scholarly journals Vitamin D and colon cancer

2012 ◽  
Vol 19 (3) ◽  
pp. R51-R71 ◽  
Author(s):  
Fábio Pereira ◽  
María Jesús Larriba ◽  
Alberto Muñoz

The most active vitamin D metabolite, 1α,25-dihydroxyvitamin D3(1,25(OH)2D3), is a pleiotropic hormone with wide regulatory actions. Classically, vitamin D deficiency was known to alter calcium and phosphate metabolism and bone biology. In addition, recent epidemiological and experimental studies support the association of vitamin D deficiency with a large variety of human diseases, and particularly with the high risk of colorectal cancer. By regulating the expression of many genes via several mechanisms, 1,25(OH)2D3induces differentiation, controls the detoxification metabolism and cell phenotype, sensitises cells to apoptosis and inhibits the proliferation of cultured human colon carcinoma cells. Consistently, 1,25(OH)2D3and several of its analogues decrease intestinal tumourigenesis in animal models. Molecular, genetic and clinical data in humans are scarce but they suggest that vitamin D is protective against colon cancer. Clearly, the available evidence warrants new, well-designed, large-scale trials to clarify the role of vitamin D in the prevention and/or therapy of this important neoplasia.

2001 ◽  
Vol 285 (4) ◽  
pp. 1012-1017 ◽  
Author(s):  
Petra Bareis ◽  
Giovanna Bises ◽  
Martin G. Bischof ◽  
Heide S. Cross ◽  
Meinrad Peterlik

2019 ◽  
Vol 20 (19) ◽  
pp. 4907 ◽  
Author(s):  
Smriti Murali Krishna

Atherosclerotic occlusive diseases and aneurysms that affect large and medium-sized arteries outside the cardiac and cerebral circulation are collectively known as peripheral arterial disease (PAD). With a rise in the rate of aging population worldwide, the number of people diagnosed with PAD is rapidly increasing. The micronutrient vitamin D is an important steroid hormone that acts on many crucial cellular mechanisms. Experimental studies suggest that optimal levels of vitamin D have beneficial effects on the heart and blood vessels; however, high vitamin D concentrations have been implicated in promoting vascular calcification and arterial stiffness. Observations from various clinical studies shows that deficiency of vitamin D has been associated with a greater risk of PAD. Epidemiological studies have often reported an inverse relation between circulating vitamin D status measured in terms of 25-hydroxivitamin D [25(OH)D] levels and increased cardiovascular disease risk; however, randomized controlled trials did not show a consistent positive effect of vitamin D supplementation on cardiovascular disease risk or events. Even though PAD shares all the major risk factors with cardiovascular diseases, the effect of vitamin D deficiency in PAD is not clear. Current evidence suggests a strong role of vitamin D in promoting genomic and epigenomic changes. This review summarises the current literature that supports the notion that vitamin D deficiency may promote PAD formation. A better understanding of underlying pathological mechanisms will open up new therapeutic possibilities which is the main unmet need in PAD management. Furthermore, epigenetic evidence shows that a more holistic approach towards PAD prevention that incorporates a healthy lifestyle, adequate exercise and optimal nutrition may be more effective in protecting the genome and maintaining a healthy vasculature.


2005 ◽  
Vol 135 (10) ◽  
pp. 2350-2354 ◽  
Author(s):  
Vin Tangpricha ◽  
Catherine Spina ◽  
Min Yao ◽  
Tai C. Chen ◽  
M. Michael Wolfe ◽  
...  

2021 ◽  
Author(s):  
Sarah Bakhamis ◽  
Faiqa Imtiaz ◽  
Khushnooda Ramzan ◽  
Edward De Vol ◽  
Osamah AlSagheir ◽  
...  

Vitamin-D deficiency remains a major cause of rickets worldwide. Nutritional factors are the major cause and less commonly inheritance causes. Recently, CYP2R1 has been reported as a major factor for 25-hydroxylation contributing to the inherited forms of vitamin D deficiency. We conducted a prospective cohort study at King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia to review cases with 25-hydroxylase deficiency and to describe their clinical, biochemical, and molecular genetic features. We analyzed 27 patients from 9 different families who presented with low 25-OH vitamin-D and not responding to usual treatment. Genetic testing identified two mutations: c.367+1G>A (12/27 patients) and c.768dupT (15/27 patients), where 18 patients were homozygous for their identified mutation and 9 patients were heterozygous. Both groups had similar clinical manifestations ranging in severity, but none of the patients with heterozygous mutation had hypocalcemic manifestations. 13/18 of homozygous patients and all the heterozygous patients responded to high doses of vitamin-D treatment, but they regressed after decreasing the dose, requiring lifelong therapy. 5/18 of homozygous patients required calcitriol to improve their biochemical data, whereas none of the heterozygous patients and patients who carried the c.367+1G>A mutation required calcitriol treatment. To date, this is the largest cohort series analyzeing CYP2R1-related 25-hydroxylase deficiency worldwide, supporting its major role in 25-hydroxylation of vitamin-D. It is suggested that a higher percentage of CYP2R1 mutations might be found in the Saudi population. We believe that our study will help in the diagnosis, treatment, and prevention of similar cases in the future.


2021 ◽  
Vol 29 (137) ◽  
pp. 352-358
Author(s):  
Hadis Musavi ◽  
Tayebeh Azramezani Kop ◽  
Anahita Ebrahimpour ◽  
Setareh Rezatabar ◽  
Afsaneh Dashtaki ◽  
...  

2004 ◽  
Vol 10 (9) ◽  
pp. 917-919 ◽  
Author(s):  
Héctor G Pálmer ◽  
María Jesús Larriba ◽  
José Miguel García ◽  
Paloma Ordóñez-Morán ◽  
Cristina Peña ◽  
...  

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