Brain regions with significantly lower glucose uptake in the PCOS compared to the Control group.

<p>All results were FDR-corrected for multiple comparisons (<i>p</i> ≤ 0.05).</p

Scatter plot of calculated insulin resistance based on homeostatic model assessment (HOMA2-IR) and average cerebral metabolic rate of glucose (CMR_glu; μmol/100 g/min) in AD-vulnerable brain regions.

<p>Scatter plot of calculated insulin resistance based on homeostatic model assessment (HOMA2-IR) and average cerebral metabolic rate of glucose (CMR_glu; μmol/100 g/min) in AD-vulnerable brain regions.</p

Additional file 1: Figure S1. of PPARGC1α gene DNA methylation variations in human placenta mediate the link between maternal hyperglycemia and leptin levels in newborns

Loci analysed in E-21. PRDM16 (A), BMP7 (B), CTBP2 (C) and PPARGC1α (D) genes CpGs epigenotyped are shown. The CpGs within BMP7-A. CTBP2-A and PPARGC1α-A locus were significantly well correlated with each other. For Gen3G, when the CpGs identified in E-21 was covered by 450k array probesets, the exact same CpGs were selected (*cg01046951; ≠cg04873098; ¥cg08550435). Since some CpGs were not covered by the 450k array, probesets covering variable CpGs in close vicinity to those identified in E-21 were selected. PRDM16: cg06814194 (1st intron) and cg23738647 (exon 6); BMP7: cg18759209 (proximal promoter); and PPARGC1α: cg11270806 and cg27514608 (both intron 5). (PDF 180 kb

Additional file 3: Table S2. of PPARGC1α gene DNA methylation variations in human placenta mediate the link between maternal hyperglycemia and leptin levels in newborns

Spearman’s correlation coefficients between placental DNA methylation and metabolic variables of newborns in E-21 and Gen3G cohorts. (PDF 268 kb

Additional file 2: Table S1. of PPARGC1α gene DNA methylation variations in human placenta mediate the link between maternal hyperglycemia and leptin levels in newborns

Assay design for pyrosequencing analysis of the DNA methylation of the PRDM16, BMP7, CTBP2 and PPARGC1α gene loci. (PDF 180 kb

Additional file 1: Figure S1. of PPARGC1α gene DNA methylation variations in human placenta mediate the link between maternal hyperglycemia and leptin levels in newborns

Loci analysed in E-21. PRDM16 (A), BMP7 (B), CTBP2 (C) and PPARGC1α (D) genes CpGs epigenotyped are shown. The CpGs within BMP7-A. CTBP2-A and PPARGC1α-A locus were significantly well correlated with each other. For Gen3G, when the CpGs identified in E-21 was covered by 450k array probesets, the exact same CpGs were selected (*cg01046951; ≠cg04873098; ¥cg08550435). Since some CpGs were not covered by the 450k array, probesets covering variable CpGs in close vicinity to those identified in E-21 were selected. PRDM16: cg06814194 (1st intron) and cg23738647 (exon 6); BMP7: cg18759209 (proximal promoter); and PPARGC1α: cg11270806 and cg27514608 (both intron 5). (PDF 180 kb

Data_Sheet_1_Promoting healthy eating in early pregnancy in individuals at risk of gestational diabetes mellitus: does it improve glucose homeostasis? A study protocol for a randomized control trial.docx

BackgroundHealthy eating during pregnancy has favorable effects on glycemic control and is associated with a lower risk of gestational diabetes mellitus (GDM). According to Diabetes Canada, there is a need for an effective and acceptable intervention that could improve glucose homeostasis and support pregnant individuals at risk for GDM.AimsThis unicentric randomized controlled trial (RCT) aims to evaluate the effects of a nutritional intervention initiated early in pregnancy, on glucose homeostasis in 150 pregnant individuals at risk for GDM, compared to usual care.MethodsPopulation: 150 pregnant individuals ≥18 years old, at ≤14 weeks of pregnancy, and presenting ≥1 risk factor for GDM according to Diabetes Canada guidelines. Intervention: The nutritional intervention initiated in the first trimester is based on the health behavior change theory during pregnancy and on Canada’s Food Guide recommendations. It includes (1) four individual counseling sessions with a registered dietitian using motivational interviewing (12, 18, 24, and 30 weeks), with post-interview phone call follow-ups, aiming to develop and achieve S.M.A.R.T. nutritional objectives (specific, measurable, attainable, relevant, and time-bound); (2) 10 informative video clips on healthy eating during pregnancy developed by our team and based on national guidelines, and (3) a virtual support community via a Facebook group. Control: Usual prenatal care. Protocol: This RCT includes three on-site visits (10–14, 24–26, and 34–36 weeks) during which a 2-h oral glucose tolerance test is done and blood samples are taken. At each trimester and 3 months postpartum, participants complete web-based questionnaires, including three validated 24-h dietary recalls to assess their diet quality using the Healthy Eating Food Index 2019. Primary outcome: Difference in the change in fasting blood glucose (from the first to the third trimester) between groups. This study has been approved by the Ethics Committee of the Centre de recherche du CHU de Québec-Université Laval.DiscussionThis RCT will determine whether a nutritional intervention initiated early in pregnancy can improve glucose homeostasis in individuals at risk for GDM and inform Canadian stakeholders on improving care trajectories and policies for pregnant individuals at risk for GDM.Clinical trial registrationhttps://clinicaltrials.gov/study/NCT05299502, NCT05299502</p