Vitamin D
not only a vitamin but also a hormone
The calicalciferol is a steroid which comes from the idrocolesterol after the sunlight exposure. It is the precursor of the biological active form of the vitamin D, known as calcitriol. This steroid goes to the liver and then to the kidney, where it is turned into in 1.25 didrossicolecalciferol which is functionally active. The active form of the vitamin can act on different tissues regulating the calcium phosphorus metabolism increasing the renal reabsorption and the intestinal absorption of these elements. As other different hormones, the ability of this vitamin steroid nature to regulate the gene expression has urged a lot of researchers to develop the biological and pharmacodynamic characteristics of these elements. These investigations have revealed new therapeutical properties comparable with some growing factors.
Herewith I’m reporting some pathologies where the vitamin administration has shown some beneficial effects.
They are:
• ARTHRITIS
Recent studies have revealed that women who ingest more than 400 IU of vitamin D day reduce their risk of developing rheumatoid arthritis by as much as 42%. Vitamin D deficiency has been associated with an increased risk of developing oreoarthritis.
• DIABETES
Diabetes mellitus type I
Studies in mice have suggested that preatreating mice that are prone to developing type I diabetes with the active form of vitamin D reduces the development of type I diabetes by 80%. This study is supported by the observation in Finland where children in the 1960’s routinely received 2,00 IU of vitamin D a day during their first year of life. When these children were followed for the next 31 years, it was observed that these children had a reduced risk of developing type I diabetes by 78%. Children who were vitamin D deficient at the same time and also followed for 31 years had an almost 300% increased risk of developing type I diabetes.
Diabetes mellitus type II
The beta islet cells that produce insulin in the pancreas have a vitamin D receptor. The active form of vitamin D stimulates the pancreas to produce insulin. It has been observed that the relative risk of developing type II diabetes is reduced by as much as 33% in men and women who increase their intake of vitamin D above 800 IU/day along with 1,000 milligrams of calcium.
• OSTEOPOROSIS
Vitamin D deficiency will cause removal of both the calcium and matrix from the bone, and as a result, will cause osteopenia and can precipitate and exacerbate osteoporosis. Unlike osteomalacia which causes bone pain, osteoporosis, which is porotic bone holes in the bones and loss of bone doesn’t cause bone pain unless there is an acute fracture. Typically this pain resolves as the fracture heals and can be easily distinguished from osteomalacia.
Other cases where the vitamins administration seems to get good results are: the epilepsy, schizophrenia, depression, cancer and obesity.
THE RELATIONSHIP BETWEEN VITAMIN D DEFICIENCY AND TYPE 1 DIABETES
Type 1 diabetes develops due to malfuctioning of the immune system. Mounting scientific evidence indicates that vitamin D plays a vital role in the normal functioning of the immune system and vitamin D deficiency can lead to the malfunctioning of the immune system.Consequentenly,your own immune system starts to attack and kill your own insulin producing in the pancreas. Once you are unable to produce insulin, you develop type 1.
Type 1 diabetes (T1D) is an autoimmune disease characterized by leukocyte infiltration into the pancreatic islets, and the treatment of adult with a vitamin D analog arrests the progression of insulitis, blocks Th1 cell infiltration into the pancreas, and markedly reduces T1D development, suggesting inhibition of chemokine production by islet cells. The vitamin D analog significantly down-regulates in vitro and in vivo proinflammatory chemokine production by islet cells, inhibiting T cell recruitment into the pancreatic islets and T1D development.
THE RELATIONSHIP BETWEEN VITAMIN D DEFICIENCY AND TYPE 2 DIABETES
Vitamin D is important for normal glucose metabolism. It acts through several mechanisms on glucose metabolism:
1. Vitamin D directly acts on insulin producing cells in the pancreas to produce more insulin
2. Vitamin D directly acts on the muscle and fat cells to improve insulin action by reducing insulin resistance.
3. Vitamin D reduces inflammation which is commonly present in patients with Insulin Resistance Syndrome and Type 2 diabetes.
4. Vitamin D indirectly improves insulin production and it’s action by improving the level of calcium inside the cells.
Now you can understand the important role vitamin D plays in keeping blood glucose normal. Intuitively, vitamin D deficiency can lead to diabetes.
-Evidence that links vitamin D deficiency to type 2
Numerous scientific studies have found vitamin D to be low in patients with Type 2 diabetes. One such remarkable study looked at the level of vitamin D, prevalence of insulin resistance and risk for Type 2 diabetes in the U.S. population. In this study, researchers concluded that people with a low level of vitamin D were at high risk for the development of insulin resistance and Type 2 diabetes.
-Evidence that vitamin D can prevent type 2 diabetes.
In a study from Finland, researchers collected health data in men and women from the ages of 40 to 74. None of these individual had Type 2 diabetes at the start of the study. They followed these individuals for 22 years to see the pattern of development of Type 2 diabetes. These researchers found that people who had higher level of vitamin D were less likely to develop Type 2 diabetes. Thus vitamin D appears to have a protective effect against the development of Type 2 diabetes.
In another study from the U.S., researchers found that vitamin D and calcium supplementation were able to reduce progression from pre-diabetes to diabetes. This protective effect of vitamin D was similar in magnitude to other measures which have been shown to reduce the progression from pre-diabetes to diabetes , such as a weight reducing diet, intense exercise and use of the drug, metformin.
In summary, vitamin D has the potential to prevent Type 1 as well as Type 2 diabetes. It can also prevent the devastating complications of diabetes such as heart attacks and kidney failure. Unfortunately, most diabetics continue to be low in vitamin D…
THE ACTION MECHANISM OF VITAMIN D
The vitamin D acts especially on proteinic component as "growing factors" type. Regulating t-cells and other protein components like laboratory tests have shown on mice.
A 1
,25-Dihydroxyvitamin D3 Analog Enhances Regulatory T-Cells and Arrests Autoimmune Diabetes in NOD Mice
Silvia Gregori,1 Nadia Giarratana,1 Simona Smiroldo,1 Milan Uskokovic,2 and Luciano Adorini1
Type 1 diabetes is a chronic progressive autoimmune disease characterized by mononuclear cell infiltration,dominated by interleukin-12 (IL-12)-dependent Th1 cells, of the pancreatic islets, with subsequent destruction of insulin-producing -cells. Here, we demonstrate that treatment of adult nonobese diabetic (NOD) mice with an analog of 1
,25-dihydroxyvitamin D3, an immunomodulatory agent preventing dendritic cell maturation, decreases lipopolysaccharide-induced IL-12 and -interferon production, arrests Th1 cell infiltration and progression of insulitis, and inhibits diabetes development
at nonhypercalcemic doses. Arrest of disease progression is accompanied by an enhanced frequency in the pancreatic lymph nodes of CD4CD25 regulatory T-cells that are able to inhibit the T-cell response to the pancreatic autoantigen insulinoma-associated protein 2 and to significantly delay disease transfer by pathogenic CD4CD25 cells. Thus, a short treatment of adult NOD mice with an analog of 1,25-dihydroxyvitamin D3 inhibits IL-12 production, blocks pancreatic infiltration of Th1 cells, enhances CD4CD25 regulatory cells, and arrests the progression of type 1 diabetes, suggesting its possible application in the
treatment of human autoimmune diabetes.
IN CONCLUSION
The Vitamin D has important interactions with trascriptional regulators and cell signaling system, including androgen receptors,estrogen receptors, IGF, TGFbeta, beta-catenin and others , to control cell growth and differentation.
