There are approximately 316,000 individuals in the United States with tetraplegia and paraplegia of which an estimated 265,000 require ongoing care. It was previously reported that there is impaired carbohydrate metabolism in individuals with spinal cord injury (SCI). Our study analyzed the effect of dietary carbohydrate on plasma glucose, insulin, and triglycerides in and whether differences exist based on tetraplegia and paraplegia. There were no significant differences in percent of calories from dietary carbohydrate in individuals with tetraplegia and paraplegia compared to able‐bodied controls. Triglycerides and insulin levels were highest in individuals with lesions to the upper thoracic region of the spine and are significantly different from controls.

Our objective was to quantify the absorption and conversion to retinoids of a 1.01-nmol, 3.7-kBq oral dose of C-14-beta-carotene in 8 healthy adults. The approach was to quantify, using AMS, the elimination of C-14 in feces for up to 16 d after dosing and in urine for up to 30 d after dosing. The levels of total C-14 in undiluted serial plasma samples were measured for up to 166 d after dosing. Also, the levels of C-14 in the retinyl ester (RE), retinol (ROH), and beta-carotene fractions that were isolated from undiluted plasma using HPLC were measured. The apparent digestibility of the C-14 was 53 +/- 13% (mean +/- SD), based on the mass balance data, and was generally consistent with the area under the curve for zero to infinite period of C-14 that was eliminated in the feces collections made up to 7.5 d after dosing. Metabolic fecal elimination, calculated as the slope per day (% C-14-dose/collection from d 7.5 to the final day), was only 0.05 +/- 0.02%. The portion of the C-14 dose eliminated via urine was variable (6.5 +/- 5.2%). Participants [except participant 6 (P6)] had a distinct plasma peak of C-14 at 0.25 d post-dose, preceded by a shoulder at similar to 0.1 d, and followed by a broad C-14 peak that became indistinguishable from baseline at similar to 40 d. Plasma C-14-RE accounted for most of the absorbed C-14 early after dosing and P1 had the longest delay in the first appearance of C-14-RE in plasma. The data suggest that plasma RE should be considered in estimating the ROH activity equivalent of ingested beta-carotene. J. Nutr. 139. 1480-1486, 2009.

Because lycopene is a powerful biological antioxidant, its delivery to humans is of major concern. cis-Lycopene isomers are more bioavailable than the all-trans isomers and thus more efficiently absorbed. Tangerine tomatoes, whose lycopene isomeric content is almost all tetra-cis, provide a useful food source for comparing cis- and trans-isomer absorption. Tangerine tomatoes were processed into sauce in the Univ. of California, Davis Pilot Plant for subsequent use in a human feeding study described in another publication. Samples were taken at several stages during processing and carotenoids extracted and analyzed for carotenoid-isomer profiles and concentrations. Analyses showed that total lycopene concentration decreased considerably during the 1st step of processing, which included heating and juicing operations. Processing resulted in a large decrease in tetra-cis lycopene concentration accompanied by increases in trans- and other cis-lycopene isomers.

Most studies show low correlations between dietary intake and serum concentrations of lycopene. We hypothesized that adjusting these terms with factors reported to influence fat‐soluble vitamin concentrations would improve this correlation. We measured dietary intakes of lycopene in 47 healthy adults with spinal cord injuries by three‐day (3D) dietary record and food frequency (FFQ). Serum lycopene was measured by reversed‐phase HPLC with diode array detection. Cholesterol, triacylglycerol, protein, and glucose concentrations were measured spectrophotometrically. C‐reactive protein was measured by ELISA. Data was analyzed with SAS. Unadjusted data gave low correlations between dietary and serum lycopene, r2 = +0.11 for 3D, +0.24 for FFQ. Adjusting data for triacylglycerol, protein, glucose and C‐reactive protein did not improve these correlations significantly. However, adjusting serum lycopene with total cholesterol concentrations resulted in significantly higher correlations, r2 = +0.65, +0.86 for 3D and FQ, respectively. We did not expect that cholesterol would have such a powerful influence. However, it is common to adjust concentrations of another fat‐soluble antioxidant, alpha‐tocopherol, by cholesterol. Our results suggest that improved correlations between dietary and serum lycopene can be attained by normalizing for cholesterol, which should aid in evaluating the impact of dietary interventions designed to increase lycopene concentrations.

BACKGROUND:We recently observed that ethanol feeding impairs 10-formyltetrahydrofolate (10-FTHF) dehydrogenase (EC 1.5.1.6.) and 10-FTHF hydrolase activity in rats. In the present study, we explored the effects of folate deficiency or sufficiency combined with alcoholic intake on 10-FTHF and possible mechanisms by which chronic ethanol ingestion produces folate deficiency. METHODS:Sprague-Dawley rats were fed either folate-sufficient (FS) or folate-deficient (FD) diets; with or without ethanol (E) for four weeks. Hepatic 10-FTHF dehydrogenase and hydrolase activity, plasma folate and homocysteine were measured at baseline and after feeding experimental diets. RESULTS:Liver weight increased slightly with either folate deficiency or ethanol consumption. In rats fed the folate-sufficient diet with ethanol (FSE), plasma folate was decreased slightly (p<0.05) and plasma homocysteine elevated compared to rats fed the FS diet without ethanol. Ethanol did not affect plasma folate and plasma homocysteine in FD rats. Red-blood cell (RBC) folate was increased similarly in rats by ethanol feeding (FSE and FDE>FS and FD). Feeding folate deficient or ethanol (FSE, FD and FDE) diets depressed hepatic activities of 10-FTHF dehydrogenase, which catalyzes the oxidative deformylation of 10-FTHF to tetrahydrofolate (THF) and carbon dioxide. Rats consuming the FDE diet had the lowest enzyme activities of the experimental groups, implying that folate deficiency and ethanol consumption each affect enzyme activity. CONCLUSIONS:We confirm that ethanol decreases hepatic 10-FTHF dehydrogenase activity and show that this decrease occurs irrespective of folate status. This shows that modulation of 10-FTHF is one possible mechanism by which ethanol intake decreases folate status and affects one-carbon metabolism.

The final step of triacylglycerol biosynthesis is catalyzed by acyl CoA:diacylglycerol acyltransferase (DGAT) enzymes. The two known DGATs, DGAT1 and DGAT2, are encoded by unrelated genes. Although both DGAT1 and DGAT2 knockout mice have reduced tissue triacylglycerol contents, they have disparate phenotypes, prompting us to investigate whether the two enzymes have unrecognized functional differences. We now report that DGAT1 exhibits additional acyltransferase activities in vitro, including those of acyl CoA:monoacylglycerol acyltransferase (MGAT), wax monoester and wax diester synthases, and acyl CoA:retinol acyltransferase (ARAT), which catalyze the synthesis of diacylglycerols, wax esters, and retinyl esters, respectively. These activities were demonstrated in in vitro assays with membranes from insect cells or homogenates from COS7 cells overexpressing DGAT1. Wax synthase and ARAT activities were also demonstrated in intact COS7 cells expressing DGAT1. Additionally, cells and tissues from DGAT1-deficient mice exhibited reduced ARAT activity, and the mice had increased levels of unesterified retinol in their livers on a high-retinol diet. Our findings indicate that DGAT1 can utilize a variety of acyl acceptors as substrates in vitro and suggest that these activities may be relevant to the in vivo functions of DGAT1.

This human study was conducted to evaluate the effect of chronic alcohol consumption on plasma concentrations of lipid and the antioxidative system in 44 Korean alcoholics and 45 age-, sex-, and nationality-matched nonalcoholic subjects. Plasma triacylglycerols and atherogenic index were higher in alcoholics than in control subjects. Plasma total cholesterol was not different among groups, but plasma high-density lipoprotein cholesterol was lower in alcoholics. There were positive correlations between ethanol consumption and plasma lipid peroxide and atherogenic index in all subjects; there were negative correlations between ethanol consumption and plasma high-density lipoprotein cholesterol in all subjects. There were no significant differences between alcoholics and control subjects in plasma concentrations of α-tocopherol, although plasma α-tocopherol/lipid tended to be lower in alcoholics. Plasma retinol was lower in alcoholics. These results suggest that chronic ethanol consumption can contribute to increased risk for vascular diseases in Korean alcoholics.

Vascular complications such as atherosclerosis hinder the treatment of diabetes. We hypothesized that moderate supplementation with β-carotene might help prevent diabetic vascular complications through its impact on lipid metabolism. Forty Sprague-Dawley rats were fed AIN-76 control diet, or the same diet supplemented with β-carotene (7.2 mg/kg diet) for 3 weeks, then diabetes was induced in half of the rats by streptozotocin. Diabetic and normal rats were fed the experimental diets for 2 more weeks. β-Carotene did not reduce blood glucose in diabetic rats. Plasma triglycerides were increased by diabetes, but reduced by β-carotene. Plasma total cholesterol was increased by diabetes. High-density lipoprotein cholesterol did not differ between groups. However, the atherogenic index of diabetic rats was higher than that of control rats, and β-carotene feeding decreased it. Fecal excretion of cholesterol and coprostanone was decreased by diabetes, and β-carotene tended to increase this excretion. Fecal excretion of bile acid showed similar tendencies, as did neutral steroids. These results suggest that dietary supplementation with β-carotene may reduce plasma triglycerides and other indices of diabetic risk, and thus may decrease the incidence of diabetic vascular complications through the normalization of lipid metabolism in patients with diabetes.

We used reversed-phase HPLC with diode array detection to simultaneously measure the major isoforms of vitamins A, E, and the carotenoids in serum from 55 healthy people with spinal cord injuries. Typically, the method measured retinol (vitamin A), alpha-tocopherol (vitamin E) and beta-carotene, alpha-carotene, lutein, lycopene, and cryptoxanthin (carotenoids). gamma-Tocopherol (vitamin E), 25-hydroxycalciferol (vitamin D), and the carotenoid zeaxanthin could also be measured when they were present in high concentrations. Healthy people with spinal cord injuries were more likely than similar people without injuries to have low concentrations of alpha-tocopherol, and to a lesser extent retinol and beta-carotene.

Dietary triacylglycerols are a major source of energy for animals. The absorption of dietary triacylglycerols involves their hydrolysis to free fatty acids and monoacylglycerols in the intestinal lumen, the uptake of these products into enterocytes, the resynthesis of triacylgylcerols, and the incorporation of newly synthesized triacylglycerols into nascent chylomicrons for secretion. In enterocytes, the final step in triacylglycerol synthesis is believed to be catalyzed primarily through the actions of acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes. In this study, we analyzed intestinal triacylglycerol absorption and chylomicron synthesis and secretion in DGAT1-deficient (Dgat1(-/-)) mice. Surprisingly, DGAT1 was not essential for quantitative dietary triacylglycerol absorption, even in mice fed a high fat diet, or for the synthesis of chylomicrons. However, Dgat1(-/-) mice had reduced postabsorptive chylomicronemia (1 h after a high fat challenge) and accumulated neutral-lipid droplets in the cytoplasm of enterocytes when chronically fed a high fat diet. These results suggest a reduced rate of triacylglycerol absorption in Dgat1(-/-) mice. Analysis of intestine from Dgat1(-/-) mice revealed activity for two other enzymes, DGAT2 and diacylglycerol transacylase, that catalyze triacylglycerol synthesis and apparently help to compensate for the absence of DGAT1. Our findings indicate that multiple mechanisms for triacylglycerol synthesis in the intestine facilitate triacylglycerol absorption.

BACKGROUND:The vitamin A activity of beta-carotene is variable and surprisingly low in women. The reasons for this are not well understood. The vitamin A activity of beta-carotene in men is still uncertain. Contributions of dietary factors compared with individual traits are largely unknown.OBJECTIVE:Our objective was to measure the intrinsic variability in the vitamin A activity of beta-carotene among healthy, well-fed men living in a controlled environment.DESIGN:We used a double-tracer test-retest design. We dosed 11 healthy men orally with 30 micromol hexadeuterated (D6) retinyl acetate (all-trans-19,19,19,20,20,20-[2H6]retinyl acetate) and then with 37 micromol D6 beta-carotene (19,19,19,19',19',19'-[2H6]beta-carotene) 1 wk later. Doses were taken with breakfasts containing 16 g fat. We measured D6 retinol, D6 beta-carotene, and trideuterated (D3) retinol (derived from D6 beta-carotene) concentrations in plasma. Areas under the plasma concentration x time since dosing curves (AUCs) were determined for D6 retinol, D6 beta-carotene, and D3 retinol.RESULTS:All men had detectable D6 retinol concentrations in plasma. The mean (+/-SE) absorption of D6 beta-carotene in all subjects was 2.235 +/- 0.925%, and the mean conversion ratio was 0.0296 +/- 0.0108 mol retinol to 1 mol beta-carotene. Only 6 of 11 men had sufficient plasma concentrations of D6 beta-carotene and D3 retinol that we could measure. The mean absorption of D6 beta-carotene in these 6 subjects was 4.097 +/- 1.208%, and the mean conversion ratio was 0.0540 +/- 0.0128 mol retinol to 1 mol beta-carotene.CONCLUSION:The vitamin A activity of beta-carotene, even when measured under controlled conditions, can be surprisingly low and variable.

Millions of people worldwide have severe chronic physical disabilities (e.g., polio, spinal cord injury). We hypothesized that these people are at risk for poor antioxidant nutrient intakes and status, because of their typically low energy expenditures and low socioeconomic status. We surveyed antioxidant nutrient intakes and concentrations in subjects with physical disabilities and age matched non-disabled controls. Only one subject with physical disabilities ate five or more servings of vegetables per day. The group had low intakes of vegetables (minus potatoes) and citrus fruits, and trends for low intakes of all antioxidant nutrients. Serum a-tocopherol and total carotenoid concentrations were lower in subjects with physical disabilities, while retinol and individual carotenoids showed non-significant lower trends. Since adequate antioxidant nutrients are associated with decreased chronic disease risk, nutrition professionals might improve the health of patients with physical disabilities by periodically monitoring their intakes and status of antioxidant nutrients.

Dietary intakes of carotenoids are highly variable in human populations as are serum carotenoid concentrations. However, there are few controlled data relating carotenoid intake to concentration. Most of the data that are available are from measurements of the absorption and decay of large pharmacologic doses of carotenoids, and are therefore of unknown physiologic relevance. Our objective was to determine the half-life (t(1/2)) of the most abundant carotenoids in blood serum from healthy adult women living under controlled conditions. As part of two carotenoid isotopic studies, we measured serum concentrations of beta-carotene, alpha-carotene, lutein, zeaxanthin, beta-cryptoxanthin and lycopene in 19 healthy young adult women that were fed controlled low carotenoid diets for approximately 10 wk. All other nutrients (vitamins A, E and C) were provided at 100-150% of the 1989 U.S. recommended dietary allowance levels. Exercise and activities were controlled throughout the studies to simulate usual activity patterns. Carotenoid concentrations were measured by reversed-phase HPLC. Serum carotenoid concentration decreases during depletion followed first-order kinetics. The half-lives determined in decreasing order were as follows: lutein (76 d) > alpha-carotene (45 d) = beta-cryptoxanthin (39 d) = zeaxanthin (38 d) = beta-carotene (37 d) > lycopene (26 d). Half-lives were unrelated to physical or demographic characteristics such as body mass, body fat, racial background or age in these relatively homogeneous groups. Carotenoids decreased by similar first-order mechanisms, although the rates differed for individual carotenoids.