Yan Chun Li, Juan Kong, Minjie Wei, Zhou-Feng Chen, Shu Q. Liu, Li-Ping Cao
Submitter: Hans Peter Rutz | firstname.lastname@example.org
Paul Scherrer Institute, Switzerland
Published August 20, 2002
In a brilliant piece of work, Li et al. have shown that the active metabolite of Vitamin D, 1,25-dihydroxyvitamin D3 (calcitriol) is an important negative regulator of the renin-angiotensin system and hence, that calcitriol is required in sufficient amounts so as to facilitate maintenance of electrolyte balance, volume and moderate blood pressure (1).
Now, considering that: in obesity, the renin-angiotensin system is up -regulated (2,3); bioavailability of vitamin D3 (cholecalciferol) is reduced due to its deposition in body fat compartments, causing obesity- associated hypovitaminosis D (4); there is diabetes and a myriad of problems with global implications (5); that: in vitamin D-deficient rats (6-8), rabbits (9) and humans (10-13), there is impaired insulin secretion and glucose tolerance; that: calcitriol levels are inversely correlated to blood pressure, VLDL trigycerides, triglyceride removal, and insulin sensitivity (14); and considering that: after calcitriol administration, there is a stimulation of insulin secretion (15-17), a reversal of insulin resistance and hyperinsulinemia (18,19) and thus, a correction of glucose intolerance in vitamin D-deficiency; that: calcitriol corrects lipid abnormalities (20,21); and that: calcitriol is responsible for maintaining a balanced renin-angiotensin system and normal blood pressure (1), it is a rather obvious conclusion that hypovitaminosis D contributes to the development of the metabolic syndrome X (22,23), which thus is both treatable and preventable by appropriate supplementation of vitamin D, as has been suggested earlier based on preliminary data (14,24). Optimized recommendations for preventive and therapeutic substitution with cholecalciferol and/or calcitriol, and optimal target plasma levels for the various metabolites of vitamin D must now be worked out.
Hans Peter Rutz, email@example.com Division of Life Sciences, Paul Scherrer Institute, CH-5232 Villigen PSI, Switzerland
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