Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D(3) from cutaneous and dietary sources because of its deposition in body fat compartments.

Sunscreens block the cutaneous absorption of UV-B radiation and prevent sunburning, premature aging, and cancer of the skin. Inasmuch as UV-B radiation is also responsible for the photosynthesis of vitamin D3, we investigated the effect of sunscreens on the cutaneous formation of vitamin D3 in vivo and in vitro. Eight normal subjects, four of whom had been protected with the sunscreen para-aminobenzoic acid (sun protection factor 8), were exposed to one minimal erythema dose of UV radiation. The mean serum vitamin D3 concentration increased from 1.5 +/- 1.0 (+/- SEM) to 25.6 +/- 6.7 ng/mL in unprotected subjects, whereas it was 5.6 +/- 3.0 and 4.4 +/- 2.4 ng/mL at these times in the subjects who were protected with para-aminobenzoic acid. Para-aminobenzoic acid also prevented the photoisomerization of 7-dehydrocholesterol to previtamin D3 in human skin slices in vitro. These results indicate that the sunscreen interferred with the cutaneous production of vitamin D3.

IntroductionTransport of vitamin D3 from its sites of cutaneous synthesis into the circulation has been assumed to be via the plasma vitamin D binding protein (DBP). We studied vitamin D transport from the skin in seven healthy volunteers who received whole body irradiation with 27 mJ /cm2 dosage of ultraviolet B light (290-320 nm). Samples of venous blood were collected serially in EDTA and immediately chilled. In KBr, plasma samples were ultracentrifuged to provide a rapid separation of proteins of density < and > 1.3 g/ml. Upper and lower phases and serial fractions were analyzed for vitamin D3 (extraction, HPLC), cholesterol (enzyme assay), and human DBP (hDBP) (radial immunodiffusion). Total plasma vitamin D (basal level < 1 ng/ml) increased by 10 h and peaked at 24 h (9 ± 1 ng/ml). 98% of the D3 remained at the density > 1.3 layers for up to 7 d, whereas cholesterol (> 85%) was detected at density < 1.3 and all of the hDBP was at density > 1. Vitamin D is a precursor ofa renal steroid hormone, 1 ,25-dihydroxyvitamin D (1). This precursor, however, cannot be provided by enzymatic synthesis. Its supply depends on ultraviolet (UV) irradiation ofthe skin or absorption from the diet. Since few natural foodstuffs contain much vitamin D (2), observers consider the endogenous, cutaneous production of cholecalciferol to be the physiological mechanism of precursor supply (2-5).Distinct differences are recognized for the cutaneous synthesis vs. diet-derived supply of vitamin D (2, 6). A more efficient and sustained supply of vitamin D is associated with UV irradiation of the skin or parenteral administration of vitamin D (2, 6). In contrast, oral vitamin D consumption leads to rapid but less sustained availability of sterol and a similar pattern of increase in the hepatic metabolite, 25-hydroxycholecalciferol (2, 6-9).Many studies have addressed the mode of vitamin D transport after oral consumption (6), but no direct studies of the plasma transport of cutaneously-derived vitamin D are reported. It has been assumed that vitamin D synthesized in skin enters the blood stream on the plasma binding protein for vitamin D and its metabolites (DBP)' and this assumption is based on in vitro studies ofthe relative potency of vitamin D in binding to DBP as compared with 7-dehydroxycholesterol, lumisterol, tachysterols3 and pre-D3 (10-12). However, other plasma carriers are recognized and some facilitate hepatic ( 13-15) and hepatocyte (16) Cutaneous irradiation. Seven subjects were exposed to 27 mJ/cm2 of . Venous blood samples were taken at baseline, 10,24, 72, and 168 h after the UV-B exposure, immediately 1. Abbreviation used in this paper: DBP, vitamin D binding protein.

No abstract

No abstract