2020
DOI: 10.1016/j.ecoenv.2020.111154
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Maternal exposure to Di-n-butyl phthalate (DBP) aggravate gestational diabetes mellitus via FoxM1 suppression by pSTAT1 signalling

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Cited by 22 publications
(18 citation statements)
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“…However, phthalate metabolites are less potent than BPA in inducing reduced viability and increased insulin release from the pancreatic β-cells in vitro (Weldingh et al 2017). In pregnant rats injected with streptozocin to induce GDM, di-n-butyl phthalate further exaggerated maternal hyperglycaemia and impaired glucose handling in vivo (Chen et al 2020). In addition, di-n-butyl phthalate impaired STAT1 signalling and led to inhibition of FoxM1 and reduced viability of β-cells in vitro (Chen et al 2020).…”
Section: Circadian Disruption During Pregnancymentioning
confidence: 99%
See 1 more Smart Citation
“…However, phthalate metabolites are less potent than BPA in inducing reduced viability and increased insulin release from the pancreatic β-cells in vitro (Weldingh et al 2017). In pregnant rats injected with streptozocin to induce GDM, di-n-butyl phthalate further exaggerated maternal hyperglycaemia and impaired glucose handling in vivo (Chen et al 2020). In addition, di-n-butyl phthalate impaired STAT1 signalling and led to inhibition of FoxM1 and reduced viability of β-cells in vitro (Chen et al 2020).…”
Section: Circadian Disruption During Pregnancymentioning
confidence: 99%
“…In pregnant rats injected with streptozocin to induce GDM, di‐ n ‐butyl phthalate further exaggerated maternal hyperglycaemia and impaired glucose handling in vivo (Chen et al . 2020). In addition, di‐ n ‐butyl phthalate impaired STAT1 signalling and led to inhibition of FoxM1 and reduced viability of β‐cells in vitro (Chen et al .…”
Section: Introductionmentioning
confidence: 99%
“…Moreover, maternal exposure to phthalates was observed to lead to gestational hypertension and gestational diabetes mellitus (Werner et al, 2015;James-Todd et al, 2016). Finally, in vivo (Chen et al, 2020) and in vitro experimental studies (Zong et al, 2015) have reached the same conclusions as the population studies. Chen et al found that exposure to din-butyl phthalate (DBP) during pregnancy promotes the insurgence of gestational diabetes mellitus by signi cantly increasing the expression of protein pSTAT1 and inhibiting that of FOXM1; the authors also found that the said exposure causes a decrease in islets β cell viability .…”
Section: Introductionmentioning
confidence: 64%
“…However, the exact pathogenic mechanisms remain a matter of debate; for instance, the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort study published in 2021 on 415 pregnant women, based on the assessment of 11 urinary metabolites (using mass spectrometry), revealed that the direct association with the glucose profile was not statistically significant, however it was with weight gain which is an indirect contributor to insulin resistance as a potential contributor to DM (47). Murine experiments revealed another mechanism involving insulin-secreting pancreatic β-cells: Di-n-butyl phthalate upregulated the expression of phosphorylated signal transducer and activator of transcription 1 (pSTAT1) which inhibited Forkhead box protein M1 (FoxM1), as a toxicity mediator of β-cell dysfunction (48). Additional effects of plastic bottles and plastic containers of foods and drinks are transferred to the fetus producing disturbances in embryonic development and growth restriction, due to the epigenetic role of phthalates ingested by pregnant women (49).…”
Section: Dm: Past and Futurementioning
confidence: 99%