Role of vitamin d in type 2 diabetes mellitus vs,club m 87 boulevard vincent auriol,homemade remedies for diabetes type 2 60v,type 2 diabetes management pdf tutorial - Test Out


Recent compelling evidence suggests a role of vitamin D deficiency in the pathogenesis of insulin resistance and insulin secretion derangements, with a consequent possible interference with type 2 diabetes mellitus. Science, Technology and Medicine open access publisher.Publish, read and share novel research. 1995 Isolation and structural identification of 1,25-dihydroxyvitamin D3 produced by cultured alveolar macrophages in sarcoidosis.
1983 Metabolism of 25-hydroxyvitamin D3 by cultured pulmonary alveolar macrophages in sarcoidosis. 2003 Tolerogenic dendritic cells induced by vitamin D receptor ligands enhance regulatory T cells inhibiting autoimmune diabetes.
2010 Glycemic changes after vitamin D supplementation in patients with type 1 diabetes mellitus and vitamin D deficiency. 2009 Genome-wide association study and a meta-analysis find that over 40 loci affect risk of type 1 diabetes.
1983 Specific high-affinity receptors for 1,25 dihydroxyvitamin D3 in human peripheral mononuclear cells: Presence in monocytes and induction in T lymphocytes following activation.
1995 Susceptibility to human type 1 diabetes at IDDM2 is determined by tandem repeat variation at the insulin gene mini satellite locus. 1994 A polymorphic locus near the insulin gene is associated with insulin-dependent diabetes mellitus. 2001 1alpha,25-Dihydroxyvitamin D3 has a direct effect on naive CD4+ T cells to enhance the development of Th2 cells. 1996 1,25-dihydroxyvitamin D3 reversibly blocks the progressions of relapsing encephalomyelitis, a model of multiple sclerosis. 1998 1,25-dihydroxyvitamin D3 prevents and ameliorates symptoms in two experimental models of human arthritis. 1998 1,25-dihydroxy-vitamin D3 restores sensitivity to cyclophosphamide-induced apoptosis in non-obese diabetic (NOD) mice and protects against diabetes. 1998 Prevention of autoimmune destruction of syngeneic islet grafts in spontaneously diabetic nonobese diabetic mice by a combination of a vitamin D3 analog and cyclosporine.
2000 Vitamin D receptor gene polymorphisms influence susceptibility to type 1 diabetes mellitus in the Taiwanese population.
1998 Prevention of type 1 diabetes in nonobese diabetic mice by late intervention with nonhyperclcemic analogs of 1,25-dihydroxyvitamin D3 in combination with a short induction course of cyclosporine A.
1997 The nonobese diabetic mouse as a model of autoimmune diabetes: Immune dysregulation gets the NOD. 1998 Inhibition of IL12 production by 1,25-dihydroxyvitamin D3: involvement of NF-?B down regulation by 1,25-dihydroxy vitamin D3.
Until now the exact mechanism of insulin secretion failure in type 2 diabetes has not been completely understood. Type 2 diabetes occurs when insulin production from pancreatic beta cells either fails, or peripheral tissues become resistant to the hormone insulin preventing the uptake of glucose from the blood stream into cells for fuel.
Designing new treatment options for type 2 diabetes has been difficult considering the exact mechanism of insulin secretion was not understood. To test the importance of Snapin in insulin secretion a drug which inhibits its production was added.
These exciting new findings will not only propel diabetic research but also help develop more accurate treatment options. People with type 1 diabetes CANNOT cordupe insulin which brings the blood sugar down so just about everything they eat causes their blood sugar to rise. A series of studies have reported a constant global rise in the incidence of type 1 diabetes. In a variety of epidemiological studies, type 1 diabetes appears to be conditioned by seasonal and geographical variation in u.v.
Further support has come from Finnish studies, which have reported a decrease in incidence in children following vitamin D supplement induction (Hypponen et ul. Vitamin D has come to be recognised to play a role in the modulation of the innate and adaptive immune system (Fig.
It acts as a transcriptional factor, inducing the expression of an antimicrobial polypeptide, cathelicidin. It leads to negative autoregulation by negative feedback of the enzymes CP24A and CP24A-SV.
Activated T cells express high levels of VDR as well, and activation by 1,25(OH)2D3 causes a decrease in proliferation and Th1 responses, but an increase in Th2 responses, Treg levels and T-cell homing. Monocytes, which express a higher number of VDRs than macrophages, stimulate further macrophage differentiation. Therefore, vitamin D plays an important role in the regulation of Th1 and Th2 balance, via the proliferation of Tregs and the release of cytokines.
However, there is evidence from adult NOD mice that type 1 diabetes is inhibited following vitamin D analogue administration. The last factor that might influence the development of the disease is genetic polymorphism of VDR. When observing the immunological mechanisms underlying each hypothesis (Table 1), one can notice certain similarities.
Taking the concept of protective vs diabetogenic factors, one might postulate that a compensatory mechanism might also occur between different hypothesised factors. A good analogy would be the use of a balancing scale with one plate on each side (each plate representing the diabetogenic and protective factors). It is likely that a multifactorial process leading to a disequilibrium between protective and diabetogenic factors is the cause of this increase. Further research, however, might be able to identify a common denominator, leading to a greater understanding as to why the incidence of type 1 diabetes is increasing.
Vitamin D may play a vital role in the prevention and treatment of diseases associated with aging, according to researchers at Loyola University Chicago Marcella Niehoff School of Nursing (MNSON). Researchers reviewed evidence that suggests an association between vitamin D deficiency and chronic diseases associated with aging such as cognitive decline, depression, osteoporosis, cardiovascular disease, high blood pressure, Type 2 diabetes and cancer. Older adults are at risk for vitamin D deficiency due to diet, reduced time outdoors and poor skin absorption of the nutrient.
The Institute of Medicine generally recommends that adults up to 70 years of age take 600 IU of vitamin D daily and adults over the age of 70 consume 800 IU of the nutrient daily. Study authors concluded that as the older population continues to grow, universal guidelines for testing and treating vitamin D deficiency are needed.
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Compared with women living in the equatorial regions of the planet, women residing in Norway and Iceland have almost five times higher risk of developing ovarian cancer. Boosting the serum vitamin D level might increase the lifespan of women diagnosed with ovarian cancer.
Despite the benefits of high serum vitamin D level, it is unclear whether consuming vitamin D supplements could boost the chance of surviving ovarian cancer. Normally 200 IU of vitamin D in the form of dietary supplement is recommended for women less than 50 years of age. You can also meet almost 100 percent of your regular vitamin D requirement by consuming 100g of an oily fish daily. However, exposing the skin to sunlight is the most effective method of boosting the vitamin D level in the body. IntroductionThis chapter will review the role of vitamin D in the pathogenesis and treatment of type 1 diabetes mellitus.
Vitamin D supplement in early childhood and risk for type 1 (insulin-dependent) diabetes mellitus. Johns Hopkins researchers believe they have uncovered the molecular switch for insulin secretion. Snapin is a protein  produced in nerve cells and plays an important role in cell communication, and has also been found in pancreatic beta cells. Epidemiological and immunological studies have demonstrated that environmental factors may influence the pathogenesis, leading to a cell-mediated pancreatic ?-cell destruction associated with humoral immunity. This will then be integrated in the pathogen-containing phagosome, leading to antimicrobial action. 1,25(OH)2D3 causes a decrease in B-cell proliferation, antibody production, memory and plasma cells. Immature dendritic cells, which also contain a higher number of VDRs, cause the suppression of the differentiation of dendritic cells and an increase in the secretion of CC-chemokine ligand 22 (CCL22), which supports the synthesis of Tregs (Adams & Hewison 2008). In these models, vitamin D prevents the maturation of dendritic cells, therefore causing a decrease in the production of IL12. Vitamin D induces the formation of a VDR complex, which binds to vitamin D3 response elements. When comparing one with the other, one can notice an opposing effect: protective vs diabetogenic.
Protective factors (vitamin D, early exposure to pathogens and breast milk) are opposed by diabetogenic factors (vitamin D deficiency, viruses and cow's milk).


In other words, an increase in vitamin D deficiency might be compensated by an increase in breast-feeding and so on.
Each plate supports a variety of weights, representing the various factors brought forward in the hypotheses described above. This in turn causes the acceleration of the diabetic process, causing an increase in childhood onset, therefore leading to an overall increase in the incidence of type 1 diabetes. With the number of people ages 65 and older expected to more than double from 2012 to 2060, the problem will become much more prevalent. Research to examine the proper dosing of vitamin D supplements necessary to prevent the chronic diseases of aging also would have significant benefit for future generations. Studies have found a direct association between deficiency of the sunshine vitamin and higher risk of developing ovarian cancer. While studying the link between serum vitamin D and ovarian cancer risk with the help of World Health Organization’s GLOBOCAN database, researchers at the Moores Cancer Center at University of California, San Diego, USA, found that countries located on the highest latitudes in the northern and southern hemispheres had the highest rate of ovarian cancer.
According to a study by researchers of the Dana-Farber Cancer Institute in Boston, mortality rate owing to ovarian cancer is lowest in women with serum vitamin D level in the upper 25% of the normal range.
Nonetheless, ovarian cancer patients might take vitamin D supplements to preserve the healthy reserve of the sunshine vitamin in the body.
Milk and dairy products are good sources of vitamin D that can be included in the diet of ovarian cancer patients. Consumption of vitamin D fortified juices and breakfast cereals could increase your serum vitamin D level. Depending upon the intensity of the ultraviolet rays of the sun, exposing the face, arms, legs and back for about 5 to 30 minutes to the sunrays, triggers synthesis of the sunshine vitamin in the skin.
In fact, vitamin D deficiency is usually detected in obesity in which insulin resistance is also a common finding. The activation of the T-cell by various stimuli (antigens), is brought by major histocompatibility complex (MHC-HLA II). At the level of the antigen-presenting cell (such as dendritic cells; DCs), 1?,25(OH)2D3 inhibits the surface expression of MHC class II-complexed antigen and of co-stimulatory molecules, in addition to production of the cytokine IL-12, thereby indirectly shifting the polarization of T cells from a Th1 towards a Th2 phenotype. The search for the triggering factor(s) has been going on for the past century, and yet they are still unknown.
The activation of TLRs by pathogens causes an increased expression of vitamin D receptor (VDR) and the vitamin D-activating enzyme CP27B (25OHD-1a-hydroxylase) in macrophages (Adams & Hewison 2008). Adapted from Adams JS & Hewison M 2008 Unexpected actions of vitamin D: new perspectives on the regulation of innate and adaptive immunity.
This has been shown to have an effect on the level of IFNg produced by Th1 cells, demonstrating a decrease in Th1 responses. This normally has a variety of calcaemic and non-calcaemic activities, of which the inhibition of the expression of IL2, INFg,TNFa and TNFb is one (Nagpal et ul.2005). One can also realise that some common ground might exist between the various hypotheses, for instance, the role of TLRs in vitamin D deficiency and hygiene hypothesis. In healthy individuals, a balance is maintained, but in patients suffering from type 1 diabetes, a shift towards diabetogenic factors occurs. In diabetic patients, this compensatory mechanism does not occur, therefore tilting the scale towards the diabetogenic side (Fig. A tablespoon of fish oil contains sufficient vitamin D to meet your minimum daily vitamin D need. The coexistence of insulin resistance and vitamin D deficiency has generated several hypotheses. This figure shows also, inhibitors of T-cell activation: cytotoxic T lymphocyte antigen 4 (CTLA-4) and lymphoid tyrosine phosphatase (LYP). In addition, 1?,25(OH)2D3 has immunomodulatory effects directly at the level of the T cell, by inhibiting the production of the Th1 cytokines IL-2 and IFN-? and stimulating the production of Th2 cytokines. We will summarize the results of in-vitro and animal studies and will conclude with a review of the relevant clinical trials.2. This review provides an overview of some of the most well-known theories found in the literature: hygiene, viral, vitamin D deficiency, breast milk and cow's milk hypotheses. This decrease has been associated with an increase in the frequency of CD4+ CD25 + Tregs, arresting the development of type 1 diabetes. In fact, one might go as far as to suggest that vitamin D deficiency alters antimicrobial effect by modulating the function of TLRs.
Some cross-sectional and prospective studies have suggested that vitamin D deficiency may play a role in worsening insulin resistance; others have identified obesity as a risk factor predisposing individuals to exhibit both vitamin D deficiency and insulin resistance.
DefinitionType 1 diabetes mellitus is an autoimmune disease in which the pancreas is unable to respond to secretagogue stimulation with appropriate insulin secretion. Although the hygiene hypothesis appears to be the most promising, positive evidence from animal, human and epidemiological studies precludes us from completely discarding any of the other hypotheses.
These alterations translate into functional VDR proteins, which in theory may lead to an abnormal synthesis of cytokines leading to type 1 diabetes. A shift might occur from a protective equilibrium towards an increase in diabetogenic factors, leading to type 1 diabetes. The available data from intervention studies are largely confounded, and inadequate considerations of seasonal effects on 25(OH)D concentrations are also a common design flaw in many studies. Both Th2 and Tregs can inhibit Th1 cells through the production of counteracting or inhibitory cytokines.
Hyperglycemia develops when more than 70-90% of the insulin-producing beta cells are destroyed. Moreover, due to contrasting evidence in the literature, a single factor is unlikely to cause an increase in the incidence of diabetes all over the world, which suggests that a multifactorial process might be involved.
In fact, association has been found in Indian, Japanese, Taiwanese and German populations (Zella & DeLuca 2003). Oral tolerance induced by the protective action of human milk might compensate for dietary antigens introduced in the last century. This change might have occurred gradually throughout the 20th century, leading to an increase in incidence.
On the contrary, there is strong evidence that obesity might cause both vitamin D deficiency and insulin resistance, leaving open the possibility that vitamin D and diabetes are not related at all. Together, these immunomodulatory effects of 1?,25(OH)2D3 can lead to the protection of target tissues, such as ? cells, in autoimmune diseases and transplantation. An autoimmune destructive process, which plays a central role in the development of type 1 diabetes mellitus, is facilitated by the subject’s own genetic susceptibility and by non-genetic factors.
Although the immunological mechanisms are still unclear, there seems to be some overlap between the various hypotheses. As breast-feeding decreased throughout the 20th century, cow's milk formulas became more popular, leading to a negative shift in oral tolerance.
Although it might seem premature to draw firm conclusions on the role of vitamin D supplementation in reducing insulin resistance and preventing type 2 diabetes, this manuscript will review the circumstances leading to vitamin D deficiency and how such a deficiency can eventually independently affect insulin sensitivity.
It is thought that the emphasis should be shifted from a single to a multifactorial process and that perhaps the ‘balance shift’ model should be considered as a possible explanation for the rise in the incidence of type 1 diabetes. Vitamin D deficiency is a non-genetic factor that appears to be associated with an increased risk of developing type 1 diabetes mellitus. It has also demonstrated the direct effect of vitamin D on Th cells by activating naive CD4+T cells with anti-CD3 and anti-CD28.
The acute complications include life-threatening conditions like severe hypoglycemia or diabetic ketoacidosis (DKA). Chronic diabetic complications can be divided into microvascular complications (retinopathy, neuropathy and nephropathy) and macrovascular complications (cardiovascular, cerebrovascular and peripheral vascular disease). I can eat an almost unlimited amount of nuts without my blood sugar going over 100 at any point. Severe microvascular and macrovascular complications can lead to renal failure (the most common cause of hemodialysis in the US), blindness or lower extremity amputations.
This indicates that vitamin D has a direct effect on Th cells, enhancing the development of Th2 cells and therefore preventing the development of type 1 diabetes.
Rather than using the Glycemic Index, I urge your friend to think about food in terms of carbohydrates.
EpidemiologyIn 2010, about 215,000 people younger than 20 years of age had diabetes (type 1 or type 2) in the United States.
He should experiment with different quantities and types of carbohydrates by eating and then testing his blood sugar.
About 27% of those with diabetes (approximately 7 million Americans) do not know they have the disease. He may learn that he’s more tolerant of carbohydrates in the afternoon or evening than the morning. Type 1 diabetes mellitus continues to be highly prevalent in many countries, with an overall annual increase estimated at 3% (International Diabetes Federation [IDF] 2010).
The Glycemic Index simply doesn’t tell us anything except for how some people without diabetes handled carbohydrates.
Natural historyThe natural history of type 1 diabetes is characterized by an autoimmune destruction of the beta cells in the islands of Langerhans in the pancreas.
The autoimmune process has cellular and humoral components, leading to the destruction of the beta cells and a decreased insulin secretion.


As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels. After 70-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. In some patients years will go by before the onset of diabetes, while other patients may never develop beta cell insufficiency, perhaps due to the regaining of tolerance.
Most patients with type 1 diabetes mellitus have one or more susceptible human leukocyte antigen (HLA) class II, and over 90% have beta cell autoantibodies present. The appearance of circulating islet cell autoantibodies is the first detectable sign of this immune process.4. However, extra-genetic components influence the penetrance of diabetes susceptibility genes. If data are obtained at a single point in time, the risk of type 1 diabetes mellitus between monozygotic twins can be as low as 30%, but if the monozygotic twins are followed long-term, the cumulative incidence of diabetes reaches 65% (Redondo et al., 2008). In the same cohort of monozygotic twins, the rate of persistent autoantibody positivity, type 1 diabetes mellitus, or both, reached 78% (Redondo et al., 2008). To better understand the genetic susceptibility to diabetes, candidate gene studies were conducted in order to identify genes that are associated with autoimmune type 1 diabetes.Human leukocyte antigen (HLA) associations have been long recognized in many autoimmune diseases. In type 1 diabetes mellitus, the HLA on chromosome 6p21 is well described and is considered to play an important role in more than 50% of the familial cases in Caucasians (Noble et al., 1996). HLA DR4-DQ8 or DR3-DQ2 haplotypes are detected in up to 90% of patients with type 1 diabetes mellitus (Devendra & Eisenbarth, 2003). First-degree relatives of the patients who carry the highest risk haplotype combination also have a higher risk of developing diabetes mellitus as compared to the relatives of diabetes patients who do not have this haplotype and who develop type 1 diabetes mellitus later in life (Gillespie et al., 2002).
Another HLA haplotype (DR15-DQ6) might have protective properties, and is found in a much larger percentage in the general population (20%) as compared to less than 1% in patients with type 1 diabetes mellitus (Eisenbarth & Gottlieb, 2004). Glutamic acid decarboxylase (GAD) antibodies are more frequent in patients with HLA DR3-DQ2, whereas insulin auto-antibodies (IAA) and protein tyrosine phosphatase-like protein antibodies (IA-2 antibodies) are more frequent in patients with HLA DR4-DQ8. The insulin gene contributes 10% to the genetic susceptibility in developing autoimmune diabetes (Bell et al., 1984). The risk of developing diabetes depends on the expression of the insulin protein in the thymus which can cause a defective central tolerance to the insulin molecule. T cells are recognized to be a major part of the immune process in diabetes mellitus, and several genes involved in T cell regulation are associated with type 1 diabetes mellitus.
Autoimmune processOne of the best animal models for type 1 diabetes mellitus is the nonobese diabetic mouse (NOD). NOD mouse develops type 1 diabetes mellitus spontaneously, over the course of a few months, allowing the investigators to study this process stage by stage. Many reports describe in detail the genetics, the immune process, the influence of the environment and most importantly, the potential therapies to prevent, delay or reverse the destructive process that leads to type 1 diabetes mellitus in this model. Delovitch and Singh (Delovitch & Singh, 1997) reviewed the use of NOD mouse in the studies of type 1 diabetes mellitus. In NOD mice, the first step is the infiltration of the peri-islet regions of the pancreatic islets by dendritic cells (DC) and macrophages, followed by T cells (CD4+ and CD8+). It is followed by a slower, progressive T cell destruction of the beta cells (insulitis), by 4-6 months of age (Delovitch & Singh, 1997). Thus, the T cells and the dendritic cells are key players in the immune process leading to type 1 diabetes mellitus.The dendritic cells (DC) are antigen-presenting cells which originate from the bone marrow.
After infiltrating the pancreas and undergoing antigenic maturation, DC secrete IL-12 and present the processed antigen (on their surface and in association with the major histocompatibility complex [MHC] class II) to other cells of the immune system (i.e. T cells) (see Fig 1).T cells are categorized mainly based on their immune actions, achieved via the different cytokines they secrete.
T helper 2 cells (Th2) are important in humoral immunity (activate B cells and antibody production, down regulating Th 1 cells) and secrete type 2 cytokines: interleukins 4, 5, 6, 9 and 10 (Rabinovitch, 1998) (Fig.
They have an inhibitory effect on the Th1 cells, which are destructive to the pancreatic beta cells. In the NOD mouse, it appears that the immunologic self-tolerance to pancreatic beta cells is lost. The disruption of the equilibrium between Th1 and Th2 cells in the thymus and in the periphery is believed to play a crucial role in the pathogenesis of autoimmune diabetes mellitus (Delovitch & Singh, 1997).
Once Th1 cells are produced they will secrete interferon ? (IFN ?) and IL-2, leading to the activation of macrophages and cytotoxic T cells, which are destructive to the pancreatic beta cells (Adorini, 2001). The same Th1 cells will stimulate the IgG2a autoantibodies against the islet beta cells autoantigens (Delovitch & Singh, 1997).
Autoimmune diabetes can be transferred from a diabetic NOD mouse to an unaffected mouse via T cells (Bendelac et al., 1987). NOD mice develop a spontaneous loss of T-cell tolerance to glutamic acid decarboxylase antibodies (GAD), leading to autoimmune diabetes (Kaufman et al., 1993).
Exposure to glutamic acid decarboxylase (GAD65 and GAD67) led to an increased T cell proliferation as early as 4 weeks of life in NOD mice, coinciding with the onset of insulitis (Tisch 1993). Some of the other beta-cell antigens elicited an increased immune response after a few more weeks, but there were other beta-cell antigens that did not trigger an immune reaction (for example, amylin) (Tisch 1993). To further support the central role of GAD antigen in autoimmune diabetes, the beta-cell-specific suppression of GAD expression in antisense GAD transgenic NOD mice was demonstrated to prevent the production of diabetogenic T cells and the onset of diabetes (Yoon et al., 1999) In humans, the pancreas becomes infiltrated with mononuclear cells.
Autoantibodies to insulin (IAA), glutamic acid decarboxylase (GAD) and insulinoma associated-2 antibody (IA-2) are demonstrated years before the clinical symptoms of diabetes. The presence of autoantibodies alone does not explain the development of diabetes, since it is recognized now that children born to type 1 diabetic mother with high antibody titers transferred through the umbilical cord do not develop diabetes more often than expected.
Environmental component The environment is implicated in the pathogenesis of type 1 diabetes mellitus by many studies.
Environmental factors have an important role in initiating an immune process that ultimately leads to pancreatic beta cell destruction and clinically apparent diabetes mellitus.
Many environmental factors have been proposed, including viruses (rubella, mumps or coxsackievirus B4), toxic substances and cytotoxins. Before the eradication of rubella in most countries, congenital rubella was strongly associated with the development of type 1 diabetes mellitus (Menser et al., 1978).
A recent meta analysis of observational studies has shown an association between type 1 diabetes and enterovirus infection (Yeung 2011). While some theories implicate viral infections in the pathogenesis of type 1 diabetes, a recent hypothesis argues that a decreased exposure to microbes may contribute to the current increase in autoimmune disease. This theory is known as “the hygiene hypothesis” (Gale, 2002).It is a known fact that the incidence of autoimmune diabetes follows a geographical pattern, with many studies reporting an association between type 1 diabetes and vitamin D status. A few large ecological studies describe a pattern of geographical variation, with an increased incidence of type 1 diabetes in the areas located north of the equator. Furthermore, seasons appear to also influence the incidence of type 1 diabetes, with the highest incidence during winter and the lowest during summer.
Typically, the treatment for type 1 diabetes mellitus involves insulin therapy, but in the last few years new therapies have been approved as well (for example, Symlin).
For newly diagnosed patients with autoimmune diabetes, combination therapy has been suggested in an attempt to minimize beta cell destruction and prolong pancreatic function.
The new therapeutic options include: immunotherapy, vaccines, drugs that influence T cell action, anti-inflammatory drugs (for example, one time use of anti-IL-1R drug), or long-term treatment with B cell components to induce regulatory T cells (oral or nasal insulin, insulin peptide therapy, GAD-Alum or the proinsulin DNA vaccines). Glucagon-like peptide 1-related drugs (GLP-1) could be also considered as a therapeutic option because they promote peritubular pancreatic cell growth (Von Herrath, 2010).5. Vitamin DAlthough initially described as a “vitamin”, vitamin D is now recognized to be a hormone, synthesized in the human body and exerting its action on other organs via a nuclear receptor (vitamin D receptor, VDR). Even though vitamin D can be obtained from the diet in small quantities, the main source of vitamin D is the skin. Under the direct influence of ultra violet B light (UVB light), 7-dehydrocholesterol (DHC) (provitamin D3) is converted into pre-vitamin D3, which is then further converted into cholecalciferol (vitamin D3) via thermal isomerization. Interestingly, if pre-vitamin D3 continues to be exposed to UVB, it will be converted into biologically inactive metabolites (tachysterol and lumisterol), preventing a potential UVB- induced vitamin D intoxication (Holick, 1999) The other source of vitamin D is the diet, which contains cholecalciferol (vitamin D3), originating from animal sources, and ergocalciferol (vitamin D2), deriving from plants (Holick, 1999).Regardless of their source, once they enter into the circulation, forms of inactive vitamin D3 or D2 bind to the vitamin D-binding protein (DBP) and are transported to the liver. The inactive vitamin D is activated through a 2-step hydroxylation process via two hydroxylases that belong to the cytochrome P450- dependent steroid hydroxylases (CYP450). In the liver, vitamin D undergoes the first hydroxylation at C-25 via some of the CYP 450 vitamin D 25-hydroxylases, forming calcidiol (25-hydroxyvitamin D) (Prosser & Jones, 2004).
The activity of 1?-hydroxylase in the immune cells is not under the regulation of parathyroid hormone and 1?-,25(OH)2D3, but rather under immune cytokine regulation.
A defect in the up-regulation of 1?-hydroxylase after immune stimulation is described in NOD mouse (Overbergh et al., 2000).
Extrarenal distribution of 1?-hydroxylase becomes important in understanding the extra-skeletal effects of vitamin D.VDR is part of the nuclear receptor super family of ligand-activated transcription factors, which also includes glucocorticoid, thyroid hormone and estrogen receptors. The gene for VDR is located on chromosome 12q12-14, and shows great polymorphism (Haussler et al., 1998). After 1,25 (OH)2D3 binds to VDR, it induces conformational changes that facilitate heterodimerization with the retinoid X receptor and the recruitment of nuclear receptor coactivator proteins, which then act on the chromatin.



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Comments

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    11.03.2016

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  4. Natavan_girl

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    11.03.2016