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2004; Dakovska & Kovacheva 2003; Zella, McCary, and DeLuca 2003).
In addition to skeletal functions, insulin resistance, and glucose intolerance, substantial volumes of research indicate that hypovitaminosis D. also contributes to systemic inflammation by virtue of more than 200 distinct gene control functions of 1,25- dihydroxyvitamin D (Holick 2007). While the etiology of rheumatoid arthritis relates to skeletal issues, the available evidence of the role of hypovitaminosis D. In systemic inflammation strongly suggests that even aspects of skeletal health are directly attributable to inflammatory responses moderated by adequate absorption of vitamin D as well (Barger-Lux, Heaney, Dowell, et al. 1998).
This anti-inflammatory function of vitamin D has been implicated in diseases affecting numerous tissues including the brain, prostate, breasts, and colon tissues, among others, all of which have vitamin D receptors and are responsive to 1,25- dihydroxyvitamin D (Holick 2007; Mathieu & Adorini 2008; Pittas, Harris, Stark, et al. 2007). The individual beneficial effects of vitamin D and calcium in isolation have not been adequately investigated by previous research, either in relation to systemic inflammation (Pittas, Harris, Stark, et al. 2007; Zittermann, Schleithoff, Tenderich, et al. 2003) or in relation to insulin resistance and glucose tolerance (Barger-Lux, Heaney, Dowell, et al. 1998; Pittas, Dawson-Hughes, Hu, et al. 2006).
Even more importantly with respect to the proposed study, systemic inflammation markers including tumor necrosis factor (TNF) and other crucial immune mediators are known to be contributors rather than consequences of diabetes since they are associated with inflammatory changes that precede the onset of diabetes (Palomer, Gonzalez- (Clemente, Blanco-Vaca, et al. 2008). This suggests that hypovitaminosis D. may contribute to the development of diabetes mellitus via two distinct mechanisms: first, by increasing insulin resistance and decreasing glucose tolerance; second, by it implication with respect to direct tumor necrosis as well (Palomer, Gonzalez-Clemente, Blanco-Vaca, et al. 2008). Avenues of future research into the relationship between hypovitaminosis D. And...
2007), as well as the inability to separate the individual effects of vitamin D and calcium (Pittas, Dawson-Hughes, Hu, et al. 2006; Pittas, Harris, Stark, et al. 2007).
References
Barger-Lux MJ, Heaney RP, Dowell S, Chen TC, Holick MF. "Vitamin D and its Major Metabolites: Serum Levels after Graded Oral Dosing in Healthy Men." Osteporos Int 1998; 8:222-30.
Chiu KC, Chu a, Go VL, Saad MF. "Hypovitaminosis D. Is Associated with Insulin Resistance and Beta Cell Dysfunction." Am J. Clin Nutr 2004; 79:820-5.
Dakovska L, Kovacheva R. The Effect of Vitamin D3 on Insulin Secretion and Peripheral Insulin Sensitivity in Type 2 Diabetic Patients. Int J. Clin Pract 2003; 57: 258-26
Holick MF. "Vitamin D Deficiency." N. Engl J. Med 2007; 357:266-81. Mathieu C, Adorini L. "The Coming of Age of 1,25-Dihydroxyvitamin D (3) Analogs as Immunomodulatory Agents." Trends Mol Med 2002; 8: 174-9.
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