Maternal GDM increased adipose mRNA levels of peroxisome proliferator-activated receptor gamma (Pparg) and adiponectin (Adipoq) in 31-week-old CD-fed male offspring, and increased mRNA levels of insulin receptor (Insr) and lipoprotein lipase (Lpl) in 31-week-old male offspring on both diets.
Only the mRNA levels of peroxisome proliferator-activated receptor gamma correlated with the levels of neonatal blood glucose in GDM patients using linear regression and Spearman's correlation analyses (r = 0.774, P = 0.001).
The aim of this study was to investigate the correlation of vitamin D (VD) levels, VD receptor (VDR), and peroxisome proliferator-activated receptor γ (PPARγ) expression with GDM in overweight or obese women.
Selenium supplementation upregulated peroxisome proliferator-activated receptor gamma (P = 0.03) and glucose transporter 1 (GLUT-1) (P = 0.01) in lymphocytes of subjects with GDM compared with the placebo.
Supplementation with polyunsaturated fatty acids in pregnant rats with mild diabetes normalizes placental PPARγ and mTOR signaling in female offspring developing gestational diabetes.
Overall, fish oil supplementation for 6 weeks in women with GDM significantly improved gene expression of PPAR-γ, IL-1, and TNF-α, but not gene expression of IL-8.
To derive a better understanding of the association between peroxisome proliferator-activated receptor gamma (PPAR-γ) rs1801282 polymorphisms and gestational diabetes mellitus (GDM) in general and in racial and ethnic subgroups and to illustrate geographic distribution of the protective of G allele of rs1801282 in women with and without GDM.
In livers of female fetuses of GDM rats, no changes in PPARγ and miR-130 were evidenced, but PPARδ was increased, a change that occurred in parallel to a reduction in the expression of miR-9, a microRNA that targets PPARδ, and was unchanged in the liver of male fetuses of GDM and control rats.
The extracellular concentration of PPARγ may be involved in the lipid transport of maternal-fetal interface cells and may play a role in the abnormal lipid metabolism of GDM patients.
Quantitative results of RT-PCR demonstrated that compared with the placebo, magnesium supplementation upregulated gene expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) (P = 0.003) and glucose transporter 1 (GLUT-1) (P = 0.004) and downregulated gene expression of oxidized low-density lipoprotein receptor (LDLR) (P = 0.001) in PBMCs of women with GDM.
In conclusion, cinnamaldehyde has safe hypoglycemic action on gestational diabetes by potentiating insulin secretion and sensitivity through activating the antioxidant defense system, suppressing pro-inflammatory cytokines production, upregulating PPARγ gene expression and alleviating the reproductive performance.
Taken together, the current study demonstrated that zinc supplementation for 6 weeks among GDM women increased the mRNA levels of PPAR-γ and GLUT1 in their newborns compared with the placebo group.
Case-control studies pertaining to the effect of the Pro12Ala polymorphism in the PPARγ protein and risk of gestational diabetes mellitus were extracted from the HuGE, PubMed, Web of Science, CNKI, and SinoMed databases after an extensive literature search.
Among pregnant women, polymorphisms in PPARγ² and IGF2BP2 were shown to be highly correlated with GDM occurrence, whereas no correlation was found for KCNQ1 polymorphisms.
These polymorphisms were in or near the following genes: TCF7L2 (rs7903146), MTNR1B (rs10830963), IGF2BP2 (rs4402960), KCNJ11 (rs5219), CDKAL1 (rs7754840), KCNQ1 (rs2237892 and rs2237895) and GCK (rs4607517); while no association was found for PPARG with GDM risk.
These results from a haplotype analysis, show for the first time that genetic variations in the PPARγ gene could play a role in the susceptibility to develop gestational diabetes.
Stepwise regression analysis revealed that RBP4 mRNA expression in SAT was independently predicted by GLUT4 mRNA expression (β= 0.59, p = 0.003) and the presence of GDM (β=0.46, p = 0.01), whereas RBP4 mRNA expression in VAT was related to PPARγ mRNA expression (β= 0.64, p = 0.0003) and the patient's age (β= -0.38, p = 0.03).
GDM was associated with significantly lower placental PPARgamma mRNA and protein, PPARalpha protein and RXRalpha protein expression, while PPAR DNA binding activity remained unchanged.
We hypothesized that interaction between PPARG2Pro12Ala and variants in the promoter region of HNF4A are associated with type 2 diabetes-related quantitative traits in Mexican-American families of a proband with previous gestational diabetes.
The other polymorphisms studied were not significantly associated with gestational diabetes mellitus (ADIPOQ +276G > T: 1.17 [1.01-1.36], p = 0.039 [Pc = 0.23]; PPARGPro12Ala: 1.06 [0.87-1.29], p = 0.53; PPARGC1A Gly482Ser: 0.96 [0.83-1.10], p = 0.54; FOXC2 -512C > T: 1.01 [0.87-1.16], p = 0.94; and ADRB3 Trp64Arg: 1.22 [0.95-1.56], p = 0.12).
We screened approximately 40 kb of PPARG in 93 nondiabetic Hispanic women (63 responders and 30 nonresponders) with previous gestational diabetes who had participated in the Troglitazone In the Prevention Of Diabetes study.
There were no significant differences in the frequency of the insulin gene variable number of tandem repeat ( INS VNTR) alleles and genotypes or the peroxisome proliferator-activated receptor-gamma 2 ( PPAR gamma 2-Pro12Ala) polymorphism between the women with gestational diabetes and the control women either in Arabian or in Scandinavian women.