Bright, Elizabeth

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Journal of the Arkansas Academy of ScienceVolume 19 Article 141965Interrelationships of Certain Metabolic Responsesto Threonine Deficiency and to Various DietaryCarbohydrates in the White RatElizabeth BrightUniversity of Arkansas, FayettevilleFollow this and additional works at: http://scholarworks.uark.edu/jaasPart of the Biochemistry Commons, Food Processing Commons, and the Zoology CommonsThis article is available for use under the Creative Commons license: Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0). Users are able toread, download, copy, print, distribute, search, link to the full texts of these articles, or use them for any other lawful purpose, without asking priorpermission from the publisher or the author.This Article is brought to you for free and open access by ScholarWorks@UARK. It has been accepted for inclusion in Journal of the Arkansas Academyof Science by an authorized editor of ScholarWorks@UARK. For more information, please contact scholar@uark.edu, ccmiddle@uark.edu.Recommended CitationBright, Elizabeth (1965) "Interrelationships of Certain Metabolic Responses to Threonine Deficiency and to Various DietaryCarbohydrates in the White Rat," Journal of the Arkansas Academy of Science: Vol. 19 , Article 14.Available at: http://scholarworks.uark.edu/jaas/vol19/iss1/1466Arkansas Academy of Science Proceedings, Vol. 19, 1965THE INTERRELATIONSHIPS OF CERTAIN METABOLICRESPONSES TO THREONINE DEFICIENCY AND TO VARIOUSDIETARY CARBOHYDRATES IN THE WHITE RATElizabeth Bright'University of ArkansasThe importance of the relative amounts of amino acids in a pro-tein is a well known and accepted fact. An amino acid imbalance re-sults from any change in the proportions of the amino acids in the dietthat results in an adverse effect which can be prevented by supple-menting the diet with a relatively small amount of the most limitingamino acid(s) (1).IThreonine deficiency has been one of the most widely studiedmbalances, partly because its manifestations in the white rat are simi-ar to those of the calorie-protein deficiency disease, kwashiorkor, inlumans.As with all nutritional factors, amino acid deficiency does notunction completely independently. One of the most pronounced symp-oms of threonine deficiency is the deposition of excess lipid in theiver. However, the amount of liver lipid appears to depend partlyon the type and the amount of carbohydrate in the diet (2).It is not known just how the dietary carbohydrate influences thedevelopment of the threonine deficiency. This particular study was de-igned to observe the effect of various carbohydrates on threonineleficiency, and at the same time to gain some information about thenfluence of the amino acid imbalance on the handling of differentarbohydrates.Male weanling rats were used, six rats in each of six groups. Allof the rations contained 9% casein as the sole protein source. At thisevel, tryptophan, methionine and threonine are the limiting aminocids. Three of the rations were supplemented with all three of thesemino acids. The other three were supplemented with only tryptophannd methionine and, therefore, were deficient in threonine.IThe dietary carbohydrate was either glucose, fructose, or a 1:1mbination of the two.After the animals had been fed the diets for two weeks, theyere sacrificed and the livers removed for analysis.IThe total amount of liver lipid was determined as well as liverlolesterol and phospholipid levels. Triglyceride values were calcu-ited by substracting the sum of the phospholipids and cholesterolom the amount of total lipid. Livers were also assayed for concen-'Graduate Research Assistant, Department of Home Economics.66Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196567Responses to Threonine Deficiencytration of glycogen and for activities of the glucose-6-phosphatase (G-6-Pase) and fructose- 1 ,6-diphosphatase (FDPase)enzyme systems.Threonine deficient diets containing each of the different car-bohydrates were as readily consumed as the corresponding threoninesupplemented diets. However, within each subgroup, that is, threoninesupplemented or threonine deficient, diets containing fructose were notas readily accepted as those containing glucose (Table 1).The threonine deficiency resulted in a decrease of weight gainwith each of the carbohydrates. However this decrease was onlyslight when the dietary carbohydrate was glucose.Generally, decreased food intakes accounted for decreased weightgain. However, there was a significant interaction of the fructose andof the threonine deficiency in depressing the food efficiency ratio ofthe group receiving this diet (Table 2).Figure 1 illustrates the relative liver weights and the major com-nents of the liver (g/100 g of body weight).The substitution of fructose or the glucose/fructose combinationor glucose in either the threonine supplemented or the threonine defi-cient diets, resulted in increased liver sizes. However, only with thehreonine deficient diets did this substitution result in an increase in themilligrams of liver lipid per 100 g of body weight.(Although the liver sizes did not vary significantly between theroup receiving threonine and the groups not receiving it with eacharbohydrate, the livers of the animals fed the threonine deficientiets contained more lipid than those of their supplemented controlroup.Levels of glycogen, protein and water were largely reflective ofthe total liver size.Some differences in the composition of the total lipid were alsoound (Fig. 2). The level of cholesterol increased with the omissionof threonine from the glucose and the glucose/fructose diets, and the)hospholipid level increased slightly with the substitution of fructoseor glucose in the threonine deficient diets. However, the total accumu-ation of lipid in the liyer appears to be chiefly due to the net depositionf triglycerides.Two types of enzyme adaptation have been proposed: an in-rease in specific activity and an increase in relative liver size (3).he total activity (i.e., units per 100 g of body weight) would representle combination of the two methods, while specific activity (i.e., units>er 100 mg of liver nitrogen) would represent the part of the adapta-on accomplished by preferential synthesis of the enzymes. The graph:ig. 3) shows both total and specific activity.both threonine supplemented and threonine deficient diets,e activities of the two enzyme systems followsimilar patterns. Dietary 67Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14http://scholarworks.uark.edu/jaas/vol19/iss1/1468Arkansas Academy of Science ProceedingsTable 1. Food intake and weight gain of rats on low protein diets,with or without supplemental threonine, and with variousdietary carbohydrates.Food Intake Weight GainDiet Total /wk Total /wkg g g gI iG + Th 114 ±52 61 ±3 43 ±3 23 ± 1II F + Th 102 ±6 55 ±3 37 ± 3 20 ± 1III G/F + Th 12113 65±1 47±2 25 ±1IV G-Th 11313 6112 38 12 20 ± 1V F-Th 9316 5013 27 +3 14 ±1VI G/F-Th 118 + 6 63 + 3 40 +2 22 11*G— glucose, F — fructose, G/F — glucose/fructose (1:1),Th — threonine2Standard error of the meanIable 2. Utilization of low protein diets, with or without supplementalthreonine, and with various dietary carbohydrates. Gramweight gain per gram food intake.DietI 'G+Th .37 ±.022II F \ Th .36 + .01III G/F +Th .39±.O1IV G-Th .341.01V F-Th .28 1.01VI G/F-Th .34 £.01'G — glucose, F — fructose, G/F — glucose/fructose (1:1), Th — threonine2Standard error of the mean68Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 1965aw Xpoq 8 QOI asd 3m0 MO -H-p ho +s2u=MC—cholesterol.6969Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14http://scholarworks.uark.edu/jaas/vol19/iss1/1470-&-S-PASE-6-6-PA8E150-pi 150 --i FDPASE r-. FDPASE>- >> p- >J 100- r- £ 100-h n*50-l_ p 50-r~GFG GFG GFG GFG GF6 ©FG 6FG GFG+ — + —TH TH TH TH TH TH TH THFigure 1 Response of the activities of glucose-6-phosphatase (G-6-Pase) and fructoa«-l,6-diphosphatase(FDPase) to low protein diets, with or without supplemental threonine, and withvarious carbohydrates. A units per 100 g body weight, B units per 100 mg liver nitrogen(specific activity). G ¦ glucose, F = fructose, OF « glucose/fructose (1:1), Th ¦ threonine,One unit of activity = the amount of enzyme which willrelease 1 Pi/ainute.70Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196571Responses to Threonine DeficiencyIructose stimulated the activities of both systems. The response to thellucose/fructose combination was generally intermediate to that to glu-ose and to fructose.The omission of threonine from the glucose diet resulted in alight decrease in the G-6-Pase activity. This depression was due en-irely to a decrease in the specific activity since the nitrogen contentsof the livers of the two glucose-fed groups were the same. In one ex-ensive study of G-6-Pase activity (4), the only treatment found to de-rease the activity of this enzyme system was the feeding of a protein-ree diet. This suggests that the effect of an amino acid imbalance isimilar to that of a protein-free diet, and not merely an indication of adecrease in the level of utilizable protein.The reaction catalyzed by G-6-Pase represents the final step innet glucose formation. The activity of FDPase could be indicative ofthe participation of the Embden-AAeyerhof pathway (EAAP) in glucoseformation.The relative changes in activities of these two enzyme systemsn response to fructose feeding could be suggestive of the proportionof glucose formation due to the EAAP. This is, a 1:1 ratio of the stimu-ation of the G-6-Pase and FDPase activities in response to fructoseeeding would be consistent with a direct conversion of fructose toglucose via the EMP. A stimulation of the activity of FDPase less thanlat of G-6-Pase would indicate that some amount of fructose wasseing converted to glucose via a route not involving fructose-1,6-phos-shate. Difference in degree of stimulation also might, indicate a changen the synthesis or breakdown of glycogen.Total G-6-Pase activity increased with the substitution of eitherructose or the glucose/fructose combination for glucose in the threonineupplemented diets. This was accompanied by a proportionatelymailer increase in the FDPase activity (figure 4), resulting in a greaterifference between the activities of the two systems as compared with-\e difference for the glucose control group. Omission of the threonineupplement from the diet resulted in a much greater stimulation ofDPase activity by both fructose and the glucose/fructose combina-on. Differences between the activities were again greater with fruc-ose than with glucose, but were less with the glucose/fructose com-aination.Presumably, the greater the differences between the activities,>e more precursors must be reaching glucose-6-phosphate by a routether the reversed glycolysis (i.e., EMP). One source of the glucose-6-losphate would be the breakdown of glycogen. However, this wasjrobabl/ not the case, since those groups having the greater differ-nces between the enzymes' activities, also showed a net increase iniver glycogen. Glycogen deposition would represent a drain on theucose-6-phosphate and would indicate an even greater utilizationf a pathway other than the EMP than is suggested by the relativenzyme activities. 71Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14http://scholarworks.uark.edu/jaas/vol19/iss1/1472Arkansas Academy of Science Proceedings-t-THTHFigure 4 Difference In the total activities of flueose-6-phosphatase (G-6-Pase) and fructo»e-l,6-diphoBphataBe (FDPaae)enzyme systems in response to low protein diets, with orwithout supplemental threonine, and with rarioua carbohydrates.G * glucose, F ¦: fructose, Of-gluoose/fruotose (ltl)# Th-"threonine.72Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196573Responses to Threonine DeficiencyThe data from the study suggest that the degree of participationof the pathways bypassing fructose-diphosphate may be modified bya deficiency of threonine. The mechanism(s) by which an amino acidmbalance can influence relative activities of alternate pathways ofcarbohydrate metabolism is not clear.The possibility that the major pathway of the conversion of fruc-tose to glucose may not be the EMP has been -proposed by severalauthors [5-7). Although most of the previous studies were with purifiedenzyme systems, the fact that the substitution of fructose for glucose inthe diet has been shown to stimulate at least two enzyme systems ofthe hexose monophosphate shunt (HAAS) (8,9) suggests that the shuntmay play an important role in fructose metabolism.There has been much recent discussion about the relationship ofipogenesis to the shunt as well as to other NADPH producing systems.'he majority of the reports indicate that the degree of lipogehesis in-luences the activity of the HAAS rather than visa versa. In any case,he levels of liver lipid found under the conditions of this study do notcorrelate with the proposed pathways of carbohydrate utilization, assuggested by the relative activities of the two enzyme systems. Otheractors, such as increased fatty acid oxidation, may possibly operateo decrease the net amount of lipid in livers in which the HAAS is quiteactive.LITERATURE CITEDr. Harper, A. E. 1959. Amino acid balance and imbalance. I. Dietarylevel of protein and amino acid imbalance. J. Nutrition 68: 405.2. Macdonald, I. 1960. Some effects of carbohydrate in experimentallow-protein diets. J. Physiol. 160: 306.I. Friedland, R. A., and A. E. Harper. 1957. Metabolic adaptation ofhigher animals. I. Dietary effect of glucose-6-phosphatase. J. Biol.Chem. 228: 743.I. Friedland, R. A., and A. E. Harper. 1958. Metabolic adaptationof higher animals. III.Quantitative study of dietary factors causingresponse in liver glucose-6-phosphatase. J. Biol. Chem. 233: 1.5. Muntz, J. A., and M. Vanka. 1962. Studies on the utilization offructose in rat liver in vivo. Fed. Proc. 21: 84.6. 1962. The metabolism of intraportally injectedfructose in rat liver in vivo. J. Biol. Chem. 237: 3583.I. Landau, B. R., and W. Merlevede. 1963. Initial reaction in themetabolism of D- and L-glyceraldehyde by rat liver. J. Biol. Chem.238: 261.(Fitch, W. M., R. Hill and I. L. Chaikoff. 1960. The effect of fruc-tose feeding on glycolytic enzyme activities of the normal rat liver.J. Biol. Chem. 234: 1048.IFitch, W. M., and I. L. Chaikoff. 1960. Extent and patterns ofadaptations of enzyme activities in liver of normal rats fed dietshigh in glucose or fructose. J. Biol. Chem. 235: 534.73Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14http://scholarworks.uark.edu/jaas/vol19/iss1/14

Interrelationships of Certain Metabolic Responses to Threonine Deficiency and to Various Dietary Carbohydrates in the White Rat

UARK (University of Arkansas )

Journal of the Arkansas Academy of Science Volume 19 Article 14 1965 Interrelationships of Certain Metabolic Responses to Threonine Deficiency and to Various Dietary Carbohydrates in the White Rat Elizabeth Bright University of Arkansas, Fayetteville Follow this and additional works at: https://scholarworks.uark.edu/jaas  Part of the Biochemistry Commons, Food Processing Commons, and the Zoology Commons Recommended Citation Bright, Elizabeth (1965) "Interrelationships of Certain Metabolic Responses to Threonine Deficiency and to Various Dietary Carbohydrates in the White Rat," Journal of the Arkansas Academy of Science: Vol. 19 , Article 14. Available at: https://scholarworks.uark.edu/jaas/vol19/iss1/14 This article is available for use under the Creative Commons license: Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0). Users are able to read, download, copy, print, distribute, search, link to the full texts of these articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This Article is brought to you for free and open access by ScholarWorks@UARK. It has been accepted for inclusion in Journal of the Arkansas Academy of Science by an authorized editor of ScholarWorks@UARK. For more information, please contact scholar@uark.edu. 66Arkansas Academy of Science Proceedings, Vol. 19, 1965THE INTERRELATIONSHIPS OF CERTAIN METABOLICRESPONSES TO THREONINE DEFICIENCY AND TO VARIOUSDIETARY CARBOHYDRATES IN THE WHITE RATElizabeth Bright'University of ArkansasThe importance of the relative amounts of amino acids in a pro-tein is a well known and accepted fact. An amino acid imbalance re-sults from any change in the proportions of the amino acids in the dietthat results in an adverse effect which can be prevented by supple-menting the diet with a relatively small amount of the most limitingamino acid(s) (1).IThreoninedeficiency has been one of the most widely studiedmbalances, partly because its manifestations in the white rat are simi-ar to those of the calorie-protein deficiency disease, kwashiorkor, inlumans.As with all nutritional factors, amino acid deficiency does notunction completely independently. One of the most pronounced symp-oms of threonine deficiency is the deposition of excess lipid in theiver. However, the amount of liver lipid appears to depend partlyon the type and the amount of carbohydrate in the diet (2).It is not known just how the dietary carbohydrate influences thedevelopment of the threonine deficiency. This particular study was de-igned to observe the effect of various carbohydrates on threonineleficiency, and at the same time to gain some information about thenfluence of the amino acid imbalance on the handling of differentarbohydrates.Male weanling rats were used, six rats in each of six groups. Allof the rations contained 9% casein as the sole protein source. At thisevel, tryptophan, methionine and threonine are the limiting aminocids. Three of the rations were supplemented with all three of thesemino acids. The other three were supplemented with only tryptophannd methionine and, therefore, were deficient in threonine.IThe dietary carbohydrate was either glucose, fructose, or a 1:1mbination of the two.After the animals had been fed the diets for two weeks, theyere sacrificed and the livers removed for analysis.IThetotal amount of liver lipid was determined as well as liverlolesterol and phospholipid levels. Triglyceride values were calcu-ited by substracting the sum of the phospholipids and cholesterolom the amount of total lipid. Livers were also assayed for concen-'Graduate Research Assistant, Department of Home Economics.66Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196567Responses to Threonine Deficiencytration of glycogen and for activities of the glucose-6-phosphatase (G-6-Pase) and fructose- 1 ,6-diphosphatase (FDPase)enzyme systems.Threonine deficient diets containing each of the different car-bohydrates were as readily consumed as the corresponding threoninesupplemented diets. However, within each subgroup, that is, threoninesupplemented or threonine deficient, diets containing fructose were notas readily accepted as those containing glucose (Table 1).The threonine deficiency resulted in a decrease of weight gainwith each of the carbohydrates. However this decrease was onlyslight when the dietary carbohydrate was glucose.Generally, decreased food intakes accounted for decreased weightgain. However, there was a significant interaction of the fructose andof the threonine deficiency in depressing the food efficiency ratio ofthe group receiving this diet (Table 2).Figure 1 illustrates the relative liver weights and the major com-nents of the liver (g/100 g of body weight).The substitution of fructose or the glucose/fructose combinationor glucose in either the threonine supplemented or the threonine defi-cient diets, resulted in increased liver sizes. However, only with thehreonine deficient diets did this substitution result in an increase in themilligrams of liver lipid per 100 g of body weight.(Althoughthe liver sizes did not vary significantly between theroup receiving threonine and the groups not receiving it with eacharbohydrate, the livers of the animals fed the threonine deficientiets contained more lipid than those of their supplemented controlroup.Levels of glycogen, protein and water were largely reflective ofthe total liver size.Some differences in the composition of the total lipid were alsoound (Fig. 2). The level of cholesterol increased with the omissionof threonine from the glucose and the glucose/fructose diets, and the)hospholipid level increased slightly with the substitution of fructoseor glucose in the threonine deficient diets. However, the total accumu-ation of lipid in the liyer appears to be chiefly due to the net depositionf triglycerides.Two types of enzyme adaptation have been proposed: an in-rease in specific activity and an increase in relative liver size (3).he total activity (i.e., units per 100 g of body weight) would representle combination of the two methods, while specific activity (i.e., units>er 100 mg of liver nitrogen) would represent the part of the adapta-on accomplished by preferential synthesis of the enzymes. The graph:ig. 3) shows both total and specific activity.both threonine supplemented and threonine deficient diets,e activities of the two enzyme systems followsimilar patterns. Dietary 67Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14https://scholarworks.uark.edu/jaas/vol19/iss1/1468Arkansas Academy of Science ProceedingsTable 1. Food intake and weight gain of rats on low protein diets,with or without supplemental threonine, and with variousdietary carbohydrates.Food Intake Weight GainDiet Total /wk Total /wkg g g gI iG + Th 114 ±52 61 ±3 43 ±3 23 ± 1II F + Th 102 ±6 55 ±3 37 ± 3 20 ± 1III G/F + Th 12113 65±1 47±2 25 ±1IV G-Th 11313 6112 38 12 20 ± 1V F-Th 9316 5013 27+3 14 ±1VI G/F-Th 118 + 6 63 + 3 40+2 22 11*G— glucose, F — fructose, G/F — glucose/fructose (1:1),Th — threonine2Standard error of the meanIable2. Utilization of low protein diets, with or without supplementalthreonine, and with various dietary carbohydrates. Gramweight gain per gram food intake.DietI 'G+Th .37 ±.022II F \ Th .36 + .01III G/F +Th .39±.O1IV G-Th .341.01V F-Th .28 1.01VI G/F-Th .34 £.01'G—glucose, F — fructose, G/F — glucose/fructose (1:1), Th — threonine2Standard error of the mean68Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 1965aw Xpoq 8 QOI asd 3m0 MO -H-p ho +s2u=MC—cholesterol.6969Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14https://scholarworks.uark.edu/jaas/vol19/iss1/1470-&-S-PASE-6-6-PA8E150-pi 150--i FDPASE r-. FDPASE>- >> p- >J 100- r- £ 100-h n*50-l_ p 50-r~GFG GFG GFG GFG GF6 ©FG 6FG GFG+ — + —TH TH TH TH TH TH TH THFigure 1 Response of the activities of glucose-6-phosphatase (G-6-Pase) and fructoa«-l,6-diphosphatase(FDPase) to low protein diets, with or without supplemental threonine, and withvarious carbohydrates. A units per 100 g body weight, B units per 100 mg liver nitrogen(specific activity). G ¦ glucose, F = fructose, OF « glucose/fructose (1:1), Th ¦ threonine,One unit of activity = the amount of enzyme which willrelease 1 Pi/ainute.70Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196571Responses to Threonine DeficiencyIructose stimulated the activities of both systems. The response to thellucose/fructose combination was generally intermediate to that to glu-ose and to fructose.The omission of threonine from the glucose diet resulted in alight decrease in the G-6-Pase activity. This depression was due en-irely to a decrease in the specific activity since the nitrogen contentsof the livers of the two glucose-fed groups were the same. In one ex-ensive study of G-6-Pase activity (4), the only treatment found to de-rease the activity of this enzyme system was the feeding of a protein-ree diet. This suggests that the effect of an amino acid imbalance isimilar to that of a protein-free diet, and not merely an indication of adecrease in the level of utilizable protein.The reaction catalyzed by G-6-Pase represents the final step innet glucose formation. The activity of FDPase could be indicative ofthe participation of the Embden-AAeyerhof pathway (EAAP) in glucoseformation.The relative changes in activities of these two enzyme systemsn response to fructose feeding could be suggestive of the proportionof glucose formation due to the EAAP. This is, a 1:1 ratio of the stimu-ation of the G-6-Pase and FDPase activities in response to fructoseeeding would be consistent with a direct conversion of fructose toglucose via the EMP. A stimulation of the activity of FDPase less thanlat of G-6-Pase would indicate that some amount of fructose wasseing converted to glucose via a route not involving fructose-1,6-phos-shate. Difference in degree of stimulation also might, indicate a changen the synthesis or breakdown of glycogen.Total G-6-Pase activity increased with the substitution of eitherructose or the glucose/fructose combination for glucose in the threonineupplemented diets. This was accompanied by a proportionatelymailer increase in the FDPase activity (figure 4), resulting in a greaterifference between the activities of the two systems as compared with-\e difference for the glucose control group. Omission of the threonineupplement from the diet resulted in a much greater stimulation ofDPase activity by both fructose and the glucose/fructose combina-on. Differences between the activities were again greater with fruc-ose than with glucose, but were less with the glucose/fructose com-aination.Presumably, the greater the differences between the activities,>e more precursors must be reaching glucose-6-phosphate by a routether the reversed glycolysis (i.e., EMP). One source of the glucose-6-losphate would be the breakdown of glycogen. However, this wasjrobabl/ not the case, since those groups having the greater differ-nces between the enzymes' activities, also showed a net increase iniver glycogen. Glycogen deposition would represent a drain on theucose-6-phosphate and would indicate an even greater utilizationf a pathway other than the EMP than is suggested by the relativenzyme activities. 71Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14https://scholarworks.uark.edu/jaas/vol19/iss1/1472Arkansas Academy of Science Proceedings-t-THTHFigure 4 Difference In the total activities of flueose-6-phosphatase (G-6-Pase) and fructo»e-l,6-diphoBphataBe (FDPaae)enzyme systems in response to low protein diets, with orwithout supplemental threonine, and with rarioua carbohydrates.G * glucose, F ¦: fructose, Of-gluoose/fruotose (ltl)# Th-"threonine.72Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14Published by Arkansas Academy of Science, 196573Responses to Threonine DeficiencyThe data from the study suggest that the degree of participationof the pathways bypassing fructose-diphosphate may be modified bya deficiency of threonine. The mechanism(s) by which an amino acidmbalance can influence relative activities of alternate pathways ofcarbohydrate metabolism is not clear.The possibility that the major pathway of the conversion of fruc-tose to glucose may not be the EMP has been -proposed by severalauthors [5-7). Although most of the previous studies were with purifiedenzyme systems, the fact that the substitution of fructose for glucose inthe diet has been shown to stimulate at least two enzyme systems ofthe hexose monophosphate shunt (HAAS) (8,9) suggests that the shuntmay play an important role in fructose metabolism.There has been much recent discussion about the relationship ofipogenesis to the shunt as well as to other NADPH producing systems.'he majority of the reports indicate that the degree of lipogehesis in-luences the activity of the HAAS rather than visa versa. In any case,he levels of liver lipid found under the conditions of this study do notcorrelate with the proposed pathways of carbohydrate utilization, assuggested by the relative activities of the two enzyme systems. Otheractors, such as increased fatty acid oxidation, may possibly operateo decrease the net amount of lipid in livers in which the HAAS is quiteactive.LITERATURE CITEDr. Harper, A. E. 1959. Amino acid balance and imbalance. I. Dietarylevel of protein and amino acid imbalance. J. Nutrition 68: 405.2. Macdonald, I. 1960. Some effects of carbohydrate in experimentallow-protein diets. J. Physiol. 160: 306.I. Friedland, R. A., and A. E. Harper. 1957. Metabolic adaptation ofhigher animals. I. Dietary effect of glucose-6-phosphatase. J. Biol.Chem. 228: 743.I. Friedland, R. A., and A. E. Harper. 1958. Metabolic adaptationof higher animals. III.Quantitative study of dietary factors causingresponse in liver glucose-6-phosphatase. J. Biol. Chem. 233: 1.5. Muntz, J. A., and M. Vanka. 1962. Studies on the utilization offructose in rat liver in vivo. Fed. Proc. 21: 84.6. 1962. The metabolism of intraportally injectedfructose in rat liver in vivo. J. Biol. Chem. 237: 3583.I. Landau, B. R., and W. Merlevede. 1963. Initial reaction in themetabolism of D- and L-glyceraldehyde by rat liver. J. Biol. Chem.238: 261.(Fitch, W. M., R. Hill and I. L. Chaikoff. 1960. The effect of fruc-tose feeding on glycolytic enzyme activities of the normal rat liver.J. Biol. Chem. 234: 1048.IFitch, W. M., and I. L. Chaikoff. 1960. Extent and patterns ofadaptations of enzyme activities in liver of normal rats fed dietshigh in glucose or fructose. J. Biol. Chem. 235: 534.73Journal of the Arkansas Academy of Science, Vol. 19 [1965], Art. 14https://scholarworks.uark.edu/jaas/vol19/iss1/14

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Interrelationships of Certain Metabolic Responses to Threonine Deficiency and to Various Dietary Carbohydrates in the White Rat

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