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1.
J Clin Endocrinol Metab ; 99(6): 2113-9, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24628554

RESUMO

CONTEXT: Irisin is a recently discovered adipomyokine that regulates the differentiation and phenotype of adipose tissue. OBJECTIVE: In this study, we investigated the levels of irisin over the three trimesters of gestation in healthy and preeclamptic women and during the follicular and luteal phase of the menstrual cycle in a cohort of healthy eumenoherric women. METHODS: Serum irisin was measured by an ELISA in a longitudinal prospective cohort study in 40 healthy pregnant women, 10 mild preeclamptic women, and 20 healthy eumenoherric women during the menstrual cycle to assess irisin levels and correlations with other metabolic parameters. We identified the protein expression of fibronectin type III domain-containing protein 5, the irisin precursor, in human placenta using immunohistochemical approaches in humans. RESULTS: Serum irisin levels are higher in the luteal than in the follicular phase in eumenorrheic women. Fibronectin type III domain-containing protein 5, the irisin precursor, is expressed in human placenta, and its serum levels are higher during the entire pregnancy when compared with nonpregnant women. Serum irisin correlates positively with the homeostasis model assessment of estimated insulin resistance in the first trimester of normal pregnancy. Serum irisin levels do not change throughout gestation in preeclamptic women; however, there were lower irisin levels during the third trimester when compared with the normal pregnant group. CONCLUSION: Our results suggest that irisin may be involved in reproductive function and in the pregnancy-associated metabolic changes, and this condition may be an irisin-resistant state during gestation.


Assuntos
Fibronectinas/sangue , Pré-Eclâmpsia/sangue , Gravidez/sangue , Adiponectina/sangue , Adolescente , Adulto , Estudos de Casos e Controles , Feminino , Fibronectinas/análise , Humanos , Estudos Longitudinais , Ciclo Menstrual/sangue , Placenta/química , Placenta/metabolismo , Progesterona/sangue , Adulto Jovem
2.
Clin Endocrinol (Oxf) ; 81(1): 141-51, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24372023

RESUMO

OBJECTIVE: Pregnancy is characterized by several metabolic changes that promote fat gain and later onset of insulin resistance. As Brain-derived neurotrophic factor (BDNF) decreases hyperglycaemia and hyperphagia, we aimed to investigate the potential role of placental and circulating BDNF levels in these pregnancy-related metabolic changes in rats and humans. DESIGN AND METHODS: We identified the mRNA and protein expression of placental BDNF and its receptor TrkB using real-time PCR, Western blot and immunohistochemical approaches in both rat and humans. Serum BDNF was measured by ELISA. We also did a longitudinal prospective cohort study in 42 pregnant women to assess BDNF levels and correlations with other metabolic parameters. RESULTS: We found that BDNF and TrkB are expressed in both rat and human placenta. In rat, both placental mRNA and serum levels are increased throughout pregnancy, whereas their protein levels are significantly decreased at the end of gestation. Serum BDNF levels in pregnant women are significantly lower in the first trimester when compared to the second and third trimester (P < 0·0148, P < 0·0012, respectively). Serum BDNF levels were negatively correlated with gestational age at birth and fasting glucose levels. CONCLUSION: Our findings suggest that both BDNF and its receptor TrkB are expressed in rodent and human placenta being regulated during pregnancy. Taken together, these findings support a role of BDNF in the regulation of several metabolic functions during pregnancy.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/sangue , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Placenta/metabolismo , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Feminino , Humanos , Imunoquímica , Gravidez , RNA Mensageiro , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase em Tempo Real , Receptor trkB/sangue , Receptor trkB/genética , Receptor trkB/metabolismo
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