Placenta expression of vitamin D and related genes in pregnant women with gestational diabetes mellitus

Wang, Yanyan; Huo, Yan; Liu, Li; Liu, Suxin; Yin, Xiaoqian; Wang, Runfang; Gao, Xingshuang

doi:10.1016/j.jsbmb.2020.105754

Cited by 16 publications

(15 citation statements)

References 30 publications

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“…However, in adolescents, placental VDR expression was inversely associated with neonatal 25(OH)D ( P = 0.012) and maternal 25(OH)D ( P = 0.080) while positively with neonatal 1,25(OH)2D ( P = 0.006) ( 22 ). In gestational diabetes, low vitamin D was reported in serum while higher levels of placental VDR; in fact, low serum levels could even up-regulate the placenta VDR gene expression via negative feedback regulation, such that the increase in the bioavailability of vitamin D might compensates for the deficiency ( 23 ). Placenta is a key organ of transfer for 25-OH-D3 that even expresses the enzyme 1-α-hydroxylase, to synthesize 1,25-(OH)2-D3 and hence to regulate inflammatory processes.…”

Section: Discussionmentioning

confidence: 99%

Calcifediol During Pregnancy Improves Maternal and Fetal Availability of Vitamin D Compared to Vitamin D3 in Rats and Modifies Fetal Metabolism

et al. 2022

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The fetus depends on the transplacental transfer of vitamin D. Calcifediol (25-OH-D3) is the vitamin D metabolite that crosses the placenta. Previously, oral 25-OH-D3 improved serum 25-OH-D3 compared to vitamin D3 in non-pregnant subjects, although no studies are available in pregnant women. We evaluated the availability of oral 25-OH-D3 compared to vitamin D3 during pregnancy, as well as, their levels in the fetus and effect on metabolism-related proteins. Twenty female rats per group were fed with 25 μg/kg of diet of vitamin D3 (1,000 UI vitamin D/kg diet) or with 25 μg/kg diet of 25-OH-D3. We analyzed 25-OH-D3 levels in maternal and fetal plasma; protein levels of vitamin D receptor (VDR), fatty acid translocase (FAT), and scavenger-receptor class B type-1 (SR-B1) in both maternal liver and placenta; and protein levels of VDR and Glutamate decarboxylase (GAD67) in fetal brain. 25-OH-D3 doubled the concentration of 25-OH-D3 in both maternal and fetal plasma compared to vitamin D3. In addition, maternal liver VDR, FAT, and SR-BI increased significantly in the 25-OH-D3 group, but no changes were found in the placenta. Interestingly, 25-OH-D3 decreased GAD67 expression in the fetal brain and it also tended to decrease VDR (P = 0.086). In conclusion, 25-OH-D3 provided better vitamin D availability for both mother and fetus when administered during pregnancy compared to vitamin D3. No adverse effects on pregnancy outcomes were observed. The effects of 25-OH-D3 on the expression of VDR and GAD67 in fetal brain require further investigation.

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Section: Discussionmentioning

confidence: 99%

Calcifediol During Pregnancy Improves Maternal and Fetal Availability of Vitamin D Compared to Vitamin D3 in Rats and Modifies Fetal Metabolism

et al. 2022

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“…On the other hand, some vitamin D-related genes modified vitamin D levels underlying GDM pathogenesis. For instance, Wang et al [ 40 ] reported that vitamin D concentrations were low and varied according to the expression levels of genes related to vitamin D among subjects with GDM compared to those without GDM.…”

Section: Discussionmentioning

confidence: 99%

Plasma 25(OH)D Concentrations and Gestational Diabetes Mellitus among Pregnant Women in Taiwan

et al. 2021

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Vitamin D’s function in the development of gestational diabetes mellitus (GDM) is not consistent in the literature. We examined the association between maternal plasma 25(OH)D concentration and GDM risk. A national cross-sectional study (1497 pregnant women) was conducted between 2017 and 2019 across Taiwan. Blood samples were drawn at recruitment to assess 25(OH)D concentrations, including vitamin D deficiency (VDD) (<20 ng/mL), insufficiency (<32 ng/mL), and sufficiency (≥32 ng/mL). GDM was detected from 24 to 28 weeks of gestation with the results extracted from the antenatal visit records. The prevalence of GDM was 2.9%. Logistic model analysis showed that 25(OH)D concentrations were not significantly associated with the risk of GDM (adjusted odds ratio (AOR) = 0.97, p = 0.144). However, subjects with VDD had a significantly greater risk of GDM (AOR = 2.26, p = 0.041), but not in those with vitamin D insufficiency (AOR = 1.20, p = 0.655). Furthermore, cubic piecewise spline regression was used to explore the relationship between five-unit intervals of 25(OH)D and the predicted probability of GDM. As the proportion of GDM increased for low 25(OH)D concentrations, it decreased at moderate concentrations and increased again at higher concentrations. These findings revealed a nonlinear relationship between 25(OH)D and GDM risk. VDD would be risky for GDM occurrence.

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“…Calcitriol shows a dual effect: anti-inflammatory (lowers inflammatory cytokines) and stimulator of the innate response (induces antimicrobial peptides expression) [ 189 , 198 , 199 , 200 ]. This suggests that the lower VD levels described in GDM [ 201 ] may worsen the inflammatory state and further decrease the innate immune response prevailing in this pathology. Specifically, hypovitaminosis-D may take its toll on placental hCTD, HBDs, and S100A9, which production depends on calcitriol transcriptional activity [ 189 , 198 , 202 ].…”

Section: Vitamin D Implications In Immune Regulation and Insulin Resistance In Gdmmentioning

confidence: 99%

“…Specifically, hypovitaminosis-D may take its toll on placental hCTD, HBDs, and S100A9, which production depends on calcitriol transcriptional activity [ 189 , 198 , 202 ]. Moreover, maternal VD deficiency has been significantly associated with insulin resistance and a greater risk of GDM [ 203 , 204 , 205 ], which may be linked to the aberrant VD metabolism that takes place in the diabetic placenta [ 201 , 206 ]. Because of the latter, VD deficiency increases the susceptibility to maternal-fetal infections, most probably by the resultant limited immune response [ 207 , 208 ].…”

Section: Vitamin D Implications In Immune Regulation and Insulin Resistance In Gdmmentioning

confidence: 99%

“…Importantly, the VD Receptor (VDR) is expressed in different organs/tissues, including the placenta and pancreas, and it is known to be involved in the regulation of glucose metabolism through modulating insulin production and secretion [ 101 , 201 , 209 ]. Indeed, VD-response elements are present in the human insulin receptor gene, which is activated by VDR-calcitriol [ 210 , 211 ].…”

Section: Vitamin D Implications In Immune Regulation and Insulin Resistance In Gdmmentioning

confidence: 99%

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Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

Olmos-Ortíz

Flores-Espinosa

Díaz

et al. 2021

IJMS

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Gestational Diabetes Mellitus (GDM) is a transitory metabolic condition caused by dysregulation triggered by intolerance to carbohydrates, dysfunction of beta-pancreatic and endothelial cells, and insulin resistance during pregnancy. However, this disease includes not only changes related to metabolic distress but also placental immunoendocrine adaptations, resulting in harmful effects to the mother and fetus. In this review, we focus on the placenta as an immuno-endocrine organ that can recognize and respond to the hyperglycemic environment. It synthesizes diverse chemicals that play a role in inflammation, innate defense, endocrine response, oxidative stress, and angiogenesis, all associated with different perinatal outcomes.

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Placenta expression of vitamin D and related genes in pregnant women with gestational diabetes mellitus

Cited by 16 publications

References 30 publications

Calcifediol During Pregnancy Improves Maternal and Fetal Availability of Vitamin D Compared to Vitamin D3 in Rats and Modifies Fetal Metabolism

Calcifediol During Pregnancy Improves Maternal and Fetal Availability of Vitamin D Compared to Vitamin D3 in Rats and Modifies Fetal Metabolism

Plasma 25(OH)D Concentrations and Gestational Diabetes Mellitus among Pregnant Women in Taiwan

Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

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