Document Detail


Molecular inflammation and adipose tissue matrix remodeling precede physiological adaptations to pregnancy.
MedLine Citation:
PMID:  22811467     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Changes in adipose tissue metabolism are central to adaptation of whole body energy homeostasis to pregnancy. To gain insight into the molecular mechanisms supporting tissue remodeling, we have characterized the longitudinal changes of the adipose transcriptome in human pregnancy. Healthy nonobese women recruited pregravid were followed in early (8-12 wk) and in late (36-38 wk) pregnancy. Adipose tissue biopsies were obtained in the fasting state from the gluteal depot. The adipose transcriptome was examined via whole genome DNA microarray. Expression of immune-related genes and extracellular matrix components was measured using real-time RT-PCR. Adipose mass, adipocyte size, and cell number increased in late pregnancy compared with pregravid measurements (P < 0.001) but remained unchanged in early pregnancy. The adipose transcriptome evolved during pregnancy with 10-15% of genes being differently expressed compared with pregravid. Functional gene cluster analysis revealed that the early molecular changes affected immune responses, angiogenesis, matrix remodeling, and lipid biosynthesis. Increased expression of macrophage markers (CD68, CD14, and the mannose-6 phosphate receptor) emphasized the recruitment of the immune network in both early and late pregnancy. The TLR4/NF-κB signaling pathway was enhanced specifically in relation to inflammatory adipokines and chemokines genes. We conclude that early recruitment of metabolic and immune molecular networks precedes the appearance of pregnancy-related physiological changes in adipose tissue. This biphasic pattern suggests that physiological inflammation is an early step preceding the development of insulin resistance, which peaks in late pregnancy.
Authors:
Veronica Resi; Subhabrata Basu; Maricela Haghiac; Larraine Presley; Judi Minium; Bram Kaufman; Steven Bernard; Patrick Catalano; Sylvie Hauguel-de Mouzon
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-07-17
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-01-07     Revised Date:  2013-10-10    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E832-40     Citation Subset:  IM    
Affiliation:
Center for Reproductive Health, MetroHealth Medical Center, 2500 MetroHealth Dr., Cleveland, OH 44109-1998, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological*
Adipokines / genetics,  immunology,  metabolism
Adipose Tissue / immunology,  physiology*
Antigens, CD / biosynthesis,  immunology
Antigens, CD14 / biosynthesis,  immunology
Antigens, Differentiation, Myelomonocytic / biosynthesis,  immunology
Chemokines / genetics,  immunology,  metabolism
Female
Humans
Inflammation / genetics,  immunology,  physiopathology*
Lipid Metabolism / genetics,  immunology,  physiology
NF-kappa B / immunology,  metabolism
Neovascularization, Physiologic / genetics,  immunology
Pregnancy
Pregnancy Trimester, First / genetics,  immunology,  physiology*
Pregnancy Trimester, Third / genetics,  immunology,  physiology*
Receptor, IGF Type 2 / biosynthesis,  immunology
Signal Transduction / genetics,  immunology,  physiology
Toll-Like Receptor 4 / immunology,  metabolism
Transcriptome / genetics,  immunology,  physiology
Grant Support
ID/Acronym/Agency:
R01-HD-022965/HD/NICHD NIH HHS; UL1 RR024989/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Adipokines; 0/Antigens, CD; 0/Antigens, CD14; 0/Antigens, Differentiation, Myelomonocytic; 0/CD68 antigen, human; 0/Chemokines; 0/NF-kappa B; 0/Receptor, IGF Type 2; 0/TLR4 protein, human; 0/Toll-Like Receptor 4
Comments/Corrections

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