartate transaminase, interleukin-6, tumour necrosis factor-alpha, liver triglycerides, steatosis, hepatic fibrogenesis, renal norepinephrine, and liver alpha1-D plus beta1-adrenoceptors, indicative of sympathetic nervous system activation. Obese dams also had raised breast milk leptin levels compared to lean dams. CONCLUSIONS: Maternal obesity programs development of a dysmetabolic and NAFLD phenotype, which is critically dependent on the early postnatal period and possibly involving alteration of hypothalamic appetite nuclei signalling by maternal breast milk and neonatal adipose tissue derived, leptin. |
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Authors:
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Jude A Oben; Angelina Mouralidarane; Anne-Maj Samuelsson; Phillippa J Matthews; Maelle L Morgan; Chad McKee; Junpei Soeda; Denise S Fernandez-Twinn; Malgorzata S Martin-Gronert; Susan E Ozanne; Barbara Sigala; Marco Novelli; Lucilla Poston; Paul D Taylor |
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Publication Detail:
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Type: Journal Article Date: 2010-04-01 |
Journal Detail:
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Title: Journal of hepatology Volume: 52 ISSN: 0168-8278 ISO Abbreviation: J. Hepatol. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-24 Completed Date: 2010-08-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8503886 Medline TA: J Hepatol Country: England |
Other Details:
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Languages: eng Pagination: 913-20 Citation Subset: IM |
Copyright Information:
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Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved. |
Affiliation:
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University College London, Centre for Hepatology, Royal Free Hospital, London, UK. j.oben@ucl.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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genetics Adipose Tissue / metabolism Animals Collagen / genetics Fatty Liver / etiology*, pathology, physiopathology Female Gene Expression / physiology Interleukin-6 / genetics Lactation* Leptin / metabolism Metabolic Syndrome X / etiology*, pathology, physiopathology Mice Mice, Inbred C57BL Milk / metabolism Obesity / complications*, metabolism, physiopathology Pregnancy Pregnancy Complications / metabolism, pathology, physiopathology* Prenatal Exposure Delayed Effects / metabolism, pathology, physiopathology* Receptors, Adrenergic, alpha-1 / genetics Signal Transduction / physiology Tumor Necrosis Factor-alpha / genetics |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Interleukin-6; 0/Leptin; 0/Receptors, Adrenergic, alpha-1; 0/Tumor Necrosis Factor-alpha; 0/adrenergic receptor alpha(1b); 0/adrenergic receptor alpha(1d); 0/alpha 2(I) collagen; 9007-34-5/Collagen |
| Comments/Corrections | |
Comment In:
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J Hepatol. 2010 Jun;52(6):788-90
[PMID:
20392513
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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