Perspective on skeletal health in inflammatory bowel disease

Bodegraven, Ad A. van; Bravenboer, Nathalie

doi:10.1007/s00198-019-05234-w

Cited by 19 publications

(16 citation statements)

References 83 publications

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“…Moreover, studies estimated that as many as 77% of patients with IBD have osteopenia and 12–41% have osteoporosis [ 41 , 45 ]. The risk of osteoporosis and osteopenia among patients with IBD is also related to insufficient intake and absorption of calcium and potassium, lower body mass index (BMI) and insufficient physical activity, low peak bone mass, and certain medications, especially glucocorticosteroids [ 46 , 47 ]. Adequate calcium intake is crucial due to IBD’s association with an increased incidence of osteoporosis, and additionally, during ongoing inflammation, pro-inflammatory cytokines affect the activity of bone cells [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Differences in Dietary Patterns of Adolescent Patients with IBD

et al. 2021

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Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC). The prevalence of both in pediatric populations has been constantly increasing. This study aimed to analyze the diet of adolescent patients with IBD in comparison to healthy controls and the current dietary standards for the Polish population to further their optimal supplementation regimen. The study group consisted of 53 patients (21 girls and 32 boys) with IBD (CD: n = 27; UC: n = 26) at a mean age of 15.4 ± 2.4 and 14.7 ± 2.2, years for girls and boys, respectively. The control group (CG) consisted of 20 patients, and 72 h of recall diaries on nutrition were collected. The nutritional data were analyzed in the Dieta 6D dietary program. When compared to Polish dietary standards, the largest differences girls with IBD and boys with IBD were found for the intake of energy (61.9 and 71.9%), iodine (61.9 and 62.6%), folates (76.2 and 87.5%), vitamin D (100 and 96.9%), potassium (61.9 and 59.4%), and calcium (85.7 and 93.8%). The overconsumption of saturated fatty acids (SFA) (61.9 and 56.3%) and sodium (76.2 and 90.6%) in girls and boys, respectively, was noted. In relation to girls with CG, girls with IBD showed a significantly higher intake of energy (1751. 3 vs. 1558.6 p = 0.0224), total protein (71.3 vs. 56.2 p = 0.0217), animal protein (47.8 vs. 34.5 p = 0.0183), total carbohydrates (237.3 vs. 196.1 p = 0.0442), and assimilable carbohydrates (219.8 vs. 180.5 p = 0.7921). Boys in the CG consumed significantly more calcium (851.8 vs. 432 p = 0.0006), phosphorus (1024.3 vs. 1357.5 p = 0.0431), lactose (11.6 vs. 6.1 p = 0.0016), and riboflavin (1.7 vs. 1.3 p = 0.0123) compared to boys with IBD. Dietician care should therefore be mandatorily provided alongside outpatient care. Based on our results, we suggest that supplementation with the selected components be considered.

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Section: Discussionmentioning

confidence: 99%

Differences in Dietary Patterns of Adolescent Patients with IBD

et al. 2021

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“…Furthermore, PTH/Pth1r, PI3K-Akt, NF-κB, and other signaling pathways were also mediated by m6A, which is important in the regulation of bone homeostasis. Roux, 2015;van Bodegraven and Bravenboer, 2019). Estrogen deficiency also increases inflammatory cytokines (Tsangari et al, 2004), followed by the activation of osteoclasts, increased bone resorption, and osteoporosis (Chen et al, 2017).…”

Section: Regulating M6a Methylation On Osteoclastsmentioning

confidence: 99%

m6A Methylation Regulates Osteoblastic Differentiation and Bone Remodeling

Huang¹,

Xu²,

Liu³

et al. 2021

Front. Cell Dev. Biol.

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Osteoporosis is a prevalent bone disease of the aging population, which is characterized by a decrease in bone mass because of the imbalance of bone metabolism. Although the prevention and treatment of osteoporosis have been explored by different researchers, the mechanisms underlying osteoporosis are not clear exactly. N6 methyladenosine (m6A) is a methylated adenosine nucleotide, which functions through its interaction with the proteins called “writers,” “readers” and “erasers.” The epigenetic regulation of m6A has been demonstrated to affect mRNA processing, nuclear export, translation, and splicing. At the cellular level, m6A modification has been known to affect cell proliferation, differentiation, and apoptosis of bone-related cells, such as bone marrow mesenchymal stem cells (BMSC), osteoblasts, and osteoclasts by regulating the expression of ALP, Runx2, Osterix, VEGF, and other related genes. Furthermore, PTH/Pth1r, PI3K‐Akt, Wnt/β‐Catenin, and other signaling pathways, which play important roles in the regulation of bone homeostasis, are also regulated by m6A. Thus, m6A modification may provide a new approach for osteoporosis treatment. The key roles of m6A modification in the regulation of bone health and osteoporosis are reviewed here in this article.

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“…The mechanism leading to low BMD and increased fracture risk caused by inflammatory bowel disease is closely related to OPG/RANKL/RANK pathway. In several studies, it has been shown that inflammatory bowel disease results in increased concentrations of proinflammatory cytokines, including tumor necrosis factor alpha (TNF- α ), interleukin (IL)-1 β , IL-6, and IL-17 [ 34 ]. It is well known that cytokines such as TNF- α , IL-1 β , and IL-6 increase the production of receptor activator of nuclear factor kappa B ligand (RANKL) by preosteoblasts, thereby promoting osteoclastogenesis.…”

Section: Discussionmentioning

confidence: 99%

QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis

Cui

Wen-hua

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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QiangGuYin (QGY) is a common Traditional Chinese medicine prescription for the treatment of osteoporosis. Previous clinical studies have found that QGY effectively improves bone mineral density (BMD) in postmenopausal women, but its underlying mechanism remains unclear. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK) pathway is a classic pathway involved in osteoporosis. Secretin levels are a serum marker of osteoporosis, but their effect on the OPG/RANKL/RANK pathway has not been reported. Hence, we investigated the relationship between the OPG/RANKL/RANK pathway and secretin and further revealed the mechanism underlying the effect of QGY in the treatment of osteoporosis. Mice were divided into secretin knockdown, secretin overexpression, and corresponding control groups. Micro-computed tomography was used to detect BMD in different groups, and the results show that QGY significantly improved BMD in mice of the secretin knockdown group. To further verify this, the serum levels of OPG, RANKL, RANK, and secretin were measured by enzyme-linked immunosorbent assays, and femur levels of OPG, RANKL, RANK, and secretin were evaluated by real-time quantitative PCR and western blotting. The results show that the expression of OPG was inhibited and that of RANKL and RANK was increased in mice from the secretin knockdown group, whereas the expression of OPG was upregulated and that of RANKL and RANK was downregulated after QGY intervention. Therefore, QGY inhibited bone resorption by promoting the expression of secretin and modulating the OPG/RANKL/RANK pathway. In addition to the effect of QGY, we also revealed the general regulatory effect of secretin on the OPG/RANKL/RANK pathway. We conclude that QGY modulates the OPG/RANKL/RANK pathway by increasing secretin levels during treatment of primary type I osteoporosis. This work provides a theoretical basis for the clinical use of QGY in the treatment of osteoporosis.

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Perspective on skeletal health in inflammatory bowel disease

Cited by 19 publications

References 83 publications

Differences in Dietary Patterns of Adolescent Patients with IBD

Differences in Dietary Patterns of Adolescent Patients with IBD

m6A Methylation Regulates Osteoblastic Differentiation and Bone Remodeling

QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis

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