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Protein utilization in humans as affected by level of dietary fat
Nutrition Research, Vol. 16, No. I, pp. 3340, 1996 Copyright 0 1995 Elsevier Science Inc. Printed in the USA. All rights reserved 0271-5317/96$15.00+.00
ELSEVIER
PROTEIN Jayanthi
0271.5317(95)02057-8
UTILIZATION
IN HUMANS AS AFFECTED
Kandiah*, Ph.D.,
Prisca Tuitoek,
BY LEVEL OF DIETARY
Ph.D.,
Constance
FAT
Kies, Ph.D.
Department of Family and Consumer Sciences, Ball State University Muncie, Indiana-47306, U.S.A., Home Economics Department, Egerton University P.O. Box 536, Njoro, Kenya, Department of Nutritional Sciences and Dietetics, 316 Ruth Leverton Hall, University of Nebraska-Lincoln 68583-0807, U.S.A.
The objective of the project was to determine the effects of level of fat with or without manganese supplementation of diets on protein status of humans. Fourteen healthy adult humans participated in a 61 day study in which they were fed a low fat diet similar to the HANES I survey or a moderate fat diet similar to the U.S. Dietary Goal recommendation with orwithoutmanganese supplementation. Mean fecal nitrogen excretions were significantly lower while subjects received moderate fat diets (p
Fat,
Manganese,
Protein,
Nitrogen,
INTRODUCTION
With the prevalence of coronary heart disease, cancer, hypertension, adult onset diabetes mellitus and obesity greater emphasis has been focused in decreasing dietary fat (l-4). In the United States, during the last two decades there has been increasing concern in the role of dietary fat and chronic disease. The most common recommendation among major scientific organizations are that individuals should reduce their fat intake to 30% of total calories (kilocalories) or less (5-7). Research has revealed that Americans, on average continue to consume a diet too high in fat (ranging from 34%-38.8% of kilocalories). The major * Corresponding
Author
33
34
J. KANDIAH etal.
contributors of dietary fat are table fats, processed meat and red meat. (8-10). The type and amount of fatty acid consumed also influences different disease state (10,ll). Though there has been a decrease in the intake of total dietary fat and saturated fat since NHANES II (1976-1980), saturated fats provide 12% of kilocalories in the diets of noninstitutionalized males and females greater than 2 months of age (9). Several trace elements have been shown to affect lipid metabolism and cholesterol synthesis (12-14). Among them is manganese, which acts as a cofactor of mevalonate kinase and farnesyl pyrophosphate synthetase, two enzymes necessary for cholesterol synthesis (15,16). In vitro studies have shown that the addition of manganese to rat liver cells increases cholesterol synthesis (17,18). However, little is known of the in vivo effect of manganese on cholesterol metabolism. Klimis-Tavantzis and coworkers reported results of a series of studies designed to investigate manganese deficiency on cholesterol and lipid metabolism in three experimental animal models (19-21). In young chicks and older laying hens, a diet deficient in manganese did not significantly alter plasma cholesterol, although liver cholesterol was significantly decreased (19). In weanling, Wistar and RICO (genetically hypercholesterolemic) rats, dietary manganese deficiency did not result in significant alterations in cholesterol and lipid metabolism (20). Recently, studies with weanling male Sprague-Dawley rats revealed liver manganese, total plasma protein and HDL cholesterol were significantly lower in manganese deficient rats (21). Diets rich in soy protein have been observed to decrease blood cholesterol levels (22-29). However, the effect of fat on the utilization of protein has not been well defined. The objective of the current study was to investigate the effects of level of fat with or without manganese supplementation on protein utilization.
METHODS
AND MATERIALS
periods of The study was composed of four experimental fourteen days each during which a measured, laboratory controlled diet was fed (Table 1). While the same foods were fed each day, some variations occurred among subjects so that caloric intakes for Subjects during could be maintained. weight maintenance experimental periods 1 and 2 received a HANES I survey (40% fat, and polyunsaturated to monounsaturated to 600 mg cholesterol, saturated fatty acids in a ratio of 4:14:14) or moderate fat diet (MF), while during experimental periods 3 and 4, subjects received Goal a similar meet the U.S. Dietary diet modified to recommendation regarding fat (30% of energy from fat, less than 300 and polyunsaturated to monounsaturated to mg. cholesterol/day, saturated fatty acids in a ratio of 1O:lO:lO) or also called a low fat diet (LF). Using a cross-over design one-half of the subjects
FAT/PROTEIN INTERACTIONS
35
received the moderate fat diet (MF) followed by the low fat diet (LF) while the reverse was followed for the other subjects. During the 5-day pre-period, subjects kept dietary diaries of kinds and amounts of food consumed, and made complete collections of urine and feces. Urine and fecal collections were compared with intake to verify completeness of 5-day dietary diaries. During the four 14-day experimental periods comprising each part, the following variations were used as shown on Table 1: basal diet alone (either moderate or low fat), or basal diet plus manganese gluconate amino acid chelate supplement. The variations resulted in alterations of protein intake. Exact quantities of the foods composing the basal diets were varied among subjects in order to make adjustments in calorie intake for weight maintenance of each individual. Subjects ranged in age from 24 to 36 years, ten were females and four were males with weight proportional to height, and twelve were Caucasian American and two were Hispanic American. All subjects received all experimental treatments; thus, each subject acted as his/her control. As in most studies of this kind, the study group was small and varied in gender, age, height and weight. This would be expected to increase the variation in other parameters of study results but not direction of response. All the subjects were undergraduate or graduate students at the University of Nebraska in the Department of Nutritional Science and Dietetics who maintained their usual study/work/social/life patterns except for eating the laboratory controlled diet in the Metabolic Research Laboratory of the Department of Nutritional Science and Dietetics and making complete collections of excreta. On the basis of health history information and pre-study blood analyses, subjects were cleared for participation by medical personnel of the University of Nebraska Division of Medical Services. Signing of Informed Consent documents prior to the start, of the study was a condition for participation. The project was approved by the University of Nebraska Institutional Committee for Projects Involving Human Subjects. Subjects made complete collections of urine and stools throughout the study. Creatinine measurements were made in repeat 24-hour urine collections in order to verify completeness of urine collections. Urine for each subject was composited on the basis of time into 24-hour lots, measured volumetrically, sampled and frozen for later analyses. Feces were divided into lots representative of food eaten during each experimental period via use of orally given fecal dyes (brilliant blue). Feces for each subject for each period were weighed, mixed, sampled, and frozen for later analyses. Fasting blood samples were drawn by professional medical technicians of the University of Nebraska Division of Medical Services on the first day of the study and at the end of each experimental period. Nitrogen concentrations in food, supplements, feces and urine were determined by the boric acid modification of the Kjeldahl method as defined by AOAC 1980. Dry fecal weights were used to estimate accuracy and completion of fecal collection on a
J.KANDIAH etal.
36
period basis. Nitrogen balances were calculated. All data were subjected to statistical analysis including Analysis of Variance and Duncan's Multiple Range Test. RESULTS AND DISCUSSION Nitrogen balance is commonly used as an index of protein nutrition and protein status in humans. Mean nitrogen intakes, corrected urinary and fecal nitrogen losses, and nitrogen balances of subjects receiving the various diets are given in Table 2. Mean intake of nitrogen during moderate fat diet was lower than the nitrogen intake on the low fat diet. Mean urinary losses of nitrogen while subjects received moderate fat plus manganese gluconate, low fat plus manganese gluconate and low fat alone were 9.33 r 1.21, 9.21 + 1.52, 9.35 + 1.24 and 9.50 f 1.23 g N/subject/day, respectively. The overall mean for all subjects for all periods while receiving moderate fat diet was 9.27 g N/subject/day and while receiving low fat diet was 9.43 g N/subject/day (p > 0.05).
TABLE 1 Experimental Plan - Study Pd.'
Intake Nitrogen# Mn*' mg/day g/day
1
2 3 4 *
# If t*t
11.24 11.24 12.58 12.58
40 40
Fat %
Cholesterol*** mg/day
40 40 30 30
600 600 <300 1300
Diet during the four experimental periods of fourteen days each composed of orange juice, tomato juice, milk, bran flakes ready-to-eat cereal, whole wheat bread, margarine, egg,. frankfurter, tuna, green beans, corn, peaches and cookies. Exact amounts varied among subjects due to differences needed for weight maintenance. Supplied by ordinary food contained in basal diet. Supplemental manganese supplied by manganese gluconate. Variations from moderate vs low fat were achieved through substitution of eggs for tuna.
FAT/PROTEIN INTERACTIONS
TABLE
2
Effect Of Altered Intakes Of Fat And Manganese On Protein Status Of Humans Trt.'
Intake g N/day 11.91a (f 0.88)
Urine g N/day 9.33= if 1.21)
Feces g N/day 1.26' f+ 0.33)
Balance g N/day 1.34= (+ 1.39)
MF + Mn
11.72' (? 0.68)
9.21a (+ 1.52)
1.26' (+ 0.37)
1.25' (-+1.48)
LF + Mn
13.22& (-+1.16)
9.35a (-+1.24)
1.60bc (+ 0.42)
2.21k (+ 1.25)
LF
13.25b (+ 1.14)
9.508 (+ 1.23)
1.60b (-+0.47)
2.17b (+ 1.11)
MF
* Moderate or low fat diets with or without manganese gluconate supplement. Mean values and SD of 14 subjects. Values with no repeated letter superscripts within each column are significantly different from one another (p < 0.05). Under the same experimental variations, mean fecal nitrogen losses were 1.26 f 0.33, 1.26 + 0.37, 1.60 + 0.42 and 1.60 -+ 0.47 g N/subject/day, respectively. The overall mean for all subjects for all periods while receiving moderate fat diet was 1.26 g N/subject/day while receiving low fat diet was 1.60 g N/subject/day (p < 0.0001). The results of mean fecal losses suggest that either the decrease in dietary fat or some other component of low fat diet caused an increase in mean fecal nitrogen excretion. Although the low fat diet was slightly higher in nitrogen content than was the moderate fat diet, this does not entirely account for the statistical difference in fecal N loss. Mean nitrogen balances calculated by subtracting urinary and fecal N from dietary nitrogen intake for the experimental treatments previously listed were 1.34 + 1.39, 1.25 f 1.48, 2.21 + 1.25 and 2.17 f 1.11. The overall mean for all subjects for all periods while receiving moderate fat diet was 1.30 g N/day and while receiving low fat diet was 2.19 g N/day (p < 0.004). As would be expected from previously discussed results on fecal loss of nitrogen, nitrogen balance tended to be less positive when the moderate fat diet was fed than when the low fat diet was fed. The overall mean urinary nitrogen losses for all subjects for all periods when they were receiving manganese supplement was 9.28 g N/day and while not receiving manganese supplement was 9.41 g N/day (p > 0.05). Mean fecal nitrogen losses while receiving same treatments as listed above were 1.43 and 1.43 g N/day, respectively
38
J. KANDIAH
etal.
(p > 0.05). Mean nitrogen balance while on the same treatments were 1.73 and 1.75 g N/day respectively (p > 0.05). Thus, no statistically significant effect of feeding manganese supplements on protein utilization were demonstrated. These results are similar to those earlier found in this laboratory (30). In conclusion, the results of this study indicate that no effects of feeding different levels of fat or manganese on nitrogen utilization or balance were demonstrated. However, feeding moderate fat diets in comparison to low fat diets tended to result in decreased nitrogen balances. Fecal nitrogen loss was higher when the low fat diets than when the moderate fat diets were fed. This suggests that protein is more poorly utilized with the feeding of lower rather than higher levels of fat.
Drs. Kandiah and Tuitoek would like to thank Dr. Kies (deceased) for her advice and contribution to the manuscript. REFERENCES 1.
Sacks FM. Dietary fat and blood pressure: A critical review of the evidence. Nutr Rev 1989; 47:291-300.
2.
Simopoulos AP. Omega 3 fatty acids in health and disease and in growth and development loss. Am J Clin Nutr 1991; 54:438463.
3.
Carroll KK. Dietary fats and cancer. Am J Clin Nutr 1991; 53:10648- 1067s.
4.
Leaf A, Weber PC. Cardiovascular effects of n-3 fatty acids. N Eng J Med 1988; 318:549-555.
5.
National cancer institute. Diet, nutrition and cancer Prevention: A guide to food choices. NIH: Washington D-C., 1987:2878.
6.
American heart association. Dietary guidelines for healthy american adults. Dallas: Texas, 1986.
7.
National research council, committee on diet and health, food and nutrition board, commission on life sciences. Diet and health: Implications for reducing chronic disease risk. Washington D.C., 1989.
FAT/PROTEIN INTERACTIONS
39
8.
Subar AF, Ziegler RG, Patterson BH, Ursin, G, Graubard B. US dietary patterns associated with fat intake: The 1987 national health interview survey. Am J Public Health 1994; 84:359-366.
9.
US Department of health and human services. Daily dietary fat and total energy intakes - third national health and nutrition examination survey, phase I, 1988-1991. J MMWR 1994; 43:116125.
10.
Ursin G, Ziegler RG, Subar AF, Graubard BI, Haile RW, Hoover R. Dietary patterns associated with a low-fat diet in the national health examination follow-up study: Identification of potential confounders for epidemiologic analyses. Am J Epidemiol 1993; 137:916-927.
11.
Dreon DM, Vranizan KM, Krauss RM, Austin MA, Wood fat vs monounsaturated effects of polyunsaturated plasma lipoproteins. JAMA 1990; 263:2462-2466.
12.
Allen KGD, Klevay copper deficiency.
13.
Koo SI, Williams DA. Relationship between the nutritional status of zinc cholesterol concentration of serum and lipoproteins in adult male rats. Am J Clin Nutr 1981; 34:23762381.
14.
Morrison LM, Schjaide A. Arterisclerosis: and regression, Illinois: Springfield,
15.
Amdur B, mevalonic
16.
Benedict C, Kett J, Porter J. Properties of farnesyl pyrophosphate synthetase of pig liver. Arch Biochem Biophys 1965; 110:611-621.
17.
Curran GL, Clute OL. Effect of cations on cholesterol synthesis by surviving rat liver. J Biol Chem 1953; 204:215219.
18.
Curran GL. Effect of certain transition group elements on hepatic synthesis of cholesterol in the rat. J Biol Chem 1954; 210:765-770.
19.
Klimis-Tavantzis DJ, Kris-Etherton of dietary manganese deficiency metabolism in the estrogen-treated Nutr 1983; 113:320-327.
20.
Klimis-Tavantzis DJ, Leach RM Jr, Kris-Etherton PM. The effect and lipid of dietary manganese deficiency on cholesterol metabolism in genetically the Wistar rat and the hypercholesterolemic RICO rat. J Nutr 1983; 113:328-336.
LM. Hyperlipoproteinemia in rats Nutr Rep Int 1980; 22:259-299.
Billing H, Bloch acid to sgualene.
PD. The fat on
due
to
Prevention treatment 1984:120-130.
K. The enzymatic conversion of J Chem Sot 1957; 79:2646-2647.
PM, Leach RM Jr. The effect on cholesterol and lipid chicken and laying hen. J
40
J. KANDIAH
etal.
21.
Klimis-Tavantzis DJ, Taylor PN, Lewis RA, Flores AL, Patterson HH. Effects of dietary manganese deficiency on high density lipoprotein composition andmetabolismin Sprague-Dawley rats. Nutrition Research 1993: 13:953-968.
22.
Thuesen L, Henriksen LB, Engby B. One year experience with a low fat, low cholesterol diet in patients with coronary heart disease. Am J Clin Nutr 1986; 44:212-219.
23.
Potter S, Bakhit RM, Essex-sorlie DL, Weingartner KE, Chapman KM, Nelson RA, Prabhudesai M, Savage WD, Nelson AI, Winter LW, Erdman JW. Depression of plasma cholesterol in men by consumption of baked products containing soy protein. Am J Clin Nutr 1993; 58:501-506.
24.
Carroll KK. Review of clinical studies on cholesterol lowering response to soy protein. J Am Diet Assoc 1991; 91:820-827.
25.
Sirtori C, Gatti E, Mantero 0. Clinical experience with the soybean protein in the treatment of hypercholesterolemia. Am J Clin Nutr 1979; 32:1645-1648.
26.
Jenkins D, Wolever T, Spiller G. Hypocholesterolemic effect of vegetable protein in a hypocaloric diet. Atherosclerosis 1989; 78:99-107.
27.
Carroll K, Giovannetti P, Huff M, Moase 0, Roberts DCK, Wolfe BM. Hypocholesterolemic effect of substituting soybean protein for animal protein in the diet of healthy young women. Am J Clin Nutr 1978; 31:1312-1321.
28.
Goldberg AP, Lim A, Kolar JB, Grundhause JJ, Steinke FH, Schonfeld G. Soybean protein independently lowers plasma hypercholesterolemia. levels in primary cholesterol Atherosclerosis 1982: 43:355-368.
29.
Gaddi A, Ciarrocchi A, Matteucci A. Dietary treatment for familial hypercholesterolemia - differential effects of dietary soy protein according to apoliprotein E phenotypes. Am J Clin Nutr 1991; 53:1191-1196.
30.
Potter SM, Kies, CV, Roihani, A. Protein fat utilization by humans as affected by calcium phosphate, calcium carbonate, and manganese gluconate supplemets. Nutr (Burbank) 1990; 6:309-312. Accepted
for
publication
June
9, 1995.
ELSEVIER
PROTEIN Jayanthi
0271.5317(95)02057-8
UTILIZATION
IN HUMANS AS AFFECTED
Kandiah*, Ph.D.,
Prisca Tuitoek,
BY LEVEL OF DIETARY
Ph.D.,
Constance
FAT
Kies, Ph.D.
Department of Family and Consumer Sciences, Ball State University Muncie, Indiana-47306, U.S.A., Home Economics Department, Egerton University P.O. Box 536, Njoro, Kenya, Department of Nutritional Sciences and Dietetics, 316 Ruth Leverton Hall, University of Nebraska-Lincoln 68583-0807, U.S.A.
The objective of the project was to determine the effects of level of fat with or without manganese supplementation of diets on protein status of humans. Fourteen healthy adult humans participated in a 61 day study in which they were fed a low fat diet similar to the HANES I survey or a moderate fat diet similar to the U.S. Dietary Goal recommendation with orwithoutmanganese supplementation. Mean fecal nitrogen excretions were significantly lower while subjects received moderate fat diets (p
Fat,
Manganese,
Protein,
Nitrogen,
INTRODUCTION
With the prevalence of coronary heart disease, cancer, hypertension, adult onset diabetes mellitus and obesity greater emphasis has been focused in decreasing dietary fat (l-4). In the United States, during the last two decades there has been increasing concern in the role of dietary fat and chronic disease. The most common recommendation among major scientific organizations are that individuals should reduce their fat intake to 30% of total calories (kilocalories) or less (5-7). Research has revealed that Americans, on average continue to consume a diet too high in fat (ranging from 34%-38.8% of kilocalories). The major * Corresponding
Author
33
34
J. KANDIAH etal.
contributors of dietary fat are table fats, processed meat and red meat. (8-10). The type and amount of fatty acid consumed also influences different disease state (10,ll). Though there has been a decrease in the intake of total dietary fat and saturated fat since NHANES II (1976-1980), saturated fats provide 12% of kilocalories in the diets of noninstitutionalized males and females greater than 2 months of age (9). Several trace elements have been shown to affect lipid metabolism and cholesterol synthesis (12-14). Among them is manganese, which acts as a cofactor of mevalonate kinase and farnesyl pyrophosphate synthetase, two enzymes necessary for cholesterol synthesis (15,16). In vitro studies have shown that the addition of manganese to rat liver cells increases cholesterol synthesis (17,18). However, little is known of the in vivo effect of manganese on cholesterol metabolism. Klimis-Tavantzis and coworkers reported results of a series of studies designed to investigate manganese deficiency on cholesterol and lipid metabolism in three experimental animal models (19-21). In young chicks and older laying hens, a diet deficient in manganese did not significantly alter plasma cholesterol, although liver cholesterol was significantly decreased (19). In weanling, Wistar and RICO (genetically hypercholesterolemic) rats, dietary manganese deficiency did not result in significant alterations in cholesterol and lipid metabolism (20). Recently, studies with weanling male Sprague-Dawley rats revealed liver manganese, total plasma protein and HDL cholesterol were significantly lower in manganese deficient rats (21). Diets rich in soy protein have been observed to decrease blood cholesterol levels (22-29). However, the effect of fat on the utilization of protein has not been well defined. The objective of the current study was to investigate the effects of level of fat with or without manganese supplementation on protein utilization.
METHODS
AND MATERIALS
periods of The study was composed of four experimental fourteen days each during which a measured, laboratory controlled diet was fed (Table 1). While the same foods were fed each day, some variations occurred among subjects so that caloric intakes for Subjects during could be maintained. weight maintenance experimental periods 1 and 2 received a HANES I survey (40% fat, and polyunsaturated to monounsaturated to 600 mg cholesterol, saturated fatty acids in a ratio of 4:14:14) or moderate fat diet (MF), while during experimental periods 3 and 4, subjects received Goal a similar meet the U.S. Dietary diet modified to recommendation regarding fat (30% of energy from fat, less than 300 and polyunsaturated to monounsaturated to mg. cholesterol/day, saturated fatty acids in a ratio of 1O:lO:lO) or also called a low fat diet (LF). Using a cross-over design one-half of the subjects
FAT/PROTEIN INTERACTIONS
35
received the moderate fat diet (MF) followed by the low fat diet (LF) while the reverse was followed for the other subjects. During the 5-day pre-period, subjects kept dietary diaries of kinds and amounts of food consumed, and made complete collections of urine and feces. Urine and fecal collections were compared with intake to verify completeness of 5-day dietary diaries. During the four 14-day experimental periods comprising each part, the following variations were used as shown on Table 1: basal diet alone (either moderate or low fat), or basal diet plus manganese gluconate amino acid chelate supplement. The variations resulted in alterations of protein intake. Exact quantities of the foods composing the basal diets were varied among subjects in order to make adjustments in calorie intake for weight maintenance of each individual. Subjects ranged in age from 24 to 36 years, ten were females and four were males with weight proportional to height, and twelve were Caucasian American and two were Hispanic American. All subjects received all experimental treatments; thus, each subject acted as his/her control. As in most studies of this kind, the study group was small and varied in gender, age, height and weight. This would be expected to increase the variation in other parameters of study results but not direction of response. All the subjects were undergraduate or graduate students at the University of Nebraska in the Department of Nutritional Science and Dietetics who maintained their usual study/work/social/life patterns except for eating the laboratory controlled diet in the Metabolic Research Laboratory of the Department of Nutritional Science and Dietetics and making complete collections of excreta. On the basis of health history information and pre-study blood analyses, subjects were cleared for participation by medical personnel of the University of Nebraska Division of Medical Services. Signing of Informed Consent documents prior to the start, of the study was a condition for participation. The project was approved by the University of Nebraska Institutional Committee for Projects Involving Human Subjects. Subjects made complete collections of urine and stools throughout the study. Creatinine measurements were made in repeat 24-hour urine collections in order to verify completeness of urine collections. Urine for each subject was composited on the basis of time into 24-hour lots, measured volumetrically, sampled and frozen for later analyses. Feces were divided into lots representative of food eaten during each experimental period via use of orally given fecal dyes (brilliant blue). Feces for each subject for each period were weighed, mixed, sampled, and frozen for later analyses. Fasting blood samples were drawn by professional medical technicians of the University of Nebraska Division of Medical Services on the first day of the study and at the end of each experimental period. Nitrogen concentrations in food, supplements, feces and urine were determined by the boric acid modification of the Kjeldahl method as defined by AOAC 1980. Dry fecal weights were used to estimate accuracy and completion of fecal collection on a
J.KANDIAH etal.
36
period basis. Nitrogen balances were calculated. All data were subjected to statistical analysis including Analysis of Variance and Duncan's Multiple Range Test. RESULTS AND DISCUSSION Nitrogen balance is commonly used as an index of protein nutrition and protein status in humans. Mean nitrogen intakes, corrected urinary and fecal nitrogen losses, and nitrogen balances of subjects receiving the various diets are given in Table 2. Mean intake of nitrogen during moderate fat diet was lower than the nitrogen intake on the low fat diet. Mean urinary losses of nitrogen while subjects received moderate fat plus manganese gluconate, low fat plus manganese gluconate and low fat alone were 9.33 r 1.21, 9.21 + 1.52, 9.35 + 1.24 and 9.50 f 1.23 g N/subject/day, respectively. The overall mean for all subjects for all periods while receiving moderate fat diet was 9.27 g N/subject/day and while receiving low fat diet was 9.43 g N/subject/day (p > 0.05).
TABLE 1 Experimental Plan - Study Pd.'
Intake Nitrogen# Mn*' mg/day g/day
1
2 3 4 *
# If t*t
11.24 11.24 12.58 12.58
40 40
Fat %
Cholesterol*** mg/day
40 40 30 30
600 600 <300 1300
Diet during the four experimental periods of fourteen days each composed of orange juice, tomato juice, milk, bran flakes ready-to-eat cereal, whole wheat bread, margarine, egg,. frankfurter, tuna, green beans, corn, peaches and cookies. Exact amounts varied among subjects due to differences needed for weight maintenance. Supplied by ordinary food contained in basal diet. Supplemental manganese supplied by manganese gluconate. Variations from moderate vs low fat were achieved through substitution of eggs for tuna.
FAT/PROTEIN INTERACTIONS
TABLE
2
Effect Of Altered Intakes Of Fat And Manganese On Protein Status Of Humans Trt.'
Intake g N/day 11.91a (f 0.88)
Urine g N/day 9.33= if 1.21)
Feces g N/day 1.26' f+ 0.33)
Balance g N/day 1.34= (+ 1.39)
MF + Mn
11.72' (? 0.68)
9.21a (+ 1.52)
1.26' (+ 0.37)
1.25' (-+1.48)
LF + Mn
13.22& (-+1.16)
9.35a (-+1.24)
1.60bc (+ 0.42)
2.21k (+ 1.25)
LF
13.25b (+ 1.14)
9.508 (+ 1.23)
1.60b (-+0.47)
2.17b (+ 1.11)
MF
* Moderate or low fat diets with or without manganese gluconate supplement. Mean values and SD of 14 subjects. Values with no repeated letter superscripts within each column are significantly different from one another (p < 0.05). Under the same experimental variations, mean fecal nitrogen losses were 1.26 f 0.33, 1.26 + 0.37, 1.60 + 0.42 and 1.60 -+ 0.47 g N/subject/day, respectively. The overall mean for all subjects for all periods while receiving moderate fat diet was 1.26 g N/subject/day while receiving low fat diet was 1.60 g N/subject/day (p < 0.0001). The results of mean fecal losses suggest that either the decrease in dietary fat or some other component of low fat diet caused an increase in mean fecal nitrogen excretion. Although the low fat diet was slightly higher in nitrogen content than was the moderate fat diet, this does not entirely account for the statistical difference in fecal N loss. Mean nitrogen balances calculated by subtracting urinary and fecal N from dietary nitrogen intake for the experimental treatments previously listed were 1.34 + 1.39, 1.25 f 1.48, 2.21 + 1.25 and 2.17 f 1.11. The overall mean for all subjects for all periods while receiving moderate fat diet was 1.30 g N/day and while receiving low fat diet was 2.19 g N/day (p < 0.004). As would be expected from previously discussed results on fecal loss of nitrogen, nitrogen balance tended to be less positive when the moderate fat diet was fed than when the low fat diet was fed. The overall mean urinary nitrogen losses for all subjects for all periods when they were receiving manganese supplement was 9.28 g N/day and while not receiving manganese supplement was 9.41 g N/day (p > 0.05). Mean fecal nitrogen losses while receiving same treatments as listed above were 1.43 and 1.43 g N/day, respectively
38
J. KANDIAH
etal.
(p > 0.05). Mean nitrogen balance while on the same treatments were 1.73 and 1.75 g N/day respectively (p > 0.05). Thus, no statistically significant effect of feeding manganese supplements on protein utilization were demonstrated. These results are similar to those earlier found in this laboratory (30). In conclusion, the results of this study indicate that no effects of feeding different levels of fat or manganese on nitrogen utilization or balance were demonstrated. However, feeding moderate fat diets in comparison to low fat diets tended to result in decreased nitrogen balances. Fecal nitrogen loss was higher when the low fat diets than when the moderate fat diets were fed. This suggests that protein is more poorly utilized with the feeding of lower rather than higher levels of fat.
Drs. Kandiah and Tuitoek would like to thank Dr. Kies (deceased) for her advice and contribution to the manuscript. REFERENCES 1.
Sacks FM. Dietary fat and blood pressure: A critical review of the evidence. Nutr Rev 1989; 47:291-300.
2.
Simopoulos AP. Omega 3 fatty acids in health and disease and in growth and development loss. Am J Clin Nutr 1991; 54:438463.
3.
Carroll KK. Dietary fats and cancer. Am J Clin Nutr 1991; 53:10648- 1067s.
4.
Leaf A, Weber PC. Cardiovascular effects of n-3 fatty acids. N Eng J Med 1988; 318:549-555.
5.
National cancer institute. Diet, nutrition and cancer Prevention: A guide to food choices. NIH: Washington D-C., 1987:2878.
6.
American heart association. Dietary guidelines for healthy american adults. Dallas: Texas, 1986.
7.
National research council, committee on diet and health, food and nutrition board, commission on life sciences. Diet and health: Implications for reducing chronic disease risk. Washington D.C., 1989.
FAT/PROTEIN INTERACTIONS
39
8.
Subar AF, Ziegler RG, Patterson BH, Ursin, G, Graubard B. US dietary patterns associated with fat intake: The 1987 national health interview survey. Am J Public Health 1994; 84:359-366.
9.
US Department of health and human services. Daily dietary fat and total energy intakes - third national health and nutrition examination survey, phase I, 1988-1991. J MMWR 1994; 43:116125.
10.
Ursin G, Ziegler RG, Subar AF, Graubard BI, Haile RW, Hoover R. Dietary patterns associated with a low-fat diet in the national health examination follow-up study: Identification of potential confounders for epidemiologic analyses. Am J Epidemiol 1993; 137:916-927.
11.
Dreon DM, Vranizan KM, Krauss RM, Austin MA, Wood fat vs monounsaturated effects of polyunsaturated plasma lipoproteins. JAMA 1990; 263:2462-2466.
12.
Allen KGD, Klevay copper deficiency.
13.
Koo SI, Williams DA. Relationship between the nutritional status of zinc cholesterol concentration of serum and lipoproteins in adult male rats. Am J Clin Nutr 1981; 34:23762381.
14.
Morrison LM, Schjaide A. Arterisclerosis: and regression, Illinois: Springfield,
15.
Amdur B, mevalonic
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