Dietary carotenoids influenced biochemical but not morphological changes in adult male rats fed a choline-deficient diet.

In a study of the effects of carotenoids, canthaxanthin (CA), beta-apo-8'-carotenal (BA), or beta-carotene in an extract of Spirulina-Dunaliella algae (AE) was fed at 0%, 0.1%, or 0.2% in a choline-deficient (CD) diet. In each of eight groups, 10 adult male Fischer 344 rats were fed diets with designated carotenoid sources and levels or a choline-sufficient diet for 12 weeks. Carotenoids altered some of the changes induced by the CD diet. Increases in enlargement of fatty livers and low plasma cholesterol levels occurred in rats fed 0.2% BA. Plasma retinol was further reduced 35% by BA or AE. BA and AE increased liver total vitamin A about 80% and 305%, respectively. Liver lipid peroxidation was enhanced and plasma alpha-tocopherol was reduced further by 1.0% AE. AE, BA, and CA (mg/g fat) depressed liver alpha-tocopherol about 49%, 67%, and 78%, respectively. The decreased liver alpha-tocopherol was concurrent with an increase in carotenoid stores of CA > BA > AE. Histopathological examination of sections of liver tissue by light microscopy showed fatty and cirrhotic changes in all rats fed CD diets. Histochemical evaluation based on a semiquantitative assay revealed a marked increase in peroxisome enzyme activity in the livers of all CD rats. None of the carotenoids appeared to have any effect on the development of morphological changes in the liver. Although carotenoids can function as antioxidants, they did not prevent changes observed in rats fed CD diets.

Canthaxanthin and excess vitamin A alter alpha-tocopherol, carotenoid and iron status in adult rats.

beta-Carotene and excess vitamin A have been shown to reduce plasma alpha-tocopherol when fed to young rats. The present study assessed the effects of beta-carotene, excess vitamin A and canthaxanthin (4,4'-diketo-beta-carotene) on carotenoid, alpha-tocopherol and iron status in adult retired breeder rats. Male 8- to 10-mo-old rats (10/group) were fed varying levels of vitamin A as retinyl palmitate, beta-carotene and canthaxanthin ad libitum for 8 wk. The AIN-76A diet was modified to contain 16% (wt/wt) fat and 50% carbohydrate (control) plus beta-carotene or canthaxanthin at 0, 0.048 (BC1 or CX1) and 0.2% (BC2 or CX2) of the diet. These compounds were fed with and without excess retinyl palmitate (RP, 220 mg/kg). Higher relative liver weights were observed in CX- and RP-fed groups. Plasma retinyl esters were detected in all RP-fed groups. Plasma retinyl palmitate was 1.6- and 1.5-fold higher in RP-BC and RP-CX groups, respectively, than in the RP groups. Plasma and liver beta-carotene and canthaxanthin were 11-54% and 26-74% lower, respectively, with excess retinyl palmitate feeding. Feeding canthaxanthin and retinyl palmitate but not beta-carotene, resulted in lower levels of plasma alpha-tocopherol. Liver non-heme iron levels were also lower in CX-fed rats irrespective of retinyl palmitate feeding. These results extend to adult rats previous findings that excess retinyl palmitate alters vitamin E and carotenoid status prior to the manifestation of clinical signs of hypervitaminosis A. Additionally, canthaxanthin feeding lowers alpha-tocopherol and iron status in adult rats.

Effects of graded dietary levels of Spirulina maxima on vitamins A and E in male rats.

The effects of ingesting the alga Spirulina maxima on the storage and utilization of vitamins A and E were investigated by feeding diets containing 0, 2.7, 10.7, 18.7 and 26.7% S. maxima to male rats for 6 wk. All diets contained 18% protein, which was contributed by S. maxima or by casein or by a mixture of them. Growth results indicated that rats did not utilize the diets containing S. maxima as well as the casein control diet (0% S. maxima) when levels were 10.7% or more of the diet. The ingestion of S. maxima caused a significant increase in dry matter and chloroform-extractable crude fat in the feces. A low level of 2.7% S. maxima caused a significant reduction in plasma, liver and heart alpha-tocopherol levels. The concentrations of alpha-tocopherol in these tissues showed a marked decline with 10.7% S. maxima in the diet, followed by a lesser decline at higher levels. Liver retinoid levels of rats increased when S. maxima was added to the diet, suggesting conversion of the naturally occurring carotenoids in S. maxima to vitamin A. However, the plasma levels of retinol decreased when S. maxima was fed at 10.7% or more. These data demonstrate that S. maxima can significantly alter the storage and utilization of vitamins A and E.

Effects of beta-carotene and retinyl palmitate on corn oil-induced superoxide dismutase and catalase in rats.

The present study was undertaken to determine the effects of beta-carotene on corn oil-induced superoxide dismutase and catalase. Six groups of male Buffalo rats were fed the following diets for 6 wk: a control diet containing recommended levels of beta-carotene and retinyl palmitate, a retinol diet containing 10 times the recommended level of retinyl palmitate, and a beta-carotene diet containing 10 times the recommended levels of beta-carotene and adequate levels of retinyl palmitate. Each vitamin combination was fed with either 5% (wt/wt) corn oil (low fat) or 20% corn oil (high fat). Plasma total beta-carotene levels were highest in the beta-carotene groups. Levels varied inversely with the level of fat in the control group and directly with fat in the beta-carotene group. Transport of beta-carotene appeared to parallel that of cholesterol in that 36 and 35%, respectively, were associated with the low density lipoprotein fraction. Accumulation of beta-carotene in the liver was apparent from the observation that levels in liver were much higher than those in plasma. Superoxide dismutase activity was much lower in the beta-carotene groups than in the retinol groups, irrespective of level of fat, and catalase activity was also lower in the beta-carotene group, but it was in proportion to the level of fat. These findings suggest that beta-carotene functions as an antioxidant in vivo.

Effects of fructose, levamisole and vanadate on insulin action in rat adipose tissue.

The effects of dietary fructose, levamisole and vanadate on insulin-stimulated conversion of D-[U-14C]glucose to 14CO2 and to 14C-labeled lipid were examined in rat epididymal adipose tissue. Male weanling rats were fed isoenergetic diets containing either 27% (wt/wt) fructose or glucose for 11 wk. During the final 4 wk, rats in each group were either untreated (control) or treated orally with 20 mg/kg body wt levamisole or 0.5 ppm vanadate via their drinking water. Basal glucose oxidation to CO2 was 45% higher in the fructose-control than in the glucose-control group. Insulin-stimulated glucose oxidation in both control groups was not higher than the basal rate in fructose-fed rats. Basal lipogenesis was 31% lower in the fructose-control than in the glucose-control group. Insulin-stimulated lipogenesis was much higher than basal, but was not different between fructose- and glucose-control groups. Levamisole increased basal lipogenesis in fructose-fed rats. Vanadate acted synergistically with fructose in greatly diminishing insulin-stimulated glucose oxidation. Fasting plasma insulin levels were lower and fasting plasma glucose and triglycerides were higher in fructose- than in glucose-fed rats, irrespective of treatment. Results suggest that adaptation to dietary fructose enhances basal oxidative capacity in an insulin-like fashion and reduces the basal lipogenic capacity of adipose tissue. Treatment with levamisole and vanadate lowers the overall rate of glucose metabolism and alters the effects of fructose.

Long-term effects of moderate fructose feeding on glucose tolerance parameters in rats.

The effects on glucose tolerance of prolonged fructose feeding, at a level approximating that currently in the American diet, were examined in weaning, male Wistar rate. Two groups of rats were fed ad libitum diets containing either 54% cooked cornstarch (w/w) [CS] or 39% cooked cornstarch plus 15% D-fructose (CSF) for 3, 5, 7, 9 and 15 months. All rats were given an oral glucose tolerance test (250 mg glucose/100 g body weight) after each designated feeding period (hereafter referred to as age groups). Serum insulin and glucose were determined from blood obtained after fasting and 1/2 1, 2 and 3 hours following the glucose load. Neither body weight nor relative food intake (g/day/100 g body weight) differed significantly with diet. Fasting serum insulin increased linearly (r = 0.97) with age in both dietary groups, but was significantly higher (P less than 0.01) in CSF- than in CS-fed rats. Fasting serum glucose levels were also higher (P less than 0.05) in CSF-than in CS-fed rats. The levels decreased with age (r = 0.61) in CS-fed rats, but increased linearly with age (r = 0.96) in CSF-fed rats. Serum insulin response to the oral glucose load was higher (P less than 0.03) in all CSF-fed than in CS-fed rats. The serum glucose response curve following the oral load was significantly higher (P less than 0.025) in CSF-fed than in CS-fed rats at 7 months but not at other ages. Liver phosphoenolpyruvate carboxykinase (PEPCK, EC 4.1.1.32) activity, measured only in the 3-month group, was higher (P less than 0.05) in the CSF-fed rats, indicating higher gluconeogenic activity.