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The Journal of Nutrition Vol. 128 No. 2 February 1998,
pp. 265-270
-Tocopherol in Rats1,2
Department of Foods and Nutrition, Kansas State University, Manhattan, KS 66506
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ABSTRACT |
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Abstract
Introduction
Methods
Results
Discussion
References
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The present study was conducted to investigate whether the intestinal absorption of vitamin E is influenced by marginal zinc deficiency. Rats trained to meal feed were divided into two groups and fed a diet containing 3 mg Zn/kg [a low zinc (LZ group)] or pair-fed (PF controls a zinc-adequate diet (30 mg Zn/kg). At 5 wk, the body weight (352 ± 5 g, mean ± SD) of LZ rats was 98.5% of that of PF rats (357 ± 8 g). Rats with lymph cannula were infused at 3 mL/h via a duodenal catheter with a lipid emulsion consisting of 568 µmol triolein, 3.56 µmol 
-tocopherol (TP) and 396 µmol Na+-taurocholate in 24 mL of phosphate-buffered saline (pH 6.4). Lymph was collected hourly for 8 h. The amounts of TP absorbed into the lymph were determined by high-performance liquid chromatography (HPLC). The hourly rate of TP absorption was significantly lower in LZ than in PF rats. A marked difference (P < 0.05) was clearly evident even at 1 h (1.8 ± 1.2 nmol/h in LZ vs. 8.5 ± 3.0 nmol/h in PF). The peak rate of absorption was significantly lower in LZ rats (67.1 ± 16.7 nmol/h at 5 h) than in PF rats (95.9 ± 7.7 nmol/h at 4 h). The total amounts of TP absorbed in 8 h in LZ and PF rats were 391.1 ± 54.4 nmol (11.0 ± 1.5% dose) and 613.9 ± 105.8 nmol (17.2 ± 3.0% dose), respectively. The lymphatic absorption of TP was correlated with the amounts of PL (r = 0.77, P < 0.05) released into the mesenteric lymph. The hourly outputs of phospholipid and oleic acid also were significantly lower in LZ rats than in PF rats up to 4 h (P < 0.05). The cumulative lymphatic outputs of phospholipid (PL) were 20.1 ± 3.7 µmol/8 h in LZ and 27.0 ± 3.9 µmol/8 h in PF rats (P < 0.05). These results show that the intestinal absorption of vitamin E is affected by the zinc status of rats. This observation along with our earlier finding of a lower intestinal absorption of retinol suggests that zinc nutriture has a profound effect on the intestinal absorption and body status of lipid soluble vitamins.
-tocopherol ·
intestinal absorption ·
fatty acid ·
rats ·
zinc deficiency
Evidence suggests that zinc may play a critical role as an antioxidant and may be involved in the antioxidant defense system (Bettger and O'Dell 1981 The observations of Bunk et al. (1989) Animals and diets.
Adult male Sprague-Dawley rats (Harlan Sprague Dawley, Indianapolis, IN) weighing 270-280 g were placed individually in plastic cages with stainless-steel wire bottoms and subjected to a daily 12-h light:dark cycle. The rats were cared for in an animal care facility that was accredited by the American Association for the Accreditation of Laboratory Animal Care. All procedures for animal care and use were approved by the Kansas State University Institutional Animal Care and Use Committee. The rats were acclimated for 1 wk and fed a zinc-adequate modified AIN-93G diet (Reeves et al. 1993
Cannulation of the mesenteric lymph duct.
At the end of 5 wk, food was withheld from the rats for 18 h, and the mesenteric lymph duct was cannulated as described previously (Ahn and Koo 1995b Measurement of the lymphatic absorption of Determination of Determination of the lymphatic outputs of PL and OA.
Lymph phospholipid (PL) was measured by the method of Raheja et al. (1973) Serum zinc analysis.
Serum was diluted 1:3 with deionized water. Zinc was determined by atomic absorption spectrophotometry with an air-acetylene flame (Perkin-Elmer, Norwalk, CT). The zinc standards were prepared from a Fisher-certified reference standard solution (Fisher Scientific, Pittsburgh, PA).
Statistical analysis.
Values presented are means ± SD. All statistical analyses were performed using PC SAS (SAS Institute, 1985). Student's t test was used to compare group means at designated time intervals. Linear regression analysis was used to determine correlation between variables. Differences were considered significant at P < 0.05, unless otherwise stated.
Body weight and zinc and
Lymphatic absorption of
Lymphatic output of OA
From 1 to 4 h, the lymphatic output of OA was significantly lower in LZ than in PF rats (Fig. 3, P < 0.05). Up to 5 h, the rates of OA output increased at 34.6 ± 4.7 µmol/h in LZ rats and at 47.4 ± 3.6 µmol/h in PF controls (P < 0.05). At 5 h and thereafter, no significant differences were observed between groups in OA output. This was due to a gradual decline in OA output in PF rats between 6 and 8 h. The total OA output for 8 h was significantly lower in LZ rats (Table 3, P < 0.05).
Lymphatic PL output.
Even when the rats were infused with glucose saline containing no lipids, the rate of PL output was significantly lower in LZ rats (0.51 ± 0.13 µmol/h) than PF rats (0.81 ± 0.22 µmol/h). During lipid infusion, the output of PL was significantly lower in LZ rats than in PF controls up to 4 h (P < 0.05), with no significant difference between groups at 5 h and thereafter (Fig. 4). The maximal hourly rates of PL output were 3.4 ± 0.3 µmol/h in LZ and 4.2 ± 0.7 µmol/h in PF rats (P < 0.05). The total output of PL for 8 h was significantly lower in LZ rats than PF rats (Table 3). The hourly patterns of PL output in both groups closely resembled those of
The present study provides new evidence that zinc deficiency in rats lowers significantly the lymphatic absorption of vitamin E. The percent absorption of
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
, Bray and Bettger 1990, Bray et al. 1986, Oteiza et al. 1995, Sullivan et al. 1980). However, the precise mechanism of its action as an antioxidant is far from clear. Several studies have suggested a possible interaction between zinc status and vitamin E in intact animals. Zinc deficiency in rats produces a decrease in plasma concentration of vitamin E (Bunk et al. 1989). In addition, supplemental vitamin E was shown to prevent the development of certain external symptoms of zinc deficiency (Bettger et al. 1980). Thus, in intact animals, it has not been clearly defined whether the increased susceptibility to oxidative damage observed in zinc deficiency is attributable solely to zinc or to alterations in vitamin E status secondary to zinc deficiency.
showed that the plasma levels of vitamin E remained lower in zinc-deficient rats than pair-fed zinc-adequate rats and failed to rise to the control levels in response to increasing dietary vitamin E levels ranging from 0.06 to 3.5 mmol/kg. The authors suggested the intestinal malabsorption of vitamin E as a possible cause of the lower plasma concentrations of vitamin E in the zinc-deficient animals. Previous studies from our laboratory have shown that the intestinal absorption of lipids in general is impaired in zinc-deficient rats (Koo and Turk 1977, Koo et al. 1986). More recently, we have demonstrated that the lymphatic absorption of retinol also is lowered markedly in marginally zinc-deficient rats (Ahn and Koo 1995a, and 1995b, Ahn et al. 1995). Results from these and earlier studies (Koo and Turk 1977, Koo et al. 1985 and 1987) suggest that the impaired absorption of lipids in zinc deficiency is due to defective formation of chylomicrons in the enterocyte. Such a defect at the intestinal level may adversely affect the absorption of other fat soluble vitamins that are incorporated into chylomicrons for their transport. Thus far, however, no direct evidence exists that the intestinal absorption of vitamin E is impaired in zinc deficiency. To gain further insight into how zinc deficiency might alter vitamin E status and metabolism, the present study was conducted to determine the intestinal absorption of vitamin E in adult male rats with a mesenteric lymph cannula and an intraduodenal catheter. This method enabled us to measure directly the amounts of vitamin E absorbed into the mesenteric lymph during its infusion into the intestinal lumen.
MATERIALS AND METHODS
Abstract
Introduction
Methods
Results
Discussion
References
) during this period. Because of a drastic decline in food intake and rapid weight loss observed in zinc-deficient rats, we trained rats to meal feed to match the food intakes and prevent the development of different feeding behaviors in zinc-deficient and pair-fed control rats. Rats were fed meals twice daily at 0830 and 1530 h according to the following protocol: after food was withheld from rats for 24 h, they were fed 6 g of the zinc-adequate diet per meal for the 1st d, 7 g/meal for the next 4 d and 8 g/meal for the next 3 d. After this training period, the rats were divided into the following two groups with 10 rats each: a low-zinc (LZ)5 group, fed a diet containing 3.0 mg of zinc/kg, and a pair-fed (PF) group, fed a zinc-adequate diet with 30 mg of zinc/kg. Both groups were matched closely in their body weight at the start and meal fed 8 g of their respective diets at 0830 h and 8 g at 1530 h for 5 wk. The total amount of diet fed (16 g/day) represented 90% of their "normal" food consumption, which was determined by averaging the last 3 days' food intake before the initiation of meal feeding. With this feeding protocol, we observed that LZ rats completely consumed the food within 4 h, whereas PF rats consumed it within 3 h. The basal diet (Table 1) was formulated by Dyets (Bethlehem, PA) according to the AIN-93G recommendations (Reeves et al. 1993) with the following modifications: egg white as the protein source, dextrose in place of sucrose and 1.0 mg of zinc/kg. The mineral mix was modified as recommended by Reeves et al. (1993) and Reeves (1996) with the use of egg white as the protein source. The diet was supplemented with zinc carbonate to provide the desired levels of zinc. The soybean oil used was not vitamin-E stripped. Both the zinc-deficient and -adequate diets provided the following amounts of tocopherols/kg diet: 75 (in mg) dl--tocopherol (all-rac), 5.3 (in mg) RRR d--tocopherol, 0.6 (in mg) 
-tocopherol, 46.3 (in mg) 
-tocopherol and 13.4 (in mg) 
-tocopherol. All rats were given free access to deionized water delivered via a stainless-steel watering system.
View this table:
Table 1.
Composition of zinc deficient diet1
, Noh and Koo 1997). Briefly, rats were anesthetized with halothane using a halothane vaporizer. After an abdominal incision was made along the midline, the major intestinal lymph duct was cannulated with polyethylene tubing (SV 31 tubing, Dural Plastics, Auburn, Australia). An indwelling infusion catheter (Silastic medical grade tubing, Dow Corning, Midland, MI) was placed via the gastric fundus into the upper duodenum and secured by a purse-string suture (4-0 Silk, Ethicon, Somerville, NJ). After the abdominal incision was closed, the rats were placed in restraining cages in a heated chamber (30°C) for postoperative recovery for 22-24 h. During this period, the rats were infused at 3 mL/h via the duodenal catheter with a maintenance solution consisting of 277 mmol glucose, 144 mmol NaCl and 4 mmol KCl per L by using an infusion pump (Harvard Apparatus, Model 935, South Natick, MA).
-tocopherol.
After postoperative recovery, each rat was infused with a lipid emulsion containing -tocopherol (TP) at 3 mL/h via the duodenal catheter in subdued light. The lipid emulsion consisted of 568 µmol triolein (99%, Sigma, St. Louis, MO), 3.56 µmol TP (all-rac--tocopherol, 97%, Aldrich Chemical, Milwaukee, WI) and 396 µmol sodium taurocholate in 24 mL of phosphate-buffered saline [which contained (in mmol/L) 6.75 Na2HPO4, 16.5 NaH2PO4, 115 NaCl and 5 KCl; pH 6.4]. The lymph samples were collected hourly for 8 h in a preweighed ice-cold centrifuge tube containing 4 mg of Na2EDTA. All samples were ice chilled and handled in subdued light. From 100-µL aliquots of lymph samples, lipids were extracted (Folch et al. 1957). The lipid extracts were filtered through a microfilter membrane (0.45 µm, Alltech Associates, Deerfield, IL) to remove particulate matters, dried under N2 and dissolved in 100 µL of methanol (Liu and Huang 1995). The concentrations of TP were determined by using a reverse-phase HPLC column (Alltima C18, 5 µm, 4.6 × 150 mm, Alltech Associates) and a Beckman HPLC with System Gold software (Beckman Instruments, Fullerton, CA). Methanol was used as the mobile phase (Liu and Huang 1995) and propelled at 2 mL/min. Detection was monitored at 292 nm (Module 166, Beckman Instruments). Under these conditions, TP was eluted at 5.2 min. The standard curve (peak area vs. ng of TP) was constructed by using TP standards. Concentrations of TP from 75 to 300 ng yielded a linear curve (r = 0.999).
TP concentrations in serum and liver.
Blood samples (2.0 mL) were collected from five rats via the orbital sinus (Riley 1960) at 1 and 3 wk. Serum was separated by centrifugation at 1000 × g for 60 min. At 5 wk, the rats were killed under halothane anesthesia. The whole livers were removed and minced finely. Lipids were extracted from 100 µL serum and 100 mg tissue samples (Folch et al. 1957). The lipid extracts were used for TP analysis, as described above.
, as modified as follows: lipids were extracted from 100-µL samples (Folch et al. 1957). To the lipid extract placed in a test tube, 400 µL of chloroform was added and gently vortexed for 5 s. Into the mixture, 100 µL of the chromogenic solution containing ammonium molybdate and mercury was added. With the tube tightly capped, it was placed in a boiling water bath for 1 min and cooled to room temperature. After adding 4.0 mL of chloroform, the mixture was vortexed gently for 2 s with the tube capped and allowed to stand at room temperature for 30 min. The lower (chloroform) layer of the mixture was separated and used to determine absorbance at 710 nm.
) from lymph samples, saponified and methylated (Slover and Lanza 1979). Methylesters of fatty acids were separated on a Stabilwax-DA capillary column (15 m × 0.53 mm; Restek, Bellefonte, PA) in a Hewlett-Packard Model 5880A GC (Hewlett-Packard, Palo Alto, CA) equipped with a flame ionization detector. Nonadecanoic acid (C19:0, Nuchek, Elysian, MN) was used as an internal standard.
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
TP levels in serum and liver.
To match closely the body weights and food intakes of LZ and PF rats, they were trained to meal feed and then were pair-fed for 5 wk. Under these conditions, food (8 g/meal) was consumed within 4 h by both LZ and PF rats. The body weights of the two groups did not differ throughout the experiment (Fig. 1). At 5 wk, the mean body weight of LZ rats was at 98.5% that of PF controls. Serum zinc concentration at 1 and 3 wk was significantly lower in LZ rats than PF controls (Table 2), but no external signs of zinc deficiency were detectable throughout 5 wk of dietary treatment. The serum TP concentrations also were significantly lower in LZ than in PF rats (Table 2). Likewise, the liver concentration and content of TP at 5 wk was significantly lower in LZ rats than in PF controls (Table 2).
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Fig 1.
Changes in the mean body weights of rats fed a low-zinc diet (LZ) and of those pair-fed a zinc-adequate diet (PF) for 5 wk. Values are means ± SD (n = 5).
View this table:
Table 2.
Serum concentrations of zinc and -tocopherol (TP) and liver TP concentrations in rats fed a low-zinc diet (LZ)
and in those pair-fed a zinc-adequate diet (PF)1
TP.
After postoperative recovery, a steady lymph flow was established at a rate of 1.9-2.2 mL/h. The rate of lymph flow was increased to 3.0-3.4 mL/h after 3 h of infusing the lipid emulsion. The average hourly lymph volumes for 8 h were 2.3 ± 0.5 mL in LZ rats and 3.0 ± 0.6 mL in PF rats (P > 0.05). Starting at 1 h, the hourly rate of TP absorption was significantly lower in LZ than in PF rats (Fig. 2, P < 0.05). Before reaching its peak, the lymphatic absorption of TP increased at a significantly slower rate (36.3 ± 4.9 nmol/h) in LZ rats than PF controls (65.0 ± 8.1 nmol/h). The cumulative absorption of TP during 8 h in LZ rats was significantly lower than in PF rats, as determined by the total amount (nmol) or percent dose of TP absorbed into the lymph (Table 3).
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Fig 2.
The lymphatic absorption of -tocopherol (TP) at hourly intervals for 8 h in rats fed a low-zinc diet (LZ) and in those pair-fed a zinc-adequate diet (PF). Values are means ± SD, n = 5. *Significantly different from LZ at the time interval, P < 0.05.
View this table:
Table 3.
Cumulative lymphatic absorption of -tocopherol (TP) and outputs of phospholipid and oleic acid during infusion of a lipid emulsion for 8 h in rats fed a low-zinc diet (LZ) and in those pair-fed a zinc-adequate diet (PF)1
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Fig 3.
The lymphatic output of oleic acid (OA) at hourly intervals for 8 h in rats fed a low-zinc diet (LZ) and in pair-fed a zinc-adequate diet (PF). Values are means ± SD. *Significantly different from LZ at the time interval, P < 0.05.
TP absorption and OA output. The hourly rates of PL output were correlated significantly with the hourly rates of TP absorption (Fig. 5, r = 0.77, P < 0.05).
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Fig 4.
The lymphatic output of phospholipid (PL) at hourly intervals for 8 h in rats fed a low-zinc diet (LZ) and in those pair-fed a zinc-adequate diet (PF). Values are means ± SD. *Significantly different from LZ at the time interval, P < 0.05.
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Fig 5.
Relationship between the hourly lymphatic absorption of -tocopherol (TP) and the hourly lymphatic output of PL in rats fed a low-zinc diet (LZ) and of those pair-fed a zinc-adequate diet (PF).
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
TP observed in the present study was within the ranges (13-17%) reported by others using rats with mesenteric lymph cannula (Gallo-Torres et al. 1971, MacMahon et al. 1971). A study by MacMahon et al. (1971), using rats with mesenteric lymph cannula and -tocopherol-bile salt micelles showed that the amount of labeled vitamin E recovered in the mesenteric lymph was 13.3% and the amount appearing in the liver was only 0.2% of the dose, suggesting that the enterohepatic circulation of TP may contribute to the total luminal pool of the vitamin. Another study using lymph-cannulated rats and a 4% triolein emulsion (Gallo-Torres et al. 1971) reported a 12% lymphatic recovery of labeled TP during a 12-h period after gastric intubation of labeled TP acetate. Traber et al. (1986) used rats with thoracic lymph cannulae and a longer duration (4 nights) of lymph collection and showed that the absorption of vitamin E from soybean oil alone was 65% when infused at a rate of 0.12 mg vitamin E/h. In the same study, however, the absorption of -tocopherol from tocopheryl polyethylene glycol 100 succinate (TPGS; water-miscible) mixed in soybean oil was 13% when infused at a rate of 3.14 mg vitamin E/h. Thus differences in the rates of intraduodenal infusion, dosages, types of test emulsions (lipid mixtures) and absorption periods employed may explain the discrepancy in the reported amounts of the vitamin absorbed. In addition, in rats without bile diversion, the lymphatic absorption of vitamin E may include that portion of vitamin E recycled via the enterohepatic circulation (MacMahon et al. 1971). Also it should be pointed out that the lymphatic absorption of TP, as measured in the present experiment and the above-cited studies, may not represent the absolute total amount of the vitamin absorbed from the intestine because some amount of absorbed TP may escape via the minor lymph ducts and the portal blood (MacMahon et al. 1971).
in weanling female rats fed a diet containing 0.9 mg zinc/kg for 3 wk. In these zinc-deficient female rats, dietary supplementation of TP at 1.5 g/kg diet for 4 wk failed to raise plasma TP to the level observed in pair-fed controls fed 0.125 g 
P/kg diet. This (Bunk et al. 1989) and our observations demonstrate the critical importance of zinc in maintaining vitamin E status in both male and female rats. Thus far, however, the nature of the interaction between zinc and vitamin E status has not been defined clearly under in vivo conditions. Using conscious rats with lymph cannulas, the present study demonstrated that the interaction between the two micronutrients exists at the intestinal level. Our results indicate that the lower levels of TP in the serum and liver of LZ rats are attributable at least partly to a defect in the intestinal absorption of the vitamin. The decline in serum and liver TP levels was modest in adult rats fed a marginal amount of dietary zinc (3 mg zinc/kg diet) and with no visible external deficiency signs. It is possible that a more marked decrease in vitamin E status is produced in growing animals with prolonged advanced zinc deficiency. Previously, in weanling rats fed a diet containing 0.9 mg Zn/kg, the plasma concentration of TP was decreased to 44% of the pair-fed control (Bunk et al. 1989). The observed decline in serum and liver TP levels in LZ rats might be associated with decreases in serum and liver lipids. However, in our most recent study, conducted under similar experimental conditions, no differences were observed between groups in serum cholesterol (2.29 ± 0.29 mmol/L in LZ and 2.05 ± 0.02 mmol/L in PF rats, n = 5) and liver total lipids (68.4 ± 1.6 mg/g in LZ and 70.0 ± 1.7 mg/g in PF rats) (unpublished data).
, the processes of intestinal TP absorption involve the following three major steps in general: incorporation of TP into micelles consisting of bile acids and lipid hydrolytic products, mucosal uptake of TP and incorporation into chylomicrons and transport into the lymphatic system. An impairment in any of these processes would result in a decrease in the rate of TP absorption and in the total amount of TP transported into the lymphatics. Evidence suggests that the primary defect may be in the intestinal incorporation and transport of TP via chylomicrons. In the present study, unesterified TP was infused intraduodenally in a lipid emulsion containing Na+-taurocholate. Therefore it is not likely that the lower TP absorption in LZ rats is due to a lack of bile acids. Vitamin E enters the enterocytes by a passive process moving with intestinal lipids (Kayden and Traber 1993). In a study using everted rat gut sacs (Hollander et al. 1974), the rate of TP uptake by enterocytes has been shown to be dependent on the concentration of TP in the perfusate over a wide range (50-1200 µmol/L). The uptake of TP is not carrier-mediated and not dependent on energy, as evidenced by no change in the uptake of TP with the addition of metabolic inhibitors and uncouplers in the incubation medium (Hollander et al. 1974). Although the present study did not examine the rate of TP uptake by enterocytes, we previously observed a massive accumulation of lipids within the enterocyte of zinc-deficient rats during fat absorption, suggesting that the mucosal uptake of lipids was not impaired in zinc-deficient rats (Koo and Turk 1977, Koo et al. 1985).
, Koo et al. 1985-1987), we proposed that a biochemical defect produced by zinc deficiency is associated with the formation of chylomicrons in the enterocyte. In zinc-deficient rats, the digestion of lipids and mucosal uptake of their hydrolytic products appear to proceed normally (Koo and Turk 1977, Koo et al. 1985). The major defect seems to stem from a lack of the surface components of chylomicrons, including PL and apolipoproteins, that are required for chylomicron production during lipid absorption. In recent studies (Ahn and Koo 1995a and 1995b, Ahn et al. 1995), we have shown that the lymphatic absorption of vitamin A (retinol) also is lowered markedly in marginally zinc-deficient rats. An important finding was that the absorption of vitamin A in those rats was restored to normal when egg phosphatidylcholine (PC) was infused intraduodenally at a physiological level (5 µmol/h) (Ahn and Koo 1995b). In the present study, the lower hourly rate of lymphatic vitamin E absorption in LZ rats also is correlated with the lower rate of lymphatic PL output. These observations provide further evidence that the major common cause of the impaired absorption of lipids and lipid soluble vitamins in zinc deficiency is an insufficient supply of PL via the biliary route to enterocytes during chylomicron formation. This, in turn, causes a delay (or defect) in chylomicron assembly and hence transport of lipid soluble nutrients from enterocytes via chylomicrons (Tso and Scobey 1978). In zinc-deficient rats, the hepatic pool of microsomal PC is reduced (Bettger and O'Dell 1981, Clejan et al. 1981, Cunnane 1988), which is an important source of biliary PL (Chanussot et al. 1990). One notable change in membrane PL in zinc-deficient animals is a decrease in essential fatty acids (EFA) (Cunnane 1988). The EFA deficiency secondary to zinc depletion has been linked to a defect in desaturation and elongation of 18:2(n-6), impaired absorption and increased susceptibility of the polyunsaturated fatty acids to oxidation due to zinc deficiency (Bettger and O'Dell 1981, Cunnane 1988). The potential importance of the EFA of biliary PL in lipid absorption has been well demonstrated previously (Clark et al. 1973). Dietary EFA deficiency in rats has been shown to lower the concentrations of 18:2(n-6) and 20:4(n-6) in biliary and intestinal microsomal PC and result in impaired fat absorption. It is postulated that in EFA deficiency, the enterocyte fails to form appropriate PL species necessary for chylomicron coating. Currently, studies are underway to determine whether zinc deficiency in fact lowers the biliary secretion of PL and alters the fatty acid makeup of biliary PL.
). However, most of these observations have been made in model systems under in vitro conditions. At present, it remains debatable whether zinc deficiency produces specific changes in these mechanisms and whether such changes, if they occur, are solely responsible for the increased production of free radicals and oxidative damage to lipids, proteins and macromolecules including DNA, as observed in zinc-deficient animals (Bettger and O'Dell 1993, Bray et al. 1986, Oteiza et al. 1995, Sullivan et al. 1980, Xu and Bray 1994). Given the compromised status of vitamin E in zinc deficient rats, as demonstrated in the present study and in previous work (Bunk et al. 1989), some of the oxidative changes and external symptoms manifested in zinc deficient animals may be linked to the cellular status of vitamin E. In fact, supplemental vitamin E has been shown to prevent the development of certain external symptoms of zinc deficiency (Bettger et al. 1980).
TP. This observation and our earlier findings (Ahn and Koo 1995a and 1995b, Ahn et al. 1995), taken together, indicate that zinc nutriture is an important determinant of the intestinal absorption of lipid soluble vitamins. The biochemical and pathologic changes observed in zinc deficiency may be associated partly with the impaired absorption and, hence, lower nutritional status of the vitamins. Further studies are needed to elucidate the mechanism underlying the impaired absorption of vitamin E and its association with the pathogenesis of zinc deficiency.
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FOOTNOTES |
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TP, -tocopherol; EFA, essential fatty acid; LZ, rats fed a low zinc diet; OA, oleic acid; PF, rats pair-fed a zinc adequate diet; PC, phosphatidylcholine; PL, phospholipid.
Manuscript received 12 June 1997. Initial reviews completed 4 August 1997. Revision accepted 8 October 1997.
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LITERATURE CITED |
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Abstract
Introduction
Methods
Results
Discussion
References
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|---|
-tocopherol in the rat.
Gastroenterology
1974;
68:1492-1499
[Medline]
-tocopherol retention in male rats is compromised by feeding diets containing oxidized frying oil.
J. Nutr.
1995;
125:3071-3080
-tocopherol and cholesterol.
Eur. J. Clin. Invest.
1971;
1:288-294
[Medline]
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