Vitamin D3 Up-Regulated Protein 1 (VDUP1) and the Immune System

2013 ◽  
pp. 57-70
Author(s):  
Hyun Suh ◽  
Haiyoung Jung ◽  
Young Park ◽  
Inpyo Choi
Keyword(s):  
Immune System ◽  
Vitamin D3

scholarly journals Endocrinology, Vitamin D and the UK’s Covid-19 Disaster

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A274-A275
Author(s):  
David Coussmaker Anderson ◽  
David S Grimes
Keyword(s):  
Vitamin D ◽  
Immune System ◽  
Vitamin D3 ◽  
Influenza Pandemic ◽  
Endocrine System ◽  
Endocrine Function ◽  
Food Sources ◽  
Endocrine Control ◽  
Blood Calcium ◽  
Ionic Calcium

Abstract The formation of cholecalciferol (Vitamin D3) in skin depends on solar UVB to break the B ring of 7-dehydrocholesterol. Its discovery more than a century ago resulted from the identification of rickets as due to deficient sunshine in latitudes far from the equator, exacerbated by the air pollution, factory work and indoor living. Rickets resulted from defective endocrine control of blood calcium, and was accompanied by epidemic tuberculosis from failure of the D3-dependent first-line immune system. The influenza pandemic of 2018 revealed the need for D3 to fight viruses. Half a century later the systemic hormone role of 1,25(OH)D3 of renal origin, under control of PTH, was a major stimulus to understanding the mechanism of action via the VDR-RXR heterodimer. It was soon realised that 1,25(OH)D3 is also produced and acts locally in many organs and tissues provided that there are adequate reserves of the (protein-bound) blood storage form, 25(OH)D. This is the common pool for 1-hydroxylation by any cells that need local activation of VDR for induction of specific genes. In the case of the immune system, the trigger is foreign proteins recognised as ‘non-self’. Local production and action of 1,25(OH)D, and then its local destruction by 24-hydroxylation must all occur below the ‘endocrine radar’, so as not to interfere with systemic calcium control. Coronaviruses through their ‘spike’ protein are internalised by interacting with the ACE-2 receptor, which in turn is down-regulated by Vitamin D. In the process, 25(OH)D is hydroxylated to the active 1,25(OH)D, which must later be degraded to 1,24,25(OH)D. So it is to be expected that when 25(OH)D reserves are low at the onset of infection, they will fall further, allowing virus to enter the cells and trigger a cytokine storm and other damage. Blood PTH will rise to claim any residual 25(OH)D for the dominating systemic role in calcium homeostasis. It follows that intake of vitamin D3 should always be much more than the minimum claimed by the globally-active endocrine system. Unfortunately, the UK’s Specialised Advisory Committee on Nutrition (SACN), does not recognise this. It is dominated by nutritionists, even though food sources of D3 are for most non-existent, and of D2, the vegetable substitute, highly variable. The 400IU of D3 reluctantly recommended for those ‘at risk’, based on endocrinology alone, is grossly inadequate; 4,000IU daily is needed to maintain a blood 25(OH)D at more than 30 ng/ml (75 nmol/l), and provide sufficient reserve for its many autocrine and paracrine functions. The dangers of letting the dominant endocrine function of 1,25(OH)D in ionic calcium control dictate the level of D3 supplements, have once again been underlined by the Covid-19 disaster.

scholarly journals Effects of vitamin D3 and methylenebisphosphonate on immune system of rats at disuse osteoporosis

2013 ◽  
Vol 7 (3) ◽  
pp. 21-32
Author(s):  
V. M. Riasnyi ◽  
◽  
L. I. Apukhovska ◽  
N. N. Veliky ◽  
I. O. Shymanskyy ◽  
...  
Keyword(s):  
Immune System ◽  
Vitamin D3 ◽  
Disuse Osteoporosis

1216: Oral Treatment with a Vitamin D3 Analogue Shows Anti Inflammatory Effects and Reduces Bladder Overactivity in Rodent Models of Chronic Cystitis

2005 ◽  
Vol 173 (4S) ◽  
pp. 330-330
Author(s):  
Peter Zvara ◽  
Fabio Benigni ◽  
Enrico Baroni ◽  
Marija Zecevic ◽  
Antonia Monno ◽  
...  
Keyword(s):  
Vitamin D3 ◽  
Oral Treatment ◽  
Rodent Models ◽  
Chronic Cystitis ◽  
Anti Inflammatory

Vitamin D3 supplementation improves glycemic control in type 2 diabetic patients: Results from an Italian clinical trial

2020 ◽  
pp. 1-10
Author(s):  
Giuseppe Derosa ◽  
Angela D’Angelo ◽  
Chiara Martinotti ◽  
Maria Chiara Valentino ◽  
Sergio Di Matteo ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Metabolic Control ◽  
Vitamin D3 ◽  
Therapy Group ◽  
Hypoglycemic Agents ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

Abstract. Background: to evaluate the effects of Vitamin D3 on glyco-metabolic control in type 2 diabetic patients with Vitamin D deficiency. Methods: one hundred and seventeen patients were randomized to placebo and 122 patients to Vitamin D3. We evaluated anthropometric parameters, glyco-metabolic control, and parathormone (PTH) value at baseline, after 3, and 6 months. Results: a significant reduction of fasting, and post-prandial glucose was recorded in Vitamin D3 group after 6 months. A significant HbA1c decrease was observed in Vitamin D3 (from 7.6% or 60 mmol/mol to 7.1% or 54 mmol) at 6 months compared to baseline, and to placebo (p < 0.05 for both). At the end of the study period, we noticed a change in the amount in doses of oral or subcutaneous hypoglycemic agents and insulin, respectively. The use of metformin, acarbose, and pioglitazone was significantly lower (p = 0.037, p = 0.048, and p = 0.042, respectively) than at the beginning of the study in the Vitamin D3 therapy group. The units of Lispro, Aspart, and Glargine insulin were lower in the Vitamin D3 group at the end of the study (p = 0.031, p = 0.037, and p = 0.035, respectively) than in the placebo group. Conclusions: in type 2 diabetic patients with Vitamin D deficiency, the restoration of value in the Vitamin D standard has led not only to an improvement in the glyco-metabolic compensation, but also to a reduced posology of some oral hypoglycemic agents and some types of insulin used.

Vitamin D3 hochdosiert dreimal jährlich reduziert Frakturrate

Praxis ◽  
2003 ◽  
Vol 92 (47) ◽  
pp. 2021-2022
Author(s):  
K. Eichler
Keyword(s):  
Vitamin D3

Learned Placebo Effects in the Immune System

2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Associative Learning ◽  
Placebo Response ◽  
Immunosuppressive Drug ◽  
Immune Functions ◽  
Placebo Effects ◽  
New Therapeutic Approaches ◽  
Biological Variables ◽  
Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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