Downregulation of peroxisome proliferator‐activated receptor gamma in the placenta correlates to hyperglycemia in offspring at young adulthood after exposure to gestational diabetes mellitus

Zhao, Qihong; Yang, Dong Rong; Gao, Lei; Zhao, Mingqiu; He, Xiu-Jie; Zhu, Meng; Tian, Chao-Qing; Liu, Gang; Li, Li; Hu, Chuanlai

doi:10.1111/jdi.12928

Cited by 12 publications

(7 citation statements)

References 32 publications

(33 reference statements)

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“…The downregulation of PPARγ in untreated GDM rats model expressed in this study is in line with the recent study by Hosni et al (2017) results, who found a decrease of PPARγ expression in the GDM rats model induced by streptozotocin intraperitoneal (Wu et al, 2017).Another study conducted by Zhao et al (2019) also found that there was downregulation of PPARγ expression on the placenta from GDM (Wu et al,2017). PPARγ is an isoform transcription factor in the peroxisome proliferator-activated receptor functions to regulate the expression of genes that regulate glucose and lipid metabolism, PPARγ activation will increase insulin sensitivity in the liver, skeletal muscle, and adipose tissue.…”

Section: Effect Of O Basilicum Extract On Histological Liver Tissues ...supporting

confidence: 92%

Basil Extract (Ocimum basilicum L) Exhibits Antidiabetic and Hepatoprotective Effects via SIRT1 and Peroxisome Proliferator-Activated Receptors (PPARγ) on Gestational Diabetes Mellitus Rats Model

et al. 2023

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Gestational Diabetes Mellitus (GDM) is a disorder of carbohydrate metabolism that causes hyperglycemia and insulin resistance during pregnancy. Sirtuin 1 (SIRT1) and Peroxisome Proliferator-Activated Receptorγ (PPARγ) are genes that play a role in glucose metabolism. Dysregulation of SIRT 1 and PPARγ is associated with the GDM. Hyperglycemia in GDM induces inflammation and oxidative stress in hepatocytes causing liver damage. Basil extract (Ocimum basilicum L) is one of indonesia medicinal plant has been used as traditional medicice in diabetic disorder. This study aims to investigate the hypoglycemic activity of basil extract by evaluating the expression of SIRT 1 and PPARγ in GDM rats and investigate the potential hepatoprotective effect of basil extract by analyzing the rat’s liver histology. Twenty-four of pregnant rats were divided into four groups; negative control, positive group induced by streptozotocin 40 mg/kg BW intraperitoneally, and two groups of GDM rats treated with 100 mg/kg BW and 200 mg/kg BW of basil extract for 14 days. Blood glucose levels were examined with a blood glucose meter. The expression of SIRT 1 and PPARγ was assessed by the RT-PCR. Histological analysis of the rat`s liver was conducted to determine the percentage of cell damage and tissue edem The data were statistically processed using SPSS. The extract of basil at a dose of 200 mg/kg BW showed an anti-diabetic effect which decreased the glucose level concentration by about two times compared to the untreated rat. It enhanced the expression of SIRT-significantly with a value of p= 0.035 (p <0.05). Basil extract-treated group showed a trend of increasing PPARγ expression, but not statistically significant. In addition, HE staining on the liver showed a tendency to improve in the group given basil extract. This Study concluded that basil extract could increase SIRT 1 and potential to be an anti-hyperglycemic therapy with a hepatoprotective effect.

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Section: Effect Of O Basilicum Extract On Histological Liver Tissues ...supporting

confidence: 92%

Basil Extract (Ocimum basilicum L) Exhibits Antidiabetic and Hepatoprotective Effects via SIRT1 and Peroxisome Proliferator-Activated Receptors (PPARγ) on Gestational Diabetes Mellitus Rats Model

et al. 2023

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“…Barker and his team confirmed that in case of failure of adaptation or inadequate placental development, fetal survival, or growth and development are severely endangered, and developmental programming of adult diseases may occur (Barker and Thornburg, 2013;Burton et al, 2016). Earlier studies had verified that the downregulation of peroxisome proliferator activated receptor gamma in placentas may predict hyperglycemia in offspring at young adulthood (Zhao et al, 2018). Analogously, offspring MetS induced by oxidative stress resulting from maternal 25 (OH)D deficiency may be caused through abnormal nutrition transformation across placenta.…”

Section: Discussionmentioning

confidence: 99%

Maternal 25-Hydroxyvitamin D Deficiency Promoted Metabolic Syndrome and Downregulated Nrf2/CBR1 Pathway in Offspring

et al. 2020

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Metabolic syndrome is a disorder of energy use and storage, which is characterized by central obesity, dyslipidemia, and raised blood pressure and blood sugar levels. Maternal 25-hydroxyvitamin D deficiency is known to cause metabolic changes, chronic disease, and increased adiposity in adulthood. However, the underlying mechanism of induced metabolic syndrome (MetS) in the offspring in vitamin D deficient pregnant mothers remains unclear. We identified that maternal 25-hydroxyvitamin D deficiency enhances oxidative stress, which leads to the development of MetS in the mother and her offspring. Further, immunohistochemical, Western blotting, and qRT-PCR analyses revealed that maternal 25-hydroxyvitamin D deficiency inhibited the activation of the Nrf2/carbonyl reductase 1 (CBR1) pathway in maternal placenta, liver, and pancreas, as well as the offspring's liver and pancreas. Further analyses uncovered that application of 25hydroxyvitamin D activated the Nrf2/CBR1 pathway, relieving the oxidative stress in BRL cells, suggesting that 25-hydroxyvitamin D regulates oxidative stress in offspring and induces the activation of the Nrf2/CBR1 pathway. Taken together, our study finds that maternal 25-hydroxyvitamin D deficiency is likely to result in offspring's MetS probably via abnormal nutrition transformation across placenta. Depression of the Nrf2/CBR1 pathway in both mothers and their offspring is one of the causes of oxidative stress leading to MetS. This study suggests that 25-hydroxyvitamin D treatment may relieve the offspring's MetS.

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“…Interestingly, the pair of genes PPARG (protein name PPAR-γ) and NOS2 (protein name iNOS) play a crucial role in modulating the M1/M2 polarization of microglia/macrophages. PPAR-γ is an isoform of peroxisome proliferator-activated receptor (PPAR) that belongs to the nuclear receptor family of transcription factors, whose expression is abundant in white adipose tissue, brown adipose tissue, and the large intestine and spleen [ 30 , 31 ]. Moreover, PPAR-γ is essential for adipogenesis, energy balance, lipid biosynthesis, and adipokine production, which also validates the results of bioinformatics analysis [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

Dong

Shen

et al. 2023

IJMS

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Emerging evidence shows that peripheral systemic inflammation, such as inflammatory bowel disease (IBD), has a close even interaction with central nervous disorders such as Alzheimer’s disease (AD). This study is designed to further clarify the relationship between AD and ulcerative colitis (UC, a subclass of IBD). The GEO database was used to download gene expression profiles for AD (GSE5281) and UC (GSE47908). Bioinformatics analysis included GSEA, KEGG pathway, Gene Ontology (GO), WikiPathways, PPI network, and hub gene identification. After screening the shared genes, qRT-PCR, Western blot, and immunofluorescence were used to verify the reliability of the dataset and further confirm the shared genes. GSEA, KEGG, GO, and WikiPathways suggested that PPARG and NOS2 were identified as shared genes and hub genes by cytoHubba in AD and UC and further validated via qRT-PCR and Western blot. Our work identified PPARG and NOS2 are shared genes of AD and UC. They drive macrophages and microglia heterogeneous polarization, which may be potential targets for treating neural dysfunction induced by systemic inflammation and vice versa.

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Downregulation of peroxisome proliferator‐activated receptor gamma in the placenta correlates to hyperglycemia in offspring at young adulthood after exposure to gestational diabetes mellitus

Abstract: The downregulation of peroxisome proliferator-activated receptor gamma in the placenta might predict hyperglycemia in offspring at young adulthood.

Cited by 12 publications

References 32 publications

Basil Extract (Ocimum basilicum L) Exhibits Antidiabetic and Hepatoprotective Effects via SIRT1 and Peroxisome Proliferator-Activated Receptors (PPARγ) on Gestational Diabetes Mellitus Rats Model

Basil Extract (Ocimum basilicum L) Exhibits Antidiabetic and Hepatoprotective Effects via SIRT1 and Peroxisome Proliferator-Activated Receptors (PPARγ) on Gestational Diabetes Mellitus Rats Model

Maternal 25-Hydroxyvitamin D Deficiency Promoted Metabolic Syndrome and Downregulated Nrf2/CBR1 Pathway in Offspring

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

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