Fetal circulating human resistin increases in diabetes during pregnancy and impairs placental mitochondrial biogenesis

Diabetes during pregnancy affects placental mitochondrial content and function, which has the potential to impact fetal development and the long-term health of offspring. Resistin is a peptide hormone originally discovered in mice as an adipocyte-derived factor that induced insulin resistance. In hu...

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Veröffentlicht in:Molecular Medicine 2020-08, Vol.26 (1), p.76-76, Article 76
Hauptverfasser: Jiang, Shaoning, Teague, April M, Tryggestad, Jeanie B, Lyons, Timothy J, Chernausek, Steven D
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Sprache:eng
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Zusammenfassung:Diabetes during pregnancy affects placental mitochondrial content and function, which has the potential to impact fetal development and the long-term health of offspring. Resistin is a peptide hormone originally discovered in mice as an adipocyte-derived factor that induced insulin resistance. In humans, resistin is primarily secreted by monocytes or macrophages. The regulation and roles of human resistin in diabetes during pregnancy remain unclear. Fetal resistin levels were measured in cord blood from pregnancies with (n = 42) and without maternal diabetes (n = 81). Secretion of resistin from cord blood mononuclear cells (CBMCs) was measured. The actions of human resistin in mitochondrial biogenesis were determined in placental trophoblastic cells (BeWo cells) or human placental explant. Concentrations of human resistin in cord sera were higher in diabetic pregnancies (67 ng/ml) compared to healthy controls (50 ng/ml, P 
ISSN:1076-1551
1528-3658
DOI:10.1186/s10020-020-00205-y