UVB radiation increases serum vitamin D level expressed as 25-hydroxyvitamin-D(3) (25(OH)D), but the influence of skin pigmentation, baseline 25(OH)D level, and total cholesterol has not been well characterized. To determine the importance of skin pigmentation, baseline 25(OH)D level, and total cholesterol on 25(OH)D production after UVB exposure, 182 persons were screened for 25(OH)D level. A total of 50 participants with a wide range in baseline 25(OH)D levels were selected to define the importance of baseline 25(OH)D level. Of these, 28 non-sun worshippers with limited past sun exposure were used to investigate the influence of skin pigmentation and baseline total cholesterol. The participants had 24% of their skin exposed to UVB (3 standard erythema doses) four times every second or third day. Skin pigmentation and 25(OH)D levels were measured before and after the irradiations. Total cholesterol was measured at baseline. The increase in 25(OH)D level after UVB exposure was negatively correlated with baseline 25(OH)D level (P<0.001) and positively correlated with baseline total cholesterol level (P=0.005), but no significant correlations were found with constitutive or facultative skin pigmentation. In addition, we paired a dark-skinned group with a fair-skinned group according to baseline 25(OH)D levels and found no differences in 25(OH)D increase after identical UVB exposure.

A new thiobarbituric acid (TBA) method for selectively determining free malondialdehyde (MDA) and lipid hydroperoxides is described. Partitioning of MDA and hydroperoxides in a Bligh and Dyer extraction was studied with pure substances. It was shown that MDA was present in the methanol-water phase exclusively, and the hydroperoxides (polar as well as nonpolar) were found in the chloroform phase. Therefore, the TBA test on these phases determines MDA directly present in the sample and the MDA formed during a ferric ion.catalyzed cleavage of hydroperoxides, respectively. The MDA present in the methanol-water phase was not hound to amino groups. Hydroperoxide values obtained with the present method corresponded well with a eolarimetric determination of peroxides and showed better linearity for higher amounts of hydroperoxides. The possibility of using an iron chelator for preventing hydroperoxide eleavage during the TBA reaction, making the determination selective for MDA without Bligh and Dyer extraction, was investigated. The iron chelator did not completely inhibit peroxide cleavage; therefore, it is necessary to perform the extraction berate the TBA determination. The method is suitable for samples with low fat content such as cod mince.The most common method for measuring oxidative changes in biological samples and food products is the thiobarbituric acid (TBA} test based on a spectrophotometric quantitation of a red-violet complex formed with malondialdehyde (MDA) (1}. This method determines both the MDA already formed naturally from hydroperoxide cleavage, and the secondary release due to the heating step in the TBA reaction. Therefore, the TBA values obtained are dependent on methodology and not easily reproduced between laboratories. The TBA test is often used for determination of lipid peroxides (2-4), but the present methods measure both free MDA and lipid peroxides. Several investigators have reported selective methods for determining free MDA by HPLC (5-9). Furthermore, HPLC has often been used for determining the MDA-TBA adduct selectively (10-12). However, the adduct measured can arise from both peroxides and free MDA.In samples with low lipid content the TBA determination on tipids isolated by a Bligh and Dyer extraction (13) has been suggested to increase the sensitivity (14), but the authors did not elucidate whether the reaction was due to MDA, hydroperoxides or both. Neither was the possible loss of MDA by evaporation accounted for.Albro et at. (] 5) described a method for measuring free MDA and "labile lipid peroxidation products" selectively. This method, however, is based on the fact that lipids Presented in part at the AOCS Annual Meeting in New Orleans, Louisiana, in May 1987. co-precipitate when proteins are precipitated with trichloroacetic acid (TCA) in a microsomal system. The method, therefore, is not applicable for most food products and oils.A selective TBA determination of free MDA and hydroperoxides, measured as MDA formed during the TBA reaction, has not been reported previously. T...

OBJECTIVETo evaluate vitamin D as a predictor of all-cause and cardiovascular mortality and risk of progression to micro- or macroalbuminuria in type 2 diabetic patients.RESEARCH DESIGN AND METHODSIn a longitudinal observational follow-up study, 289 type 2 diabetic patients with normoalbuminuria (n = 172), microalbuminuria (n = 73), and macroalbuminuria (n = 44) at baseline were followed for a median (range) of 15.0 (0.2–23) years. Mean ± SD age was 54 ± 9 years. Plasma 25-hydroxyvitamin D3 levels were determined by high-performance liquid chromatography/tandem mass spectrometry on baseline samples. Severe vitamin D deficiency was defined as the lower 10th percentile (<13.9 nmol/l).RESULTSMedian (range) vitamin D level was 35.7 (5–136.7) nmol/l. Vitamin D levels were not associated with age, sex, estimated glomerular filtration rate, urinary albumin excretion rate (UAER), or A1C at baseline, but low levels were weakly associated with elevated systolic blood pressure (R = 0.13, P = 0.03). During follow-up, 196 (68%) patients died. All-cause mortality was increased in patients with severe vitamin D deficiency (hazard ratio 1.96 [95% CI 1.29–2.98]). The association persisted after adjustment for UAER, A1C, diabetes duration, and conventional cardiovascular risk factors (2.03 [1.31–3.13]). Severe vitamin D deficiency was associated with increased cardiovascular mortality (1.95 [1.11–3.44]), and the association persisted after adjustment (1.90 [1.15–3.10]). Severe vitamin D deficiency at baseline did not predict progression to micro- or macroalbuminuria.CONCLUSIONSIn type 2 diabetic patients, severe vitamin D deficiency predicts increased risk of all-cause and cardiovascular mortality, independent of UAER and conventional cardiovascular risk factors. Whether vitamin D substitution improves prognosis remains to be investigated.

OBJECTIVETo evaluate vitamin D as a predictor of all-cause mortality, progression from normoalbuminuria to micro- or macroalbuminuria, and the development of background or proliferative retinopathy in patients with type 1 diabetes.RESEARCH DESIGN AND METHODSA prospective observational follow-up study in which an inception cohort of type 1 diabetic patients was followed from onset of diabetes diagnosed between 1979 and 1984. Plasma vitamin D [25(OH)D3] levels were determined by high performance liquid chromatography/tandem mass spectrometry in 227 patients before the patients developed microalbuminuria. Values equal to or below the 10% percentile (15.5 nmol/L) were considered severe vitamin D deficiency.RESULTSMedian (range) vitamin D was 44.6 (1.7–161.7) nmol/L. Vitamin D level was not associated with age, sex, urinary albumin excretion rate (UAER), or blood pressure. During follow-up, 44 (18%) patients died. In a Cox proportional hazards model, the hazard ratio for mortality in subjects with severe vitamin D deficiency was 2.7 (1.1–6.7), P = 0.03, after adjustment for UAER, HbA1c, and conventional cardiovascular risk factors (age, sex, blood pressure, cholesterol, smoking). Of the 220 patients, 81 (37%) developed microalbuminuria and 27 (12%) of these progressed to macroalbuminuria. Furthermore, 192 (87%) patients developed background retinopathy, whereas 34 (15%) progressed to proliferative retinopathy. Severe vitamin D deficiency at baseline did not predict the development of these microvascular complications.CONCLUSIONSIn patients with type 1 diabetes, severe vitamin D deficiency independently predicts all-cause mortality but not development of microvascular complications in the eye and kidney. Whether vitamin D substitution in type 1 diabetic patients can improve the prognosis remains to be investigated.

The increase in 25(OH)D depends mainly on the UVB dose; however, for small UVB doses the area of irradiated body surface is important.