| Multiparity leads to obesity and inflammation in mothers and obesity in male offspring. | |
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MedLine Citation:
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PMID: 22127227 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Multiparity is an independent risk factor for obesity in parous females. In addition to being a health issue for the mother, offspring of multiparous females may also be at risk for obesity later in life. The aim of the current study was to establish a mouse model that mimics the human pathology of multiparity and determine the effects of multiparity-induced obesity (MIO) on offspring in adulthood. C57BL/6 mice were mated and studied when primiparous (1st pregnancy) or multiparous (4th pregnancy). Dams became obese with multiparity, an effect that was independent of the age of the dam. Multiparous dams also had increased markers of inflammation (JNK activation, cytokine expression) in adipose tissue and liver that was greater than inflammation in nulliparous females made obese with a high-fat diet. Placental inflammation was prevalent in multiparous vs. primiparous dams as well. Male offspring of the multiparous dams developed increased adiposity by 24 wk of age relative to the progeny of primiparous dams, although food consumption was similar in both groups. Lipid metabolism was altered in liver and fat in that mRNA levels of regulatory genes (PGC-1α) as well as metabolic genes (CPT I) and Akt phosphorylation were decreased in offspring of multiparous dams. Thus, in mice, as in humans, multiparity increases adiposity and is associated with hepatic and placental inflammation and abnormal glucose tolerance. Importantly, MIO leads to increased body fat and metabolic dysfunction in the offspring, suggesting a role in the propagation of obesity. |
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Authors:
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Sandra L Rebholz; Thomas Jones; Katie T Burke; Anja Jaeschke; Patrick Tso; David A D'Alessio; Laura A Woollett |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-11-29 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 302 ISSN: 1522-1555 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-02-06 Completed Date: 2012-03-30 Revised Date: 2013-04-12 |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E449-57 Citation Subset: IM |
Affiliation:
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Department of Pathology and Laboratory Medicine, University of Cincinnati Medical School, Cincinnati, OH 45237-0507, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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metabolism Adiposity Animals Carnitine O-Palmitoyltransferase / metabolism Diet, High-Fat Eating Female Inflammation / metabolism* Lipid Metabolism Liver / metabolism Male Mice Mice, Inbred C57BL Models, Animal* Obesity / metabolism* Parity* Placenta / metabolism Pregnancy Proto-Oncogene Proteins c-akt / metabolism Trans-Activators / biosynthesis |
| Grant Support | |
ID/Acronym/Agency:
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DK-059630/DK/NIDDK NIH HHS; HD-34089/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Ppargc1a protein, mouse; 0/Trans-Activators; EC 2.3.1.21/Carnitine O-Palmitoyltransferase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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