Dietary Protein and Utilization of Carotene or Retinyl Acetate in Rats

Kamath, Savitri K.; MacMillan, Joan B.; Arnrich, Lotte

doi:10.1093/jn/102.12.1579

Cited by 13 publications

(4 citation statements)

References 12 publications

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“…However, it seems to markedly increase the conversion of p-carotene to retinol and retinyl esters at the high dietary protein concentration ( Figure 6). These results are in accord with earlier findings on the beneficial effects of protein on the conversion of P-carotene to vitamin A in rats (33,34). Dietary carbohydrate also has no significant effect on the absorption and accumulation of dietary P-carotene, because Vol.…”

Section: Discussionsupporting

confidence: 92%

The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary β‐carotene in ferrets

Lakshman

Liu

Sapp

et al. 1996

Nutrition and Cancer

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Dietary beta-carotene has been shown to have cancer chemopreventive action on the basis of epidemiologic evidence and studies in animals. Because the anticarcinogenic property of beta-carotene may be exerted per se, it is desirable to achieve the maximum absorption and accumulation of intact beta-carotene in various parts of the body. Therefore the effects of dietary taurocholate, fat, protein, and carbohydrate on the absorption, accumulation, and fate of dietary beta-carotene (3.730 nmol/g diet) in selected tissues of ferrets were explored. Taurocholate (0.2-1.0% wt/wt) and fat (6-23% wt/wt) caused two- to threefold (p < 0.05) increases in the absorption and accumulation of beta-carotene in the liver, lungs, and adipose tissue in a dose-dependent manner. In contrast, neither dietary protein (10-40% wt/wt) nor carbohydrate (25-55% wt/wt) affected the absorption and accumulation of beta-carotene in various tissues. Significantly, taurocholate, 23% fat, or 40% protein also markedly increased the amounts of hepatic retinol and retinyl esters derived from dietary beta-carotene. These results indicate that dietary taurocholate, fat, and high protein have a marked influence on the exposure of beta-carotene to intestinal carotene cleavage enzyme or its activity. Thus an ideal combination of dietary components (wt/wt) in ferrets for the maximal absorption and accumulation of beta-carotene in different tissues is 0.5% taurocholate and 13.4% fat, whereas 1% taurocholate, 23% fat, or 40% protein stimulates its conversion to vitamin A.

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Section: Discussionsupporting

confidence: 92%

The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary β‐carotene in ferrets

Lakshman

Liu

Sapp

et al. 1996

Nutrition and Cancer

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“…Mittal (1983) reported that rats fed on carotene as the only source of vitamin A and later made deficient, responded better (in terms of plasma retinol) to carotene-based repletion than those fed on retinol, but the biochemical basis for this adaptation was not investigated. There have been reports that the level of dietary protein may affect the hepatic deposition of retinol formed from carotene (Jagannathan & Patwardhan, 1960;Deshmukh & Ganguly, 1964;Kamath et al 1972;Kamath & Arnrich, 1973), that the quality of protein may be important (Berger et al 1962;Geervani & Devi, 1981), and that dietary fat can also affect hepatic deposition (Korycka et al 1969;Jayarajan et al 1980: Geervani & Devi, 1981. The nature of the carotene source (Rajalakshmi et al 1975) and the magnitude of the carotene load (Bondi & Sklan, 1984) affect the efficiency of intestinal uptake, and the presence of bile salts (El-Gorab et al 1975) or of zinc deficiency (Honory, 1978;Takruri & Thurnham, 1981) may affect efficiency of conversion.…”

Section: Discussionmentioning

confidence: 99%

Carotene dioxygenase (EC1. 13. 11. 21) activity in rat intestine: effects of vitamin A deficiency and of pregnancy

Villard

Bates

1986

Br J Nutr

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1. Female weanling rats were fed on a purified diet containing either no vitamin A, apart from traces present in casein (deficient groups), or the same diet containing 1.55 mg retinol as retinyl acetate/kg (control groups). In one experiment the deficient groups were given 1 μg retinol/d after 10 weeks, to permit successful reproduction under conditions of marginal vitamin A status. A proportion were mated at 11 weeks after weaning, and fetal development was permitted for 7 d or for 20 d before killing.2. Carotene dioxygenase (EC 1. 13.11.21) activity was measured in a supernatant fraction from intestinal mucosal scrapings. For each group, activity was 20–30% greater in the vitamin-A-deficient animals than in the controls, and the difference reached statistical significance for the virgin and 7 d pregnant animals in the first experiment (severe deficiency) and for the 20 d pregnant animals in the second experiment (less-severe deficiency).3. It is suggested that low tissue vitamin A levels may feedback to increase carotene dioxygenase activity, by mechanisms at present unknown, presumably to ensure a more efficient use of precursor dietary carotenoids.

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“…Treatment with the special diet was initiated at 27 days of age and continued until approximately 9 months of age. Group 4: 50 µg retinoic acid (Eastman Kodak, Rochester, New York); this supplement is retinol-free since the acid cannot be converted to the alcohol form of the vitamin, and this dose is adequate to prevent death and to maintain growth (Kamath, MacMillan &Arnrich, 1972). Group 2: 5000 i.u.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of cyclic ovarian activity in rats treated chronically with vitamin A

Rj¹

1977

Reproduction

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The effects of altering the dietary level of vitamin A on cyclic ovarian activity, and serum and hepatic vitamin A concentrations were studied in female rats. High but non-toxic oral doses of retinyl palmitate (5000 i.u., 3 times/week) significantly advanced the age at vaginal opening but had no effect on vaginal and ovarian cycles after 15 weeks of treatment. Hepatic stores of vitamin A were significantly elevated but serum levels were unchanged. Retinol-deficient rats given a supplement of retinoic acid had a normal vaginal opening age but displayed cornified vaginal cells for many of the days that smears were taken. Hepatic and serum vitamin A concentrations were markedly reduced. When treatment with high doses of retinyl palmitate was continued for 9 months, animals developed polycystic anovulatory ovaries which were significantly lighter than those of controls. Retinol-deficient rats given retinoic acid and demonstrating depleted hepatic vitamin A reserves had ovaries of normal weight and containing corpora lutea, indicating that retinol is not necessary for ovulatory activity. Short-term treatment (16 days) of rats with toxic doses of retinyl palmitate (50,000 i.u. daily) sufficient to raise serum and hepatic retinol levels significantly did not alter ovarian cyclicity; corpora lutea were present and ovarian weight was normal.These data indicate that long-term treatment with high but non-toxic doses of vitamin A inhibits cyclic ovulatory activity, perhaps via alteration of a steroidogenic mechanism in the ovary or adrenal since other studies indirectly support the existence of such a relationship. Furthermore, retinoic acid is a sufficient form of vitamin A replacement to maintain cyclic ovarian activity.

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Dietary Protein and Utilization of Carotene or Retinyl Acetate in Rats

Cited by 13 publications

References 12 publications

The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary β‐carotene in ferrets

The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary β‐carotene in ferrets

Carotene dioxygenase (EC1. 13. 11. 21) activity in rat intestine: effects of vitamin A deficiency and of pregnancy

Inhibition of cyclic ovarian activity in rats treated chronically with vitamin A

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