Epigenetic regulation of fetal bone development and placental transfer of nutrients: progress for osteoporosis

Bocheva, Georgeta; Boyadjieva, Nadka

doi:10.2478/v10102-011-0026-6

Cited by 23 publications

(20 citation statements)

References 46 publications

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“…38 In addition, intrauterine nutrition shortage can lead to reduced level of circulating IGF-1 in the fetus and thus inhibit fetal linear growth and weight gain. 12,13 A novel finding of this study was that SGA newborns with cooccurrence of maternal smoking and inadequate GWG during pregnancy had much higher risk of stunting and lower mean height-for-age z score at age 5 years, while SGA newborns with only 1 of them did not have significantly higher risk of stunting or lower mean height-for-age z score, compared with SGA newborns without these 2 risk factors. It might be explained by the fact that SGA newborns with cooccurrence of these 2 SGA risk factors may undergo "double hits" of linear growth restriction in utero and also that 1 adverse exposure may increase the fetus's susceptibility to the other.…”

Section: Discussionmentioning

confidence: 66%

“…In addition, maternal smoking during pregnancy and inadequate GWG may both lead to IGF gene hypermethylation and thus reduced IGF levels. 13,41 Therefore, it is even more critical for smoking mothers to gain adequate weight during pregnancy if they cannot quit smoking.…”

Section: Discussionmentioning

confidence: 99%

“…10,11 SGA newborns with maternal short stature may have limited genetic potential of linear growth. 12 SGA newborns with maternal smoking, alcohol use, and infectious diseases during pregnancy may have toxicant-induced epigenetic changes 13 and growth hormone deficiency due to impaired hypothalamic-pituitary-adrenal axis functions. [14][15][16][17] SGA newborns with maternal smoking and alcohol use during pregnancy are more likely to have poor family dietary habits such as high fat and sugar but low calcium, vitamin D, and protein intake.…”

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confidence: 99%

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Stunting at 5 Years Among SGA Newborns

et al. 2016

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To compare risk of stunting at 5 years across etiological subgroups of small for gestational age (SGA) newborns. METHODS:We analyzed data of a subsample (N = 1100) of the Early Childhood Longitudinal Study-Birth Cohort. We defined SGA as birth weight <10th percentile, then classified subjects into etiological subgroups by each of 8 risk factors (ie, maternal prepregnancy underweight, short stature, smoking during pregnancy, alcohol use during pregnancy, inadequate gestational weight gain [GWG], hypertension, genital herpes infection, and multiple births) or by cooccurrence of 2 often intertwined risk factors (smoking and inadequate GWG). We defined stunting as 5 years height-for-age z score below -2. We fitted logistic regression models to test whether the risk of stunting differed across SGA subgroups, adjusting for confounders.RESULTS: SGA subgroup with maternal short stature (odds ratio [OR] = 3.88; 95% confidence interval [CI] = 2.16-6.96) or inadequate GWG (OR = 2.18; 95% CI = 1.23-3.84) had higher risk of stunting at 5 years, compared with the SGA subgroup without the corresponding risk factor. SGA newborns with both maternal smoking and inadequate GWG during pregnancy had much higher risk of stunting at 5 years (OR = 3.10; 95% CI = 1.21-7.91), compared with SGA newborns without any of these 2 SGA risk factors. CONCLUSIONS:Etiological subgroups of SGA differed in risk of stunting at 5 years. SGA newborns of inadequate GWG mothers who smoke and SGA newborns of short mothers were at particularly high risk of stunting.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Stunting at 5 Years Among SGA Newborns

et al. 2016

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“…The significantly higher levels of serum calcium in the offspring of global CTRKO mothers than in the offspring of control mothers for the same range of serum PTH values may reflect a change in the set point in the ionized calcium levels for PTH secretion in the absence of maternal CTR. It is well established that there is epigenetic regulation of the placental transfer of nutrients, with the key nutrients calcium and vitamin D being likely to influence fetal bone development (39). These intriguing findings provide evidence for a role of the CTR in the epigenetic regulation of serum calcium that warrants further investigation.…”

Section: Discussionmentioning

confidence: 93%

A Role for the Calcitonin Receptor to Limit Bone Loss During Lactation in Female Mice by Inhibiting Osteocytic Osteolysis

et al. 2015

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During lactation, the large transfer of calcium from the mother to the milk is primarily sourced from the maternal skeleton. To determine whether the calcitonin receptor (CTR) plays a physiological role to protect the skeleton from excessive resorption during lactation, we assessed the maternal skeleton of global CTR knockout (CTRKO) and littermate control mice at the end of lactation (postnatal day 21). Micro-computed tomography analyses showed no effect on trabecular or cortical bone in the distal femur and L1 vertebra of maternal global CTR deletion at the end of lactation in global CTRKO mice compared with that in control mice. Bone resorption, as assessed by osteoclast number and activity at the end of lactation, was unaffected by maternal CTR deletion. Cathepsin K, carbonic anhydrase 2, matrix metalloproteinase 13, and receptor activator of nuclear factor-κB ligand mRNA levels, however, were markedly elevated by 3- to 6.5-fold in whole bone of lactating global CTRKO females. Because these genes have been shown to be up-regulated in osteocytes during lactation when osteocytes resorb their surrounding bone matrix, together with their reported expression of the CTR, we determined the osteocyte lacunar area in cortical bone. After lactation, the top 20% of osteocyte lacunar area in global CTRKO mice was 10% larger than the top 20% in control mice. These data are consistent with an increased osteocytic osteolysis in global CTRKO mice during lactation, which is further supported by the increased serum calcium observed in global CTRKO mice after lactation. These results provide evidence for a physiological role for the CTR to protect the maternal skeleton during lactation by a direct action on osteocytes to inhibit osteolysis.

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“…Thus, a systematic review of randomized clinical trials suggests that calcium supplementation generates small but statistically significant weight loss in overweight and obese individuals (Onakpoya et al, 2011). However, calcium has not been associated but indirectly with epigenetic modifications (Bocheva and Boyadjieva, 2011) and many more studies are necessary to discard that calcium could be a protective factor for obesity by acting through epigenetic mechanisms.…”

Section: Different Minerals Have Been Associated With Changes In Epigmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

252

161

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Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

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Epigenetic regulation of fetal bone development and placental transfer of nutrients: progress for osteoporosis

Cited by 23 publications

References 46 publications

Stunting at 5 Years Among SGA Newborns

Stunting at 5 Years Among SGA Newborns

A Role for the Calcitonin Receptor to Limit Bone Loss During Lactation in Female Mice by Inhibiting Osteocytic Osteolysis

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

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