Is there a Relationship Between Vitamin D and Endometriosis? An Overview of the Literature

2019 ◽  
Vol 25 (22) ◽  
pp. 2421-2427 ◽  
Author(s):  
Pierluigi Giampaolino ◽  
Luigi D. Corte ◽  
Virginia Foreste ◽  
Giuseppe Bifulco

Background: Vitamin D is involved in the physiological functions of several tissues, however, its deficiency may contribute to the development of various disorders. Recent research has been focusing on the role of vitamin D in the pathogenesis of endometriosis based on the evidence of the presence of vitamin D receptor and the enzymes required for vitamin D synthesis in the ectopic endometrium. Endometriosis, defined as the presence of endometrial glands and stroma in ectopic locations, is considered an estrogen-dependent disease and Vitamin D seems to have a role in modulation of the inflammatory state and proliferation of endometriotic cells. Objective: This study aimed to review the available literature regarding the relationship between vitamin D and endometriosis as well as the effects of vitamin D supplementation. Methods: A search on PubMed database has been performed. Results: The relationship between endometriosis and Vitamin D has been analyzed through the evaluation of vitamin D serum level, the polymorphism of vitamin D receptor and the role of vitamin D-binding protein in patient with endometriosis. The possible role of Vitamin D in the endometriosis therapy has also been investigated, in particular, the effect of vitamin D on pain relief, on endometriotic lesion in vitro and in rat models and in addition to a future target immunotherapy. Conclusion: Although promising, the data analyzed are not sufficient to evidence a cause-effect relationship between VD status and endometriosis, therefore further studies are needed in order to better clarify the association between vitamin D and endometriosis, especially in the context of the possibility of new treatment options.

2021 ◽  
Vol 1 (2) ◽  
pp. 057-061
Author(s):  
Hasna Osman Fadalla Mohamed ◽  
Omer Fadol Edris ◽  
Gad Allah Modawe ◽  
Suhair Abdelrahman Ahmed

Background: Vitamin D deficiency is a worldwide health issue and its role as an immune modulator has recently been emphasized. Evidence increasingly indicates the important role of vitamin D in reducing the incidence of autoimmune diseases. However, at this time the search for its role in autoimmune diseases and thyroid is not critical. Objectives: The study aimed to assess the relationship between vitamin D deficiency in Sudanese patients with hypothyroidism. Methods: Analytical case control hospital based study, conducted in Fadil Hospital and Police Hospital, Khartoum city, Khartoum state. The study carried out from March 2018 to September 2018. A total of 100 subjects were enrolled in the study. Vitamin D deficiency was set at levels below 20 ng / ml. Thyroid hormones (TSH, T3 and T4) were assessed in all participants using auto analyzer TOSOH AIA 313,while vitamin D was estimated using ELIZA. The data were analyzed using SPSS version (21). Results: The study included 76(76%) females and 24(24%) males, no significance differences between thyroid profile among study population.75 (75%) deficiency of vitamin D and 25(25%) normal vitamin D. vitamin D deficiency was significantly lower in female than male with( p =0.001). Conclusion: The results indicated that patients with hypothyroidism suffer from vitamin D deficiency significantly associated with the degree and severity of hypothyroidism. This encourages the desirability of vitamin D supplementation and recommends the detection of vitamin D deficiency for all hypothyroidism patients.


2020 ◽  
Vol 318 (3) ◽  
pp. C536-C541 ◽  
Author(s):  
Stephen P. Ashcroft ◽  
Joseph J. Bass ◽  
Abid A. Kazi ◽  
Philip J. Atherton ◽  
Andrew Philp

Vitamin D deficiency has been linked to a reduction in skeletal muscle function and oxidative capacity; however, the mechanistic bases of these impairments are poorly understood. The biological actions of vitamin D are carried out via the binding of 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) to the vitamin D receptor (VDR). Recent evidence has linked 1α,25(OH)2D3 to the regulation of skeletal muscle mitochondrial function in vitro; however, little is known with regard to the role of the VDR in this process. To examine the regulatory role of the VDR in skeletal muscle mitochondrial function, we used lentivirus-mediated shRNA silencing of the VDR in C2C12 myoblasts (VDR-KD) and examined mitochondrial respiration and protein content compared with an shRNA scrambled control. VDR protein content was reduced by ~95% in myoblasts and myotubes ( P < 0.001). VDR-KD myoblasts displayed a 30%, 30%, and 36% reduction in basal, coupled, and maximal respiration, respectively ( P < 0.05). This phenotype was maintained in VDR-KD myotubes, displaying a 34%, 33%, and 48% reduction in basal, coupled, and maximal respiration ( P < 0.05). Furthermore, ATP production derived from oxidative phosphorylation (ATPOx) was reduced by 20%, suggesting intrinsic impairments within the mitochondria following VDR-KD. However, despite the observed functional decrements, mitochondrial protein content, as well as markers of mitochondrial fission were unchanged. In summary, we highlight a direct role for the VDR in regulating skeletal muscle mitochondrial respiration in vitro, providing a potential mechanism as to how vitamin D deficiency might impact upon skeletal muscle oxidative capacity.


Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 243 ◽  
Author(s):  
Clara Yongjoo Park

Older adults are recommended vitamin D to prevent fractures. Though this population is also at risk of osteoarthritis (OA), the effect of vitamin D on OA is unclear and may differ by disease state. The relationship between vitamin D and OA during OA initiation and progression were considered in this narrative review of in vivo and in vitro studies. Regarding OA initiation in humans, the small number of published observational studies suggest a lack of association between induction of OA and vitamin D status. Most randomized controlled trials were performed in White OA patients with relatively high vitamin D status (>50 nmol/L). These studies found no benefit of vitamin D supplementation on OA progression. However, subset analyses and one randomized controlled pilot trial indicated that vitamin D supplementation may alleviate joint pain in OA patients with low vitamin D status (<50 nmol/L). As the etiology of OA is recently being more fully uncovered, better animal and cell models are needed. According to currently available clinical results, evidence is lacking to set a vitamin D level to prevent OA, and increasing vitamin D status above 50 nmol/L does not seem to benefit OA patients.


2021 ◽  
Author(s):  
Jasna Letícia Pinto Paz ◽  
Maria do Perpétuo Socorro Corrêa Amador Silvestre ◽  
Letícia Siqueira Moura ◽  
Ismari Perini Furlaneto ◽  
Yan Corrêa Rodrigues ◽  
...  

The transmission and evolution of leprosy depends on several aspects, including immunological and genetic factors of the host, as well as genetic factors of Mycobacterium leprae. This study evaluated the association of single nucleotide polymorphisms (SNPs) on the FokI (rs2228570), TaqI (rs731236), ApaI (rs7975232) regions of the vitamin D receptor (VDR) gene with leprosy. A total of 405 individuals were evaluated, composed by groups of 100 multibacillary and 57 paucibacillary patients, and 248 healthy contacts. Blood samples were collected from patients and contacts. The genotyping was performed by sequencing of the interest regions. The alleles of the studied SNPs, and of SNP FokI genotypes, were not associated with leprosy. For the SNP on TaqI region, the relationship between the tt genotype, and for the SNP ApaI, the AA genotype, revealed an association with susceptibility to MB form, while Aa genotype with protection. The extended genotypes AaTT and AaTt of ApaI and TaqI were associated with protection to against MB form. Futher studies analyzing the expression of the VDR gene and the correlation with its SNPs might help to clarify the role of polymorphisms on the immune response in leprosy.


2019 ◽  
Author(s):  
Stephen P. Ashcroft ◽  
Joseph J. Bass ◽  
Abid A. Kazi ◽  
Philip J. Atherton ◽  
Andrew Philp

ABSTRACTVitamin D deficiency has been linked to a reduction in skeletal muscle function and oxidative capacity, however, the mechanistic basis of these impairments are poorly understood. The biological actions of vitamin D are carried out via the binding of 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) to the vitamin D receptor (VDR). Recent evidence has linked 1α,25(OH)2D3 to the regulation of skeletal muscle mitochondrial function in vitro, however, little is known with regard to the role of the VDR in this process. To examine the regulatory role of the VDR in skeletal muscle mitochondrial function, we utilised lentiviral mediated shRNA silencing of the VDR in C2C12 myoblasts (VDR-KD) and examined mitochondrial respiration and protein content compared to shRNA scrambled control. VDR protein content was reduced by ~95% in myoblasts and myotubes (P < 0.001). VDR-KD myoblasts displayed a 30%, 30% and 36% reduction in basal, coupled and maximal respiration respectively (P < 0.05). This phenotype was maintained in VDR-KD myotubes, displaying a 34%, 33% and 48% reduction in basal, coupled and maximal respiration (P < 0.05). Furthermore, ATP production derived from oxidative phosphorylation (ATPox) was reduced by 20% suggesting intrinsic impairments within the mitochondria following VDR-KD. However, despite the observed functional decrements, mitochondrial protein content as well as markers of fusion and fission were unchanged. In summary, we highlight a direct role for the VDR in regulating skeletal muscle mitochondrial respiration in vitro, providing a potential mechanism as to how vitamin D deficiency might impact upon skeletal muscle oxidative capacity.


Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 273 ◽  
Author(s):  
Guido Gembillo ◽  
Valeria Cernaro ◽  
Antonino Salvo ◽  
Rossella Siligato ◽  
Alfredo Laudani ◽  
...  

Diabetes mellitus (DM) poses a major public health problem worldwide, with ever-increasing incidence and prevalence in recent years. The Institute for Alternative Futures (IAF) expects that the total number of people with type 1 and type 2 DM in the United States will increase by 54%, from 19,629,000 to 54,913,000 people, between 2015 and 2030. Diabetic Nephropathy (DN) affects about one-third of patients with DM and currently ranks as the first cause of end-stage kidney disease in the Western world. The complexity of interactions of Vitamin D is directly related with progressive long-term changes implicated in the worsening of renal function. These changes result in a dysregulation of the vitamin D-dependent pathways. Various studies demonstrated a pivotal role of Vitamin D supplementation in regression of albuminuria and glomerulosclerosis, contrasting the increase of glomerular basement membrane thickening and podocyte effacement, with better renal and cardiovascular outcomes. The homeostasis and regulation of the nephron’s function are absolutely dependent from the cross-talk between endothelium and podocytes. Even if growing evidence proves that vitamin D may have antiproteinuric, anti-inflammatory and renoprotective effects in patients with DN, it is still worth investigating these aspects with both more in vitro studies and randomized controlled trials in larger patient series and with adequate follow-up to confirm the effects of long-term vitamin D analogue supplementation in DN and to evaluate the effectiveness of this therapy and the appropriate dosage.


Author(s):  
Vladimir Vranic ◽  
Milena Potic Floranovic ◽  
Milan Petrovic ◽  
Srdjan Starcevic ◽  
Gordana Supic

Abstract Osteoarthritis is a degenerative, painful and irreversible disease that affects millions of people worldwide. The causes and mechanisms of osteoarthritis have not been fully understood. Vitamin D is an essential factor in bone metabolism. Its actions are mediated by the vitamin D receptor, a transcription factor that controls gene expression, thus maintaining calcium and phosphate homeostasis. Vitamin D has been hypothesized to play essential role in a number of musculoskeletal diseases including osteoarthritis, and its deficiency is prevalent among osteoarthritis patients. A large number of studies have been done regarding the effects of vitamin D in pathogenesis and progression of osteoarthritis, as well as its use a therapeutic agent. Up to date, studies have provided controversial results, and no consensus concerning this matter was achieved. With this review, we aim to explore current data on the possible role of vitamin D and its receptor in pathogenesis of osteoarthritis and assess the efficiency of vitamin D supplementation as a therapeutic strategy.


2008 ◽  
Vol 36 (10) ◽  
pp. 2058-2063 ◽  
Author(s):  
Tsutomu Matsubara ◽  
Kouichi Yoshinari ◽  
Kazunobu Aoyama ◽  
Mika Sugawara ◽  
Yuji Sekiya ◽  
...  

2019 ◽  
Vol 8 (7) ◽  
pp. 1070-1081
Author(s):  
Amarjit Saini ◽  
Linda Björkhem-Bergman ◽  
Johan Boström ◽  
Mats Lilja ◽  
Michael Melin ◽  
...  

The CC genotype of the vitamin D receptor (VDR) polymorphism TaqI rs731236 has previously been associated with a higher risk of developing myopathy compared to TT carriers. However, the mechanistic role of this polymorphism in skeletal muscle is not well defined. The effects of vitamin D on patients genotyped for the VDR polymorphism TaqI rs731236, comparing CC and TT carriers were evaluated. Primary human myoblasts isolated from 4 CC carriers were compared with myoblasts isolated from four TT carriers and treated with vitamin D in vitro. A dose-dependent inhibitory effect on myoblast proliferation and differentiation was observed concurrent with modifications of key myogenic regulatory factors. RNA sequencing revealed a vitamin D dose–response gene signature enriched with a higher number of VDR-responsive elements (VDREs) per gene. Interestingly, the greater the expression of muscle differentiation markers in myoblasts, the more pronounced was the vitamin D-mediated response to suppress genes associated with myogenic fusion and myotube formation. This novel finding provides a mechanistic explanation to the inconsistency regarding previous reports of the role of vitamin D in myoblast differentiation. No effects in myoblast proliferation, differentiation or gene expression were related to CC vs TT carriers. Our findings suggest that the VDR polymorphism TaqI rs731236 comparing CC vs TT carriers did not influence the effects of vitamin D on primary human myoblasts and that vitamin D inhibits myoblast proliferation and differentiation through key regulators of cell cycle progression. Future studies need to employ strategies to identify the primary responses of vitamin D that drive the cellular response towards quiescence.


2020 ◽  
Vol 25 (41) ◽  
pp. 4357-4367 ◽  
Author(s):  
Loai Alzghoul

: Autism spectrum disorder (ASD) is a pervasive developmental disorder with heterogeneous etiology. Vitamin D can function as a fat-soluble vitamin as well as a hormone, and can exert its effect through both genomic and non-genomic mechanisms. In the last decades, several studies have examined the relationship between vitamin D levels and ASD. These studies demonstrated that low vitamin D status in early development has been hypothesized as an environmental risk factor for ASD. Both in vivo and in vitro studies have demonstrated that vitamin D deficiency in early life can alter brain development, dysregulates neurotransmitter balance in the brain, decreases body and brain antioxidant ability, and alters the immune system in ways that resemble pathological features commonly seen in ASD. In this review, we focused on the association between vitamin D and ASD. In addition, the above-mentioned mechanisms of action that link vitamin D deficiency with ASD were also discussed. Finally, clinical trials of vitamin D supplementation treatment of ASD have also been discussed.


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