Female rats 4 weeks old were fed diets including beef tallow or safflower oil in combination with sucrose or rice starch. At 8 weeks of age, half the rats were orally administered 2 of estrogen (mestranol) in 5 μl of safflower oil and half were fed the vehicle only. After 10 to 14 days of estrogen treatment, rats were fasted and exsanguinated. Alterations were found in weight gain, liver weights, and levels of various lipids in plasma and liver. Most lipid levels were influenced by an interaction of mestranol with one of the dietary factors. No changes were observed in blood clotting activity as measured by prothrombin time and levels of plasma fibrinogen

Clevidence, Beverly A.

English

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Journal of the Arkansas Academy of ScienceVolume 30 Article 141976Dietary Fat-Carbohydrate Combinations: TheirEffects on Lipid Metabolism in Estrogen-TreatedRatsBeverly A. ClevidenceUniversity of Arkansas, FayettevilleFollow this and additional works at: http://scholarworks.uark.edu/jaasPart of the Biochemistry 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 CitationClevidence, Beverly A. (1976) "Dietary Fat-Carbohydrate Combinations: Their Effects on Lipid Metabolism in Estrogen-TreatedRats," Journal of the Arkansas Academy of Science: Vol. 30 , Article 14.Available at: http://scholarworks.uark.edu/jaas/vol30/iss1/14Arkansas Academy of Science Proceedings, Vol. XXX,197636Dietary Fat-Carbohydrate Combinations: Their Effectson LipidMetabolism inEstrogen-Treated RatsBEVERLY A.CLEVIDENCEDepartment ot Home Economics,University of Arkansas, Fayetteville, Arkansas 72701ABSTRACTFemale rats 4 weeks old were fed diets including beef tallow or safflower oil incombination with sucrose or rice starch. At 8 weeks of age, half the rats were orallyadministered 2 of estrogen (mestranol) in5 Ml of safflower oil and half were fed thevehicle only. After 10 to 14 days of estrogen treatment, rats were fasted and exsanguinated.Alterations were found in weight gain, liver weights, and levels of various lipids inplasmaand liver.Most lipid levels were influenced by an interaction of mestranol with one of thedietary factors. No changes were observed in blood clotting activity as measured byprothrombin time and levels of plasma fibrinogen.INTRODUCTIONOral contraceptives (OCs) are known to elevate plasma lipids andto increase thromboembolism in women (Mann et al. 1975). It ispossible that certain dietary histories predispose women tothrombosis. Estrogens from OCs may act synergistically with certaindietary patterns. Plasma and liver lipids and blood clotting activity inrats are known to be influenced by the interaction of OCs withdietary fat (Tabacchi and Kirksey 1973). Plasma and liver lipids areknown tobe influenced by type of carbohydrate fed with various fats(Carroll and Bright 1965). The purpose of this investigation was tostudy liverand plasma lipidlevels and blood clotting activityofyoungfemale rats treated with estrogen and fed diets of varied fat-carbohydrate composition.MATERIALS ANDMETHODSThe experiment was designed as a 2 X2 X2 factorial with 5or 6 ratsto each of 8 treatment combinations. Experimental variables werethe type ofdietary fat. beef tallow (BT)or safflower oil (SO): the typeofdietary carbohydrate, sucrose (S) or rice starch (RS); and estrogentreatment, with mestranol 1(+M)orwithout mestranol (-M).At 4 weeks of age, female rats of the Sprague-Dawley 1strain wereassigned at random to treatment groups. Ina temperature controlledroom, rats were housed individually in wire-bottomed cages wherethey had free access to water and ration (Table I).At 8 weeks of age.half the rats fed each of the 4diets were orally administered .' /< t: <>lmestranol, a common estrogen in OCs, in 5 M1 of safflower oil andhalf were fed the vehicle only. This quantity of mestranol isapproximately the minimum dosage of estrogen used in combinationwith a progestin to prevent conception in rats (Aftergood and AllinSlater 1971). In proportion to body weight, this dosage in rats isapproximately 10 times the quantity ofestrogen taken by women whouse OCs.After 10 to 14 days of estrogen treatment, rats were fasted for 4hours, anesthetized with sodium pentobarbital, and exsanguinatedfrom the abdominal aorta. Liver and plasma were assayed for lipidcontent. Triglyceride was assayed by the method of Mendez et al.(1975). The method of Zlatkis et al. (1953) was used to determinecholesterol. Phospholipid was hydrolyzed by the method of Young-berg and Youngberg (1930), and the inorganic phosphorus thusreleased was determined by the method of Fiske and Subbarow(1925). Plasma coagulation properties assayed were prothrombintime (Faulkner and King 1970) and level of plasma fibrinogen(Ratnoff and Menzie 1964). Data were examined by analysis ofvariance in a completely random design. Significance wasdetermined from /"-values.'Amersham Searle Chemicals, Inc., Chicago, Illinois.'Hormone Assay Laboratories, Chicago, Illinois.RESULTS ANDDISCUSSIONMestranol depressed weight gain by 46% (Table II). Rats treatedwith mestranol not only ate less ration than did their counterparts,but also used food consumed less efficiently for weight gain. Rats fedSO had heavier livers inrelation to body weight than did those fedBT.Relative liver weights of rats treated withmestranol were greaterbecause of lower body weights. Values forliverlipidswere stated per100 mg of liver protein in order to make comparisons unaffected byliver or body weights.Total liver lipids and liver triglycerides were altered by an inter-action of the carbohydrate and estrogen factors (Fig. la, b). Withoutmestranol, liver lipid was greater when the dietary carbohydrate wasRS rather than S. However, when the treatment included mestranol.RS was unable to elevate total liver lipidsand triglycerides.It is not clear why, in the absence of mestranol, RS but not Selevated liver lipids.Carroll and Bright (1965), who fed low carbohy-drate-high fat diets, found that accumulation of liver lipidsinmalerats was dependent on both the type of carbohydrate and the type offat fed. In that study, liver lipid was decreased when rats were fedfructose with corn oilrather than glucose with corn oil,or eithercarbohydrate withhydrogenated coconut oil.The fate of RS in the presence of mestranol is unknown. Cortisol,which increases gluconeogenesis and inhibits fatty acid synthesis inthe liver, is known to be elevated in plasma of rats treated withmestranol (Renaud 1970). Perhaps glucose from RS undergoeslipogenesis in the absence of mestranol but is utilized by cells orconverted to glycogen inthe presence of mestranol.Livercholesterol was elevated by SO and by the interaction of SOwith RS, regardless of whether or not mestranol was administered(Fig. lc).Plasma cholesterol was depressed by mestranol, an actionindependent of the type of fat or carbohydrate fed (Table III).Thus,the elevation of liver cholesterol and the depression of plasmacholesterol were unrelated and not the result of transfer from plasmato liver.Plasma phospholipids were elevated by BTover SO, and depressedby the interaction of SO with mestranol. Although mestranol had noinfluence on plasma phospholipids when the dietary fat was BT.phospholipids were greatly decreased by mestranol when SO was fed(Fig. Id). Aftergood and Alfin-Slater (1971) reported that plasmaphospholipids were decreased in female rats fed a stock diet andtreated withan OC.Plasma cholesterol and plasma phospholipids of rats weredepressed in this experiment by mestranol or by an interaction thatincluded mestranol. Yet these lipids commonly are elevated in theplasma of women who take OCs. In contrast, plasma triglyceridesseem to be elevated in both women and rats by most OCs and byestrogen. Although plasma triglycerides were not measured in thisstudy, it is suspected that this lipidwas elevated by mestranol (Kekkiand Nikkila 1971, Tabacchi and Kirksey 1973, Kudzma et al. 1975).The liverof an estrogen-fed animal is likelytobe overburdened withfatty acids because estrogen elevates plasma cortisol levels and36Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14Published by Arkansas Academy of Science, 1976Beverly A.Clevidencecortisol mobilizes fatty acids from adipose tissue. The liver, which LITERATURE CITEDcannot use fatty acids for gluconeogenesis, may incorporate theminto triglycerides and transfer them to the blood as lipoproteins. AFTERGOOD, L.and R.B. ALFIN-SLATER. 1971. Further studiesNo difference in blood clotting activity among treatments was of the effects of an anovulatory drug on lipidmetabolism inthefound as measured by prothrombin time or level of plasma rat. J. LipidRes. 12:306-312.i fibrinogen. Tabacchi and Kirksey (1973) reported that OCsi containing mestranol elevated levels of plasma fibrinogen in 7- CARROLL,C. and E. BRIGHT.1965. Influence of carbohydrate-to-| month-old female rats when the diet included coconut oil or fat ratio on metabolic changes induced in rats by feeding; cholesterol. Negative results of the present experiment may have different carbohydrate-fat combinations. J. Nutr. 87:202-210.; been due to the youthof the rats tested.I The results of this study indicate that young female rats undergo FAULKNER, W.R. and J.W. KING, eds. 1970. Chemical Rubberchanges in liver and plasma lipids inresponse to the type of dietary Company manual of clinical laboratory procedures. ChemicalI fat or carbohydrate, and that these changes can be modified by Rubber Co., Cleveland. P. 191.> administration of mestranol. Yet certain blood clotting factors do not¦; appear to be altered either by mestranol or by dietary fat or carbohy- FISKE, C.H. and Y.SUBBAROW. 1925. The colorimetric determi-I drate. nation of phosphorus. J. Biol. Chem. 66:375-400.j Table I.Composition of Diets KEKKI,M.and E.A. NIKKILA.1971. Plasma triglyceride turnoverg/100 g diet duringuseof oral contraceptives. Metabolism 20:878-889.I Vitamin-free casein* 19.6m ,..,.„.! n, KUDZMA, D.J., F. ST. CLAIRE, L. DeLALLO and S.J.i " 7 p „ 2 Sn FRIEDBERG. 1975. Mechanism of avian estrogen-induced• Salts, R, H. 5.0 hypertriglyceridemia: evidence for overproduction of{ Vitamin Mixture-3 0.3 triglyceride. J. LipidRes. 16:123-133.Choline Chloride 0,2Fat 4 20.0 MANN, J.I., M.P. VESSEY, M. THOROGOOD and R. DOLL,j Carbohydrate^ 30.0 1975 - Myocardial infarction in young women with special! Alphacel* 24 5 reference to oral contraceptive practice. Brit.Med. J. 2:241-245.I *ICN Pharmaceuticals, Inc., Cleveland, OH.J Table II.Weight Gain. Food Intake, and Food Efficiency RatioI p_ _ _ , „ , _ ,«*- During Period ofMestranol TreatmentI 0. P. and Harper, A. E. 1965.I J. Nutr. 87: 267-273. Weight Rain Food intake FER 200 (b)I 3mg/100 g of ration: thiamine HC1, 0,8; Fat ,j pyridoxine, 0.4; Ca pantothenate, 4,0; so 12niacin, 5.0; inositol, 20.0; folic acid, carbohydrate0.4; vitamin B12(triturated 3000^ per g), £s' 1.33; biotin, 0.02; vitamin A powder EstrogenI (20,000 IU per g), 10.0; calciferol (850,000j IU per g), 0.18; DL-«( -tocopherol powder(250 IU per g), 30.0; menadione, 0.38; significant f valuesriboflavin, 0.6; and sucrose, 176.89. (p<o.oo 5) E.t E.t(P< 0.05) Esttallow or Saf flower Oil.'BT-beef tallow, SO-saf flower oil, S ¦= sucrose, RS-ricestarch,-M-without mestranol, +M = with mestranol.I Sucrose Or rice Starch. 2 Food efficiency ratio ¦ r welRht Rain/100 s> food intake.\ C V -S 12 r1an \ a \ 2 m[ B, SO - \ u \ C Jt \ o \ S 3 ~ >^ »h 130 "1 I I -—1 \.& I* " S | BT | SO \^¦ I |? « 2 - -a 110-6 2 I I % * 1 L_ g K. 1 1 =£ I L_-M +M=-M +M >, S RS -M +Mbo—(a)'(b) & (c) (d)Figure 1. Interaction means ofliver and plasma lipids. RS = rice starch. S = sucrose, -M = without mestranol, +M = with mestranol. SO =safflower oil, BT =beef tallow.! Arkansas Academy of Science Proceedings, Vol. XXX,1976 3737Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14http://scholarworks.uark.edu/jaas/vol30/iss1/14iArkansas Academy of Science Proceedings, Vol.XXX,197638Dietary Fat-Carbohydrate CombinationsMENDEZ. J.. B. FRANKLIN and H. GAHAGAN. 1975. Simplemanual procedure for determination of serum triglycerides.Clin.Chem. 21:768-770.RATNOFF.O.D. and C. MENZIE.1964. Estimation of fibrinogen insmall samples of plasma. Pages 224-226 in L.M. Tocantins andL.A. Kazal. eds. Blood coagulation, hemorrhage andthrombosis. Grue and Stratton. New York.RENAUD. S. 1970. Thrombosis and atherosclerosis prevention byestrogens in hyperlipemic rats. Atherosclerosis 12:467-473.Table III.Composition of Liverand Plasma LipidsTABACCHI. M.H. and A. KIRKSEY. 1973. Influence of dietarylipids on plasma and hepatic lipids and on blood clottingproper-ties in rats fed oralcontraceptives. J. Nutr. 103:1270-1278.YOUNGBERG, B. and M. YOUNGBERG. 1930. Phosphorusmetabolism. I.A system of blood phosphorus analysis. J. Lab.Clin. Med. 16:158.ZLATKIS. A..B. ZAK and A.J. BOYLE. 1953. A new method forthe direct determination of serum cholesterol. J. Lab.Clin. Med.41:486-492.Liver lipids Plasma lipidsTotal Triglyc-Lipid erideCholes-terolCholes- Phospho-terol lipidmg/100 mg liver protein nig/100 ml plasmaFatBT1 24.6726.416.805.292.293.1395.189.9137SO 118CarbohydrateS 94.091.012822.7828.454.557.702.452.95 127RSEstrogen-M 27.4723.687.434.752.722.67102.483.1132+M 124Significant F values(P< 0.005) CHO, Est, CHO, Est, Fat, CHO,CHO X Est CHO X EstEst Fat(P< 0.05) Fat X CHO Fat X Est*BT = beef tallow, SO = safflower oil, S = sucrose, RS = rice starch,-M = without mestranol, +M = with mestranol.38Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14Published by Arkansas Academy of Science, 1976

Dietary Fat-Carbohydrate Combinations: Their Effects on Lipid Metabolism in Estrogen-Treated Rats

UARK (University of Arkansas )

Journal of the Arkansas Academy of Science Volume 30 Article 14 1976 Dietary Fat-Carbohydrate Combinations: Their Effects on Lipid Metabolism in Estrogen-Treated Rats Beverly A. Clevidence University of Arkansas, Fayetteville Follow this and additional works at: https://scholarworks.uark.edu/jaas  Part of the Biochemistry Commons Recommended Citation Clevidence, Beverly A. (1976) "Dietary Fat-Carbohydrate Combinations: Their Effects on Lipid Metabolism in Estrogen-Treated Rats," Journal of the Arkansas Academy of Science: Vol. 30 , Article 14. Available at: https://scholarworks.uark.edu/jaas/vol30/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. Arkansas Academy of Science Proceedings, Vol. XXX,197636Dietary Fat-Carbohydrate Combinations: Their Effectson LipidMetabolism inEstrogen-Treated RatsBEVERLY A.CLEVIDENCEDepartment ot Home Economics,University of Arkansas, Fayetteville, Arkansas 72701ABSTRACTFemale rats 4 weeks old were fed diets including beef tallow or safflower oil incombination with sucrose or rice starch. At 8 weeks of age, half the rats were orallyadministered 2 of estrogen (mestranol) in5 Ml of safflower oil and half were fed thevehicle only. After 10 to 14 days of estrogen treatment, rats were fasted and exsanguinated.Alterations were found in weight gain, liver weights, and levels of various lipids inplasmaand liver.Most lipid levels were influenced by an interaction of mestranol with one of thedietary factors. No changes were observed in blood clotting activity as measured byprothrombin time and levels of plasma fibrinogen.INTRODUCTIONOral contraceptives (OCs) are known to elevate plasma lipids andto increase thromboembolism in women (Mann et al. 1975). It ispossible that certain dietary histories predispose women tothrombosis. Estrogens from OCs may act synergistically with certaindietary patterns. Plasma and liver lipids and blood clotting activity inrats are known to be influenced by the interaction of OCs withdietary fat (Tabacchi and Kirksey 1973). Plasma and liver lipids areknown tobe influenced by type of carbohydrate fed with various fats(Carroll and Bright 1965). The purpose of this investigation was tostudy liverand plasma lipidlevels and blood clotting activityofyoungfemale rats treated with estrogen and fed diets of varied fat-carbohydrate composition.MATERIALS ANDMETHODSThe experiment was designed as a 2 X2 X2 factorial with 5or 6 ratsto each of 8 treatment combinations. Experimental variables werethe type ofdietary fat. beef tallow (BT)or safflower oil (SO): the typeofdietary carbohydrate, sucrose (S) or rice starch (RS); and estrogentreatment, with mestranol 1(+M)orwithout mestranol (-M).At 4 weeks of age, female rats of the Sprague-Dawley 1strain wereassigned at random to treatment groups. Ina temperature controlledroom, rats were housed individually in wire-bottomed cages wherethey had free access to water and ration (Table I).At 8 weeks of age.half the rats fed each of the 4diets were orally administered .' /< t: <>lmestranol, a common estrogen in OCs, in 5 M1 of safflower oil andhalf were fed the vehicle only. This quantity of mestranol isapproximately the minimum dosage of estrogen used in combinationwith a progestin to prevent conception in rats (Aftergood and AllinSlater 1971). In proportion to body weight, this dosage in rats isapproximately 10 times the quantity ofestrogen taken by women whouse OCs.After 10 to 14 days of estrogen treatment, rats were fasted for 4hours, anesthetized with sodium pentobarbital, and exsanguinatedfrom the abdominal aorta. Liver and plasma were assayed for lipidcontent. Triglyceride was assayed by the method of Mendez et al.(1975). The method of Zlatkis et al. (1953) was used to determinecholesterol. Phospholipid was hydrolyzed by the method of Young-berg and Youngberg (1930), and the inorganic phosphorus thusreleased was determined by the method of Fiske and Subbarow(1925). Plasma coagulation properties assayed were prothrombintime (Faulkner and King 1970) and level of plasma fibrinogen(Ratnoff and Menzie 1964). Data were examined by analysis ofvariance in a completely random design. Significance wasdetermined from /"-values.'Amersham Searle Chemicals, Inc., Chicago, Illinois.'Hormone Assay Laboratories, Chicago, Illinois.RESULTS ANDDISCUSSIONMestranol depressed weight gain by 46% (Table II). Rats treatedwith mestranol not only ate less ration than did their counterparts,but also used food consumed less efficiently for weight gain. Rats fedSO had heavier livers inrelation to body weight than did those fedBT.Relative liver weights of rats treated withmestranol were greaterbecause of lower body weights. Values forliverlipidswere stated per100 mg of liver protein in order to make comparisons unaffected byliver or body weights.Total liver lipids and liver triglycerides were altered by an inter-action of the carbohydrate and estrogen factors (Fig. la, b). Withoutmestranol, liver lipid was greater when the dietary carbohydrate wasRS rather than S. However, when the treatment included mestranol.RS was unable to elevate total liver lipidsand triglycerides.It is not clear why, in the absence of mestranol, RS but not Selevated liver lipids.Carroll and Bright (1965), who fed low carbohy-drate-high fat diets, found that accumulation of liver lipidsinmalerats was dependent on both the type of carbohydrate and the type offat fed. In that study, liver lipid was decreased when rats were fedfructose with corn oilrather than glucose with corn oil,or eithercarbohydrate withhydrogenated coconut oil.The fate of RS in the presence of mestranol is unknown. Cortisol,which increases gluconeogenesis and inhibits fatty acid synthesis inthe liver, is known to be elevated in plasma of rats treated withmestranol (Renaud 1970). Perhaps glucose from RS undergoeslipogenesis in the absence of mestranol but is utilized by cells orconverted to glycogen inthe presence of mestranol.Livercholesterol was elevated by SO and by the interaction of SOwith RS, regardless of whether or not mestranol was administered(Fig. lc).Plasma cholesterol was depressed by mestranol, an actionindependent of the type of fat or carbohydrate fed (Table III).Thus,the elevation of liver cholesterol and the depression of plasmacholesterol were unrelated and not the result of transfer from plasmato liver.Plasma phospholipids were elevated by BTover SO, and depressedby the interaction of SO with mestranol. Although mestranol had noinfluence on plasma phospholipids when the dietary fat was BT.phospholipids were greatly decreased by mestranol when SO was fed(Fig. Id). Aftergood and Alfin-Slater (1971) reported that plasmaphospholipids were decreased in female rats fed a stock diet andtreated withan OC.Plasma cholesterol and plasma phospholipids of rats weredepressed in this experiment by mestranol or by an interaction thatincluded mestranol. Yet these lipids commonly are elevated in theplasma of women who take OCs. In contrast, plasma triglyceridesseem to be elevated in both women and rats by most OCs and byestrogen. Although plasma triglycerides were not measured in thisstudy, it is suspected that this lipidwas elevated by mestranol (Kekkiand Nikkila 1971, Tabacchi and Kirksey 1973, Kudzma et al. 1975).The liverof an estrogen-fed animal is likelytobe overburdened withfatty acids because estrogen elevates plasma cortisol levels and36Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14Published by Arkansas Academy of Science, 1976Beverly A.Clevidencecortisol mobilizes fatty acids from adipose tissue. The liver, which LITERATURE CITEDcannot use fatty acids for gluconeogenesis, may incorporate theminto triglycerides and transfer them to the blood as lipoproteins. AFTERGOOD, L.and R.B. ALFIN-SLATER. 1971. Further studiesNo difference in blood clotting activity among treatments was of the effects of an anovulatory drug on lipidmetabolism inthefound as measured by prothrombin time or level of plasma rat. J. LipidRes. 12:306-312.i fibrinogen. Tabacchi and Kirksey (1973) reported that OCsi containing mestranol elevated levels of plasma fibrinogen in 7- CARROLL,C. and E. BRIGHT.1965. Influence of carbohydrate-to-| month-old female rats when the diet included coconut oil or fat ratio on metabolic changes induced in rats by feeding; cholesterol. Negative results of the present experiment may have different carbohydrate-fat combinations. J. Nutr. 87:202-210.; been due to the youthof the rats tested.I The results of this study indicate that young female rats undergo FAULKNER, W.R. and J.W. KING, eds. 1970. Chemical Rubberchanges in liver and plasma lipids inresponse to the type of dietary Company manual of clinical laboratory procedures. ChemicalI fat or carbohydrate, and that these changes can be modified by Rubber Co., Cleveland. P. 191.> administration of mestranol. Yet certain blood clotting factors do not¦; appear to be altered either by mestranol or by dietary fat or carbohy- FISKE, C.H. and Y.SUBBAROW. 1925. The colorimetric determi-I drate. nation of phosphorus. J. Biol. Chem. 66:375-400.j Table I.Composition of Diets KEKKI,M.and E.A. NIKKILA.1971. Plasma triglyceride turnoverg/100 g diet duringuseof oral contraceptives. Metabolism 20:878-889.I Vitamin-free casein* 19.6m ,..,.„.! n, KUDZMA, D.J., F. ST. CLAIRE, L. DeLALLO and S.J.i"7 p „ 2 Sn FRIEDBERG. 1975. Mechanism of avian estrogen-induced• Salts, R, H. 5.0 hypertriglyceridemia: evidence for overproduction of{ Vitamin Mixture-3 0.3 triglyceride. J. LipidRes. 16:123-133.Choline Chloride 0,2Fat 4 20.0 MANN, J.I., M.P. VESSEY, M. THOROGOOD and R. DOLL,j Carbohydrate^ 30.0 1975 - Myocardial infarction in young women with special! Alphacel* 24 5 reference to oral contraceptive practice. Brit.Med. J. 2:241-245.I *ICN Pharmaceuticals, Inc., Cleveland, OH.J Table II.Weight Gain. Food Intake, and Food Efficiency RatioI p_ _ _ , „ , _ ,«*- During Period ofMestranol TreatmentI 0. P. and Harper, A. E. 1965.I J. Nutr. 87: 267-273. Weight Rain Food intake FER 200 (b)I 3mg/100 g of ration: thiamine HC1, 0,8; Fat ,j pyridoxine, 0.4; Ca pantothenate, 4,0; so 12niacin, 5.0; inositol, 20.0; folic acid, carbohydrate0.4; vitamin B12(triturated 3000^ per g), £s' 1.33; biotin, 0.02; vitamin A powder EstrogenI (20,000 IU per g), 10.0; calciferol (850,000j IU per g), 0.18; DL-«( -tocopherol powder(250 IU per g), 30.0; menadione, 0.38; significant f valuesriboflavin, 0.6; and sucrose, 176.89.(p<o.oo 5) E.t E.t(P< 0.05) Esttallow or Saf flower Oil.'BT-beef tallow, SO-saf flower oil, S ¦= sucrose, RS-ricestarch, -M-without mestranol, +M = with mestranol.I Sucrose Or rice Starch. 2 Food efficiency ratio ¦ r welRht Rain/100 s> food intake.\ C V -S 12 r1an \ a \ 2 m[ B, SO - \ u \ C Jt \ o \ S 3~ >^ »h 130 "1 I I -—1 \.& I* " S | BT | SO \^¦ I |? « 2 - -a 110-6 2 I I % * 1 L_ g K. 1 1 =£ I L_-M +M=-M +M >, S RS -M +Mbo—(a)'(b) & (c) (d)Figure 1. Interaction means ofliver and plasma lipids. RS = rice starch. S = sucrose, -M = without mestranol, +M = with mestranol. SO =safflower oil, BT =beef tallow.! Arkansas Academy of Science Proceedings, Vol. XXX,1976 3737Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14https://scholarworks.uark.edu/jaas/vol30/iss1/14iArkansas Academy of Science Proceedings, Vol.XXX,197638Dietary Fat-Carbohydrate CombinationsMENDEZ. J.. B. FRANKLIN and H. GAHAGAN. 1975. Simplemanual procedure for determination of serum triglycerides.Clin.Chem. 21:768-770.RATNOFF.O.D. and C. MENZIE.1964. Estimation of fibrinogen insmall samples of plasma. Pages 224-226 in L.M. Tocantins andL.A. Kazal. eds. Blood coagulation, hemorrhage andthrombosis. Grue and Stratton. New York.RENAUD. S. 1970. Thrombosis and atherosclerosis prevention byestrogens in hyperlipemic rats. Atherosclerosis 12:467-473.Table III.Composition of Liverand Plasma LipidsTABACCHI. M.H. and A. KIRKSEY. 1973. Influence of dietarylipids on plasma and hepatic lipids and on blood clottingproper-ties in rats fed oralcontraceptives. J. Nutr. 103:1270-1278.YOUNGBERG, B. and M. YOUNGBERG. 1930. Phosphorusmetabolism. I.A system of blood phosphorus analysis. J. Lab.Clin. Med. 16:158.ZLATKIS. A..B. ZAK and A.J. BOYLE. 1953. A new method forthe direct determination of serum cholesterol. J. Lab.Clin. Med.41:486-492.Liver lipids Plasma lipidsTotal Triglyc-Lipid erideCholes-terolCholes- Phospho-terol lipidmg/100 mg liver protein nig/100 ml plasmaFatBT1 24.6726.416.805.292.293.1395.189.9137SO 118CarbohydrateS 94.091.012822.7828.454.557.702.452.95 127RSEstrogen-M 27.4723.687.434.752.722.67102.483.1132+M 124Significant F values(P< 0.005) CHO, Est, CHO, Est, Fat, CHO,CHO X Est CHO X EstEst Fat(P< 0.05) Fat X CHO Fat X Est*BT = beef tallow, SO = safflower oil, S = sucrose, RS = rice starch,-M = without mestranol, +M = with mestranol.38Journal of the Arkansas Academy of Science, Vol. 30 [1976], Art. 14Published by Arkansas Academy of Science, 1976

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Dietary Fat-Carbohydrate Combinations: Their Effects on Lipid Metabolism in Estrogen-Treated Rats

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