Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D deficiency is epidemic and its manifestations are protean. Vitamin D deficiency is associated with autoimmune diseases (particularly multiple sclerosis and type 1 diabetes) and has been associated with infection, allergy, asthma, and dermopathies (particularly psoriasis). Asthma may be worsened by vitamin D deficiency and correction of the deficiency has been shown to improve the manifestations of asthma. Vitamin D deficiency has been associated with multiple cancers, including those of the breast, colon, ovary, and prostate. Due mainly to increased insulin resistance but also to an impairment in insulin release, vitamin D deficiency is associated with the development of type 2 diabetes. In addition, the complications of diabetes may be worsened by vitamin D deficiency.
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PMID:Protean manifestations of vitamin D deficiency, part 2: deficiency and its association with autoimmune disease, cancer, infection, asthma, dermopathies, insulin resistance, and type 2 diabetes. 2160 12

Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism.
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PMID:[Diabetes and osteoporosis]. 2171 81

Experimental evidence indicates that vitamin D may play a role in the defense against type 1 diabetes (T1D) as well as type 2 diabetes (T2D). Epidemiological data have established a link between vitamin D deficiency and an increased incidence of both T1D and T2D, whereas early and long-term vitamin D supplementation may decrease the risk of these disorders. The protective effects of vitamin D are mediated through the regulation of several components such as the immune system and calcium homeostasis. However, an increasing amount of evidence suggests that vitamin D also affects beta cells directly thereby rendering them more resistant to the types of cellular stress encountered during T1D and T2D. This review evaluates the role of vitamin D signaling in the pathogenesis of T1D and T2D with a special emphasis on the direct effects of vitamin D on pancreatic beta cells.
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PMID:Vitamin D and diabetes: its importance for beta cell and immune function. 2188 71

Vitamin D has an important role in bone-metabolism (and its deficiency can cause preterm osteopenia, craniotabe and rickets), but it has also non-calcitropic functions. In fact, vitamin D deficiency is correlated to chronic kidney disease, respiratory infections, type 1 diabetes, psoriasis, Crohn disease and neonatal hypocalcemia. Because of the vitamin D deficiency is a global problem, its role as a drug is fundamental for the human health in all ages.
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PMID:Vitamin D as a drug. 2194 82

Vitamin D is widely known for its role in bone metabolism, but this sterol hormone also has important immunomodulatory properties. Vitamin D is produced by the conversion of D3 in the skin following UVB exposure, or after ingestion of D2 or D3. At the extremes of latitude, there is insufficient UVB intensity in the autumn and winter months for adequate synthesis of vitamin D to occur. Growing evidence implicates vitamin D deficiency in early life in the pathogenesis of nonskeletal disorders (e. g., type 1 diabetes and multiple sclerosis) and, more recently, atopic disorders. Several studies have reported higher rates of food allergy/anaphylaxis or proxy measures at higher absolute latitudes. Although causality remains to be determined, these studies suggest a possible role for sunlight and/or vitamin D in the pathogenesis of food allergy/anaphylaxis.
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PMID:Latitude, sunlight, vitamin D, and childhood food allergy/anaphylaxis. 2200 65

Vitamin D plays a key role in calcium-phosphorus homeostasis and bone metabolism, but it is also involved in numerous others tissues. Vitamin D deficiency among pregnant women is frequent in many populations over the world. It is associated with an increased risk of preeclampsia, gestational diabetes mellitus, and caesarean section. Consequences in newborns are low birth weight, neonatal rickets, a risk of neonatal hypocalcemia, asthma and/or type 1 diabetes. Therefore, prevention of vitamin D deficiency among pregnant women is essential. The currently recommended supplementation amount of vitamin D is not sufficient to maintain a value of 25 hydroxy vitamin D above 30 ng/ml, during pregnancy. Randomized controlled trials during pregnancy are necessary to evaluate the amount of vitamin D sufficient to avoid the consequences of vitamin D deficiency.
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PMID:[Vitamin D and pregnancy]. 2200 74

Although specific viruses have been associated with autoimmune diseases, none fulfill Koch's criteria of causation. The etiologies of such diseases appear to be complex and multifactorial. For example, one might propose that the etiology of type 1 diabetes mellitus results from a toxic metabolite of nitrosamines during an enteroviral infection. Multiple sclerosis might result from a cascade of events involving several herpes virus infections activated during periods of vitamin D deficiency. We encourage investigators to consider Rotman's sufficient-component causal model when developing hypotheses for testing for the etiology of chronic diseases. Delineating the web of causation may lead to additional strategies for prevention and treatment of several autoimmune diseases.
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PMID:Viruses and vitamin D in the etiology of type 1 diabetes mellitus and multiple sclerosis. 2211 99

Circulating maternal concentrations of hormonally active vitamin D [calcitriol, 1,25(OH)(2)D] rise early in the first trimester, doubling by the end of the third trimester. The early rise in calcitriol is believed to be necessary for enabling the immunological adaptation by the mother required for the maintenance of a normal pregnancy. This immunological adaptation is characterized by downregulation of the T helper type 1 (Th1) cytokine responses and a shift towards domination by the Th2 type responses. Attenuation of the Th1-mediated immune response is one of the influences of calcitriol on regulatory T cell activity and dendritic cell maturation. There is accumulating evidence that vitamin D supplementation may be able to prevent the immune maladaptation and loss of tolerance that occur in preeclampsia, with evidence for an association obtained from various types of observational studies and clinical trials. There is also evidence from observational studies for potential long-term programming effects of vitamin D supplementation on immunological diseases (such as type 1 diabetes and allergic diseases), with evidence supporting the role of active vitamin D as a potent immunomodulator. This paper highlights the complex effects of active vitamin D on immunomodulation with long-term implications for the risk of immunological diseases. It is suggested that it is essential to avoid vitamin D deficiency during pregnancy, and while accumulating evidence suggests important benefits of further increases in the intake, further research is required to fully establish the influence of high dosages.
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PMID:Preventing vitamin D deficiency in pregnancy: importance for the mother and child. 2212 34

Vitamin D deficiency and insufficiency is common in children. Vitamin D deficiency is defined as a 25-hydroxyvitamin D <20 ng/mL and insufficiency as 21-29 ng/mL. The major sources of vitamin D are sun exposure, diet, and supplements. In young children, vitamin D deficiency causes a mineralization defect of the skeleton, resulting in rickets. Vitamin D deficiency has been linked to many chronic diseases, including multiple sclerosis, type 1 diabetes, infectious diseases, heart disease, and type 2 diabetes. In utero vitamin D deficiency increases risk for preeclampsia and the need for a cesarean section. Children living at higher latitudes and who are presumed to be at increased risk for vitamin D deficiency are at higher risk for developing type 1 diabetes and multiple sclerosis later in life. The Institute of Medicine recommends that children 0-1 year and 1-18 years need 400 and 600 IU/d, respectively, of vitamin D for maximal skeletal health. The Endocrine Society's Clinical Guidelines recommended that to prevent and treat vitamin D deficiency, children 0-1 year and 1-18 years need 400-1000 and 600-1000 IU/d, respectively.
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PMID:The D-lightful vitamin D for child health. 2217 24

Maternal adaptations during pregnancy and lactation appear to provide calcium to fetus and neonate without relying on vitamin D or calcitriol. Consequently, the blood calcium, calciotropic hormones, and skeleton appear normal at birth in the offspring of mothers who are severely vitamin D deficient or who lack calcitriol or its receptor. It remains unclear whether skeletal or extraskeletal problems will develop postnatally from exposure to vitamin D deficiency in utero. During the neonatal period, calcitriol-stimulated intestinal calcium absorption becomes the dominant mechanism of calcium delivery. The vitamin D-deficient neonate is at risk to develop hypocalcemia, rickets, and possibly extraskeletal disorders (e.g., type 1 diabetes). Breastfed babies are at higher risk of vitamin D deficiency because normally little vitamin D or 25-hydroxyvitamin D passes into breast milk. Dosing recommendations during pregnancy and lactation should ensure that the baby is born vitamin D sufficient and maintained that way during infancy and beyond.
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PMID:The role of vitamin D in pregnancy and lactation: insights from animal models and clinical studies. 2248 92


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