OBJECTIVES: Reduced increase in serum placental growth factor (PLGF) levels frequently occurs in patients with pre-eclampsia (PE) and thus has been used as a predictive factor for developing PE. However, it has remained elusive how shortage of PLGF could affect pancreatic endocrine homoeostasis and function in pregnancy to lead to development of gestational diabetes mellitus (GDM). MATERIALS AND METHODS: We used l-NAME injection in mice, as a model of human PE, in which PLGF levels were significantly reduced. RESULTS: We not only confirmed reduced serum PLGF levels in patients with PE but also detected strong correlation of serum PLGF levels and presence of GDM. We found that growth of beta cell mass during pregnancy was significantly impaired by l-NAME injection, as a result of reduced beta cell proliferation. This may explain the higher risk of developing GDM in patients with PE. Moreover, provision of exogenous PLGF in l-NAME-treated pregnant mice significantly rescued beta cell proliferation, with subsequent increase in beta cell mass, suggesting that shortage in PLGF may be responsible for impaired beta cell growth and higher occurrence of GDM in patients with PE. CONCLUSIONS: Our study highlighted a pivotal role for PLGF in prevention and treatment of GDM in patients with PE.
OBJECTIVES: Reduced increase in serum placental growth factor (PLGF) levels frequently occurs in patients with pre-eclampsia (PE) and thus has been used as a predictive factor for developing PE. However, it has remained elusive how shortage of PLGF could affect pancreatic endocrine homoeostasis and function in pregnancy to lead to development of gestational diabetes mellitus (GDM). MATERIALS AND METHODS: We used l-NAME injection in mice, as a model of human PE, in which PLGF levels were significantly reduced. RESULTS: We not only confirmed reduced serum PLGF levels in patients with PE but also detected strong correlation of serum PLGF levels and presence of GDM. We found that growth of beta cell mass during pregnancy was significantly impaired by l-NAME injection, as a result of reduced beta cell proliferation. This may explain the higher risk of developing GDM in patients with PE. Moreover, provision of exogenous PLGF in l-NAME-treated pregnant mice significantly rescued beta cell proliferation, with subsequent increase in beta cell mass, suggesting that shortage in PLGF may be responsible for impaired beta cell growth and higher occurrence of GDM in patients with PE. CONCLUSIONS: Our study highlighted a pivotal role for PLGF in prevention and treatment of GDM in patients with PE.
Authors: Camila Oliveira de Souza; Maria Terezinha Serrão Peraçoli; Ingrid Cristina Weel; Camila Ferreira Bannwart; Mariana Romão; Erika Nakaira-Takahagi; Leonardo Teixeira Lopes de Medeiros; Márcia Guimarães da Silva; José Carlos Peraçoli Journal: Life Sci Date: 2012-07-07 Impact factor: 5.037
Authors: Fong Cheng Pan; Eric D Bankaitis; Daniel Boyer; Xiaobo Xu; Mark Van de Casteele; Mark A Magnuson; Harry Heimberg; Christopher V E Wright Journal: Development Date: 2013-01-16 Impact factor: 6.868