Increased placental expression of fibroblast growth factor 21 in gestational diabetes mellitus

Dekker Nitert, Marloes, Barrett, Helen L., Kubala, Marta H., Scholz Romero, Katherin, Denny, Kerina J., Woodruff, Trent M., David McIntyre, H. David and Callaway, Leonie K. (2014) Increased placental expression of fibroblast growth factor 21 in gestational diabetes mellitus. Journal of Clinical Endocrinology and Metabolism, 99 4: E591.1-E591.8. doi:10.1210/jc.2013-2581

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Author Dekker Nitert, Marloes
Barrett, Helen L.
Kubala, Marta H.
Scholz Romero, Katherin
Denny, Kerina J.
Woodruff, Trent M.
David McIntyre, H. David
Callaway, Leonie K.
Title Increased placental expression of fibroblast growth factor 21 in gestational diabetes mellitus
Journal name Journal of Clinical Endocrinology and Metabolism   Check publisher's open access policy
ISSN 1945-7197
Publication date 2014
Sub-type Article (original research)
DOI 10.1210/jc.2013-2581
Open Access Status
Volume 99
Issue 4
Start page E591.1
End page E591.8
Total pages 8
Place of publication Chevy Chase, MD, United States
Publisher Endocrine Society
Collection year 2015
Formatted abstract
Background: Fibroblast growth factor 21 (FGF21) can regulate glucose and lipid metabolism. The placenta actively synthesizes and secretes many hormones, but it is unknown whether this includes FGF21. This study aimed to analyze the placental expression of FGF21 in women with or without gestational diabetes mellitus (GDM).

Methods: FGF21 and peroxisome proliferator-activated receptor (PPAR)- mRNA and protein expression were measured in the placentae of 20 women with and 18 without GDM.m RN Aexpression of PPAR-, FGF receptors 1-4, the coreceptor -klotho, and glucose transporter (GLUT)-1, -3, and -4 was investigated. Maternal and fetal circulating FGF21 levels were assessed in 10 mother-baby dyads per condition.

Results: FGF21 was expressed in the placenta and its mRNA expression increased in women with GDM [10.75 (interquartile range 3.28-125.6 AU)] vs control [0.83 (0.22- 4.78), P <001], as is its protein expression [GDM 2.89 (1.44 -5.10)] vs control [0.42 (0.05-1.98), P <05]. PPAR- mRNA but not protein expression was increased in GDM[2.94 (0.70 -7.26)] vs control [0.99 (0.43-2.17), P-.05] and was positively correlated to FGF21 mRNA expression (ρ 0.43, P <01). Placental mRNA expression of FGF receptors and GLUT1 was unchanged, and-klotho, GLUT3, and GLUT4 showed increased expression in GDM. Maternal circulating FGF21 levels were similar [GDM 323 (75-921) vs control 269 (49-731) pg/mL, P <81]. FGF21 was undetected in fetal cord blood.

Conclusions: FGF21 is expressed in the placenta and its expression is increased in GDM. The absence of FGF21 in fetal cord blood suggests that neither placental FGF21 nor maternal circulating FGF21 is secreted into the fetal circulation. Placental FGF21 may be a regulator of placental metabolism.
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