Human adipose tissue expansion in pregnancy is impaired in gestational diabetes mellitus

Aims/hypothesis During pregnancy, adipose tissue (AT) must expand to support the growing fetus and the future nutritional needs of the offspring. Limited expandability of AT is associated with insulin resistance, attributed to ectopic lipid deposition. This study aimed to investigate human AT expand...

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Veröffentlicht in:Diabetologia 2015-09, Vol.58 (9), p.2106-2114
Hauptverfasser: Rojas-Rodriguez, Raziel, Lifshitz, Lawrence M., Bellve, Karl D., Min, So Yun, Pires, Jacqueline, Leung, Katherine, Boeras, Crina, Sert, Aylin, Draper, Jacqueline T., Corvera, Silvia, Moore Simas, Tiffany A.
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Sprache:eng
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Zusammenfassung:Aims/hypothesis During pregnancy, adipose tissue (AT) must expand to support the growing fetus and the future nutritional needs of the offspring. Limited expandability of AT is associated with insulin resistance, attributed to ectopic lipid deposition. This study aimed to investigate human AT expandability during pregnancy and its role in the pathogenesis of gestational diabetes mellitus (GDM). Methods This cross-sectional study of omental (OM) and subcutaneous (SQ) AT collected at Caesarean delivery included 11 pregnant and three non-pregnant women with normal glucose tolerance (NGT), five with GDM, three with type 2 diabetes mellitus. Adipocyte size, capillary density, collagen content and capillary growth were measured. Affymetrix arrays and real-time PCR studies of gene expression were performed. Results Mean OM adipocyte size was greater in women with GDM than in those with NGT ( p  = 0.004). Mean OM and SQ capillary density was lower in GDM compared with NGT ( p  = 0.015). Capillary growth did not differ significantly between groups. The most differentially expressed AT transcript when comparing non-pregnant and pregnant women corresponded to the IGF binding protein (IGFBP)-5, the expression levels of which was found by subsequent quantitative real-time PCR to be lower in women with GDM vs women with NGT ( p  
ISSN:0012-186X
1432-0428
DOI:10.1007/s00125-015-3662-0