Increased mitochondrial DNA copy number in maternal peripheral blood is associated with low birth weight in Lombok, Indonesia

Priliani, Lidwina; Febinia, Clarissa A.; Kamal, Badru; Shankar, Anuraj H.; Malik, Safarina G.

doi:10.1016/j.placenta.2018.08.001

Cited by 13 publications

(9 citation statements)

References 21 publications

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“…In 2018, Priliani et al examined the association between maternal mitochondrial function, as expressed by the mtDNA copy number in venous blood, and birth weights in 528 randomly selected mothers [ 128 ]. A real-time quantitative PCR assay of archived blood samples and a regression analysis, adjusting for other major determinants of birth weight, showed that their mtDNA copy numbers were inversely correlated with birth weight ( p < 0.001), especially in the third trimester ( p < 0.001).…”

Section: Environmental Factors During Pregnancy and Mtdna Copy Number In Newbornsmentioning

confidence: 99%

Mitochondrial DNA Copy Number and Developmental Origins of Health and Disease (DOHaD)

Fukunaga

2021

IJMS

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Mitochondrial dysfunction is known to contribute to mitochondrial diseases, as well as to a variety of aging-based pathologies. Mitochondria have their own genomes (mitochondrial DNA (mtDNA)) and the abnormalities, such as point mutations, deletions, and copy number variations, are involved in mitochondrial dysfunction. In recent years, several epidemiological studies and animal experiments have supported the Developmental Origin of Health and Disease (DOHaD) theory, which states that the environment during fetal life influences the predisposition to disease and the risk of morbidity in adulthood. Mitochondria play a central role in energy production, as well as in various cellular functions, such as apoptosis, lipid metabolism, and calcium metabolism. In terms of the DOHaD theory, mtDNA copy number may be a mediator of health and disease. This paper summarizes the results of recent epidemiological studies on the relationship between environmental factors and mtDNA copy number during pregnancy from the perspective of DOHaD theory. The results of these studies suggest a hypothesis that mtDNA copy number may reflect environmental influences during fetal life and possibly serve as a surrogate marker of health risks in adulthood.

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Section: Environmental Factors During Pregnancy and Mtdna Copy Number In Newbornsmentioning

confidence: 99%

Mitochondrial DNA Copy Number and Developmental Origins of Health and Disease (DOHaD)

Fukunaga

2021

IJMS

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“…Previous studies have reported that oxidative stress increased with gestational age during normal pregnancy, especially in the third trimester, marked by the rise of plasma lipid hydroperoxides, urinary 8-hydroxydeoxyguanosine, and plasma 8-isoprostane (29–31), and that peripheral blood mtDNA-CN was higher when exposed to oxidative stress (32, 33). Oxidative stress in pregnant women can lead to reduced birth weight (34), and although we did not measure oxidative stress directly, which is another limitation of the study, our previous study in this population, along with other studies, reported that elevated levels of mtDNA-CN were associated with LBW (17–19).…”

Section: Discussionmentioning

confidence: 95%

“…MtDNA-CN has been reported to correlate inversely with pregnancy outcomes. Higher mtDNA-CN was found in IUGR pregnancy (17, 18), and we recently reported that higher maternal mtDNA-CN in peripheral blood was associated with reduced birth weight (19). MMN deficiencies observed in an ageing population showed a reduction of mitochondrial efficiency (20), leading to compensatory increases in mtDNA-CN.…”

Section: Introductionmentioning

confidence: 87%

“…DNA extraction was performed on packed cell samples using the Geneius Micro gDNA Extraction Kit (Geneaid). Determination of mtDNA-CN was done by real-time qPCR assay with SYBR Select MasterMix (Applied Biosystems), using primers for mitochondrial tRNA leu and nuclear β-2 microglobulin genes, based on the protocol from Venegas et al (24), using the 7500 Real-Time PCR System (Applied Biosystems), as previously described (19). Primers, PCR mixture, and qPCR conditions for the mtDNA transfer RNA leucine gene (GenBank: KM102154.1) and the single-copy nDNA β-2 microglobulin gene (GenBank: NM_004048.2) amplifications are described in Supplemental Table 1 .…”

Section: Methodsmentioning

confidence: 99%

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Maternal Multiple Micronutrient Supplementation Stabilizes Mitochondrial DNA Copy Number in Pregnant Women in Lombok, Indonesia

Priliani

Prado

Restuadi

et al. 2019

The Journal of Nutrition

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Background The Supplementation with Multiple Micronutrients Intervention Trial (SUMMIT) in Lombok, Indonesia showed that maternal multiple micronutrients (MMN), as compared with iron and folic acid (IFA), reduced fetal loss, early infant mortality, and low birth weight. Mitochondria play a key role during pregnancy by providing maternal metabolic energy for fetal development, but the effects of maternal supplementation during pregnancy on mitochondria are not fully understood. Objective The aim of this study was to assess the impact of MMN supplementation on maternal mitochondrial DNA copy number (mtDNA-CN). Methods We used archived venous blood specimens from pregnant women enrolled in the SUMMIT study. SUMMIT was a cluster-randomized double-blind controlled trial in which midwives were randomly assigned to distribute MMN or IFA to pregnant women. In this study, we selected 108 sets of paired baseline and postsupplementation samples (MMN = 54 and IFA = 54). Maternal mtDNA-CN was determined by real-time quantitative polymerase chain reaction in baseline and postsupplementation specimens. The association between supplementation type and change in mtDNA-CN was performed using rank-based estimation for linear models. Results In both groups, maternal mtDNA-CN at postsupplementation was significantly elevated compared with baseline (P < 0.001). The regression revealed that the MMN group had lower postsupplementation mtDNA-CN than the IFA group (β = −4.63, P = 0.003), especially for women with mtDNA-CN levels above the median at baseline (β = −7.49, P = 0.007). This effect was rapid, and observed within 33 d of initiation of supplementation (β = −7.39, P = 0.017). Conclusion Maternal MMN supplementation rapidly stabilized mtDNA-CN in pregnant women who participated in SUMMIT, indicating improved mitochondrial efficiency. The data provide a mechanistic basis for the beneficial effects of MMN on fetal growth and survival, and support the transition from routine IFA to MMN supplementation. This trial was registered at www.isrctn.com as ISRCTN34151616.

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“…Deficiencies of minerals such as zinc, selenium, copper and iodine have also been associated with complications in pregnancy, childbirth or fetal development [ 74 – 76 ]. We recently showed that increases in mitochondrial DNA copy number during pregnancy are associated with LBW, and that maternal MMN supplementation stabilized mitochondrial DNA copy number in peripheral blood mononuclear cells of SUMMIT women, indicating its effects on improved energy efficiency and reduced oxidative damage [ 77 , 78 ].…”

Section: Discussionmentioning

confidence: 99%

Maternal biomarker patterns for metabolism and inflammation in pregnancy are influenced by multiple micronutrient supplementation and associated with child biomarker patterns and nutritional status at 9-12 years of age

et al. 2020

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Maternal nutritional status influences fetal development and long-term risk for adult noncommunicable diseases. However, the underlying mechanisms remain poorly understood. We examined whether biomarkers for metabolism and inflammation during pregnancy were associated with maternal health and with child biomarkers and health at 9-12 years of age in 44 maternal-child dyads from the Supplementation with Multiple Micronutrients Intervention Trial (SUMMIT, ISRCTN34151616) in Lombok, Indonesia. Archived blood for each dyad from maternal enrollment, later in pregnancy, postpartum, and from children at 9-12 years comprised 132 specimens. Multiplex microbead immunoassays were used to quantify vitamin D-binding protein (D), adiponectin (A), retinol-binding protein 4 (R), C-reactive protein (C), and leptin (L). Principal component analysis (PCA) revealed distinct variance patterns, i.e. principal components (PC), for baseline pregnancy, bp.pc1.D#A#R# and bp.pc2. C#L"; combined follow-up during pregnancy and postpartum, dp-pp.pc1.D"#A"R"#L# and dp-pp.pc2.A"C"L"; and children, ch.pc1.D"R"C" and ch.pc2.D#A"L". Maternal multiple micronutrient (MMN) supplementation led to an association of baseline maternal bp.pc2. C#L" with decreased post-supplementation maternal dp-pp.pc2.A"C"L" (p = 0.022), which was in turn associated with both increased child ch.pc1.D"R"C" (p = 0.036) and decreased child BMI z-score (BMIZ) (p = 0.022). Further analyses revealed an association between maternal dp-pp.pc1.D"#A"R"#L# and increased child BMIZ (p = 0.036). Child ch.pc1. D"R"C" was associated with decreased birth weight (p = 0.036) and increased child BMIZ (p = 0.002). Child ch.pc2.D#A"L" was associated with increased child BMIZ (p = 0.005), decreased maternal height (p = 0.030) and girls (p = 0.002). A pattern of elevated maternal adiponectin and leptin in pregnancy was associated with increased C-reactive protein,

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Increased mitochondrial DNA copy number in maternal peripheral blood is associated with low birth weight in Lombok, Indonesia

Cited by 13 publications

References 21 publications

Mitochondrial DNA Copy Number and Developmental Origins of Health and Disease (DOHaD)

Mitochondrial DNA Copy Number and Developmental Origins of Health and Disease (DOHaD)

Maternal Multiple Micronutrient Supplementation Stabilizes Mitochondrial DNA Copy Number in Pregnant Women in Lombok, Indonesia

Maternal biomarker patterns for metabolism and inflammation in pregnancy are influenced by multiple micronutrient supplementation and associated with child biomarker patterns and nutritional status at 9-12 years of age

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