Liver and serum lipids and lipoproteins of rats fed 5% L-lysine

Soybean protein and casein supplemented with 1% Arg were compared for their ability to prevent fatty livers caused by excess dietary Lys. The concentrations of serum lipids and lipoproteins of rats fed 5% Lys and having vatty livers were also compared with those of rats fed the identical diet but lacking fatty livers when killed. The total liver lipids, triglycerides and cholesterol of rats fed 15% casein +5% Lys were 3.9, 12.4 and 2 times control values, respectively. Rats fed 5% Lys +1% Arg or 5% Lys with 15% soybean protein had liver lipid concentrations similar to controls fed no supplemental Lys. Serum total lipids, triglycerides, cholesterol, phospholipids and free fatty acids also did not change, and serum ketone bodies were slightly elevated with Lys feeding whether the rats had fatty livers or not. The concentrations of circulating HDL were slightly depressed in all rats fed 5% Lys while LDL were significantly elevated, particularly in rats without fatty livers. Serum VLDL did not change with 5% dietary Lys. Overall, excessive dietary Lys caused fatty livers which were prevented by varying the diet or length of feeding. Excess Lys feeding altered lipoprotein metabolism shown by decreased serum HDL and a substantial elevation in LDL. The latter was more apparent when the fat accumulation in liver was less severe or absent. The data suggest that the fatty liver from Lys excess is probably unrelated to increased fat mobilization from storage, decreased fat oxidation or to a major block in the transport of triglycerides from the liver to the circulation.     

Serum cholesterol,triglycerides and total lipid fatty acids of rats in response to okra(hibiscus escuientus) seed oil

Tender pods of okra are commonly consumed vegetables in India. Okra seed kernel, like soybean, is a rich source of protein and fat. Its fat, with its appreciable linoleic acid content (>42%), prompted us to look into its metabolic utility in comparison with commonly consumed groundnut oil. Serum lipid profiles, with respect to cholesterol, triglycerides and total lipid fatty acids were determined in rats receiving okra seed oil at a level of 10% in the casein based diet which was adequate with respect to vitamins, minerals, etc. The control group received a casein based diet in which groundnut oil was the source of fat. Serum lipid profiles in this group were similarly monitored. The feeding trial was carried out for a period of 90 days. Results showed that serum cholesterol content of rats receiving okra seed oil was significantly lower compared to those consuming groundnut oil. A decreasing trend in total lipids as well as triglycerides was also evident in animals fed okra seed oil. Serum fatty acid profiles showed a relatively higher proportion of long chain and polyunsaturated fatty acids in this group as compared to the group receiving groundnut oil. These results indicate that okra seed oil consumption has a potential hypocholesterolemic effect. To whom correspondence to be addressed. ¹Part of this work was presented at 45th Annual Meeting of Oil Technologists Association of India, New Delhi-Feb. 9–10, 1990.     

Deposition of dietary epoxides in tissues of rats

Epididymal fat pad lipids from rats fed trivernolin at the 4.8% level in the diet for 90 days were found to contain 6.1% epoxyoleic acid. No epoxides were detected in the serum lipids and only trace amounts were found in the liver lipids. TLC, GLC and a specific color reaction with picric acid were used to identify this fatty epoxide in the tissues. Epoxyoleic acid was shown to be present as a mixture of predominately monovernoloyl triglycerides with some divernoloyl triglycerides and small amounts of trivernolin. Lipase hydrolysis of the first two triglycerides has demonstrated that the vernoloyl groups are present mostly in the 1,3 positions. In a separate experiment, rats were fed cholesterol epoxide at the 0.5% and 1.5% levels in the diet for 90 days. TLC and GLC examination of lipids from these rats failed to reveal the presence of any cholesterol epoxide. Only one-half of the sterol fed could be accounted for in the fecal lipids. Presented in part at the AOCS Meeting, Chicago, October 1967.     

Changes in serum lipids in rats treated with oral cooper

Disturbances in lipid metabolism during copper deficiency in rats are well recognized. Copper deficiency is associated with the spontaneous retention of hepatic iron. Previous studies have reported that hypercholesterolemia and hypertriglyceridemia are associated with elevated hepatic iron concentrations in copper deficient rats. There was a direct relationship between the magnitude of blood lipids and the concentration of hepatic iron. Based on these data, it has been hypothesized that iron was responsible for the development of lipemia of copper deficiency. In this study was determined the effect of increasing doses of Cu(10, 20 and 50 ppm) in the diet, on the serum total lipids, total cholesterol, triglycerides (triacylglicerols), phospholipids, non-esterified fatty acids (NEFA) and liver iron and zinc concentrations in normal rats. The results were compared with normal rats that received a balanced diet containing 0.6 and 6 ppm of Cu, respectively. The results show that Cu-supplement diminished the cholesterol and triglyceride serum levels, increased the level of phospholipids, NEFA and concomitantly decreased the hepatic concentrations of Fe and Zn. There was a statistically significant (p < 0.05) simple correlation between triglycerides and liver Fe (r = 0.917; R2 = 64.03%), cholesterol and liver Zn (r = 0.872; R2 = 76.07%), cholesterol and liver Fe (r = 0.995; R2 = 99.10%), liver Fe and liver Cu (r = -0.612), liver Fe and liver Zn (r = 0.837), liver Cu and liver Zn (r = -0.612), and serum triglycerides and liver Zn (r = 0.967). The mechanism(s) by which Fe and Zn determine these changes is not known; none of the enzymes that act in cholesterol and triglyceride metabolism and biosynthesis require Fe and/or Zn. The increase of NEFA is due to changes in the process of lipolysis and re-esterification of the fatty acids in blood. However, additional studies are needed for the precise mechanisms of this interrelationships to be clarified.     

Dietary proteins modulate the effects of fish oil on triglyceridemia in the rat

Sprague-Dawley rats were fed purified diets varying in both protein (20%) and lipid (11%) content for 28 d to verify the independent and interactive effects of dietary proteins and lipids on serum and hepatic lipids, and on tissue lipoprotein lipase (LPL) activity in both fasted and postprandial states. These diets consisted of either casein-menhaden oil, casein-coconut oil, soy protein-menhaden oil (SPMO), soy protein-coconut oil, cod protein-menhaden oil, or cod protein-coconut oil. A randomized 3×2 factorial design was used. A significant protein-lipid interaction was seen on serum triglyceride levels: menhaden oil, compared with coconut oil, induced a decrease in serum triglyceride levels when combined with soy protein but not when combined with cod protein and casein. The lower serum triglyceride concentrations observed in the SPMO-fed rats could be the result of decreased hepatic triglycerides when soy protein was compared with casein and when menhaden oil was compared with coconut oil. Total LPL activity in the heart was higher in menhaden oil-fed rats than in coconut oil-fed rats in the postprandial state. The higher LPL activity in the heart could, however, explain only 10% of the reduction of serum triglycerides, contributing slightly to the lowering effects of SPMO diet on serum triglycerides. Therefore, the present results indicate that dietary proteins can modulate the effects of fish oil on triglyceridemia in the rat, and that could be mainly related to specific alterations in hepatic lipid concentrations.     

Synthesis of cholesterol and total lipid by male and female rats fed beef tallow or corn oil

Male and female weanling rats were fed diets containing 2 or 42% of calories as corn oil or 40% as beef tallow plus 2% as corn oil until they were 12 or 18 weeks of age. Incorporation of C¹⁴-acetate into lipids of serum and liver and concentration of lipids in serum, liver, and carcass at the end of these periods were determined. Net synthesis of noncholesterol lipid was repressed by changing the diet from 2% to 42% of calories from either dietary fat in both sexes and at both ages. Cholesterol net synthesis was enhanced 29-fold in males and 22-fold in females fed 42% corn oil compared to 2% corn oil to the age of 12 weeks. It was enhanced only 2.6-fold for males and 3.4-fold for females by 40% beef tallow plus 2% corn oil. At 18 weeks of age cholesterol synthesis in males fed 42% corn oil was 7.3 and in females 9.1 times the value for those fed 2% corn oil. At this age the values for rats fed 40% beef tallow plus 2% corn oil were 1.2 and 3.7 times those for 2% corn oil fed rats of the respective sexes.     

Effects of low casein and fish oil on hyperlipidemia and proteinuria in nephritic rats

The effects of amino acid-fortified low casein and fish oil (FO) diets on hyperlipidemia and proteinuria were studied in rats with nephrotoxic serum nephritis. After an antiserum injection, rats were maintained for 14 d on four different experimental diets: a 20% casein diet containing corn oil (CO) or FO, or an 8% casein diet supplemented with cystine plus threonine containing CO or FO. The 8% casein diets reduced urinary protein excretion in nephritic rats without inducing severe growth retardation or fatty liver compared with the basal 20% casein diets. Both the 8% casein diet and the FO diet decreased serum cholesterol, triglyceride and phospholipid levels in nephritic rats, and nonesterified fatty acid levels were decreased by FO feeding. In nephritic animals, hepatic cholesterol synthesis was decreased by the 8% casein diets compared with the 20% casein diets, and tended to be reduced by FO feeding between groups at the same casein levels. No effect of diet was observed on fatty acid synthesis among the nephritic rats. FO administration to the nephritic animals suppressed fecal steroid excretion. While lipoprotein lipase activity was unchanged among the nephritic rats, hepatic triglyceride lipase activity was reduced by either the 8% casein or FO diet. The results suggest that the hypolipidemic action of low casein diets may, at least in part, be due to reduced hepatic cholesterol synthesis and suppressed triglyceride secretion from the liver. They also suggest that the hypolipidemic action of FO may, at least in part, be due to reduced hepatic cholesterol synthesis and decreased fatty acid mobilization from peripheral adipose tissue.     

Changes in the activities of lipoprotein lipase and the lipogenic enzymes in tumor-bearing rats

The effects of tumor growth on lipid metabolism were investigated by evaluating serum lipids, lipoprotein lipase activity (LPLA), the lipogenic enzymes, urinary catecholamines along with serum insulin and glucagon levels. We injected 1.5×10⁶ cells of rat mammary tumor, AC33, and killed the rats on the 18th day. Serum triglycerides and free fatty acids of the tumor-bearing (TB) rats increased 4 and 5 times, respectively, more than the control (C) rats. Total liver lipids were not significantly different between the two groups. Tumor growth produced a 70% decrease in total epididymal fat pad LPLA; there were no changes in soleus muscle LPLA. Serum insulin levels of the TB rats were 49% less than the C rats. The TB rats had significantly lighter epididymal fat pads and lower activities of adipose fatty acid synthetase and citrate cleavage enzyme. Urinary catecholamines of the TB rats were reduced over 30% compared with the C rats. These results show that the hypertriglyceridemia of the TB rats may be due, in part, to a deficiency of adipose tissue LPLA. The data also suggest that the effects of the tumor on lipid metabolism may be mediated through insulin.     

Separate effects of dietary protein and fat on serum cholesterol levels: another view of amino acid content of proteins

Casein or soy protein with vegetable or animal fat were used to determine the dietary protein or fat effects and their possible interaction on serum cholesterol levels. Young, male New Zealand white rabbits with a mean weight of 2.1 kg were divided into groups of six and fed one of four different diets containing 20% of the calories as protein, 30% as fat (according to dietary guidelines for the United States) and 50% as carbohydrate. The diets contained casein or soy (lysine/arginine ratio = 2.2 or 0.9, respectively) as the protein sources with fat from either almond oil or butter. There was no significant difference in weight gain among the diet groups. Total serum cholesterol level was highest among animals fed the diet containing butter with casein (177 +/- 25 mg/dl) or soy protein (189 +/- 50 mg/dl), it was intermediate in animals fed the vegetable oil with casein (121 +/- 14 mg/dl), and lowest in the soy protein with vegetable oil group (58 +/- 12 mg/dl). There was a significant difference in serum cholesterol levels due to the protein effect when vegetable oil was used (p less than 0.05) but not with butter. There was also a significant fat effect on serum cholesterol when the diet contained soy protein (p less than 0.005) but not when the protein was casein. No significant interaction was observed between the dietary fat and protein sources on serum cholesterol levels, which suggests that dietary protein and fat independently affect the levels of serum cholesterol. Thus, dietary protein has a significant effect on serum cholesterol levels and may be a factor in the low levels of serum cholesterol observed among vegetarians and in humans of Third World countries where the diets is primarily of vegetable origin.     

The effects of fat-free,saturated and polyunsaturated fat diets on rat liver and plasma lipids

The liver and plasma lipids and fatty acid composition of rats fed synthetic diets of differing fat type and content were studied. All animals were starved for 48 hr and then refed a high carbohydrate, fat-free diet for 48 hr. They were then divided into three groups and fed for an additional 48 hrs the following: group 1, the fat-free diet; group 2, a diet containing 44% of calories from corn oil; and group 3, a diet containing 44% calories from completely hydrogenated soybean oil. The total lipid concentration of the liver in the animals on the fat-free diet was elevated at 72 and 96 hr. The addition of either saturated or unsaturated fat in the diet at 48 hr prevented this accumulation. The total phospholipid and cholesterol concentrations of the liver were relatively uninfluenced by any diet in this study. Plasma total fatty acid concentration was elevated at 72 hr in the animals on a fat-free diet compared to those fed the stock diet, starved for 48 hr or fed the fat-containing diets. By 96 hr, however plasma fatty acid concentrations in all groups were similar to those in animals fed only the stock diet. The release of de novo synthesized fatty acids into plasma from the liver was strongly inhibited by dietary fat, either saturated or polyunsaturated. With the fat-free diet there was a significant increase in the saturated and monounsaturated fatty acids in both liver and plasma. The addition of corn oil to the diet facilitated a reversion of the fatty acid composition in liver and plasma to that found in the animals fed the stock diet ad libitum, but saturated fat did not. No effect of diet on the fatty acid composition of the red cells was observed during the course of this study. Exogenous saturated fatty acids, although similar chemically to the fatty acids synthesized by the liver, may have physiological actions that differ from endogenously synthesized fat.     

Tissue lipid responses to 3-hydroxy-3-methylglutaric acid with different dietary fats

Simultaneous administration of 3-hydroxy-3-methylglutaric acid (HMG) for 4 weeks to rats fed 20% saturated fats prevented rise of serum cholesterol, triglycerides, and phospholipids. Except phospholipids, other liver lipids were significantly decreased. HMG administration for 4 weeks along with atherogenic diet significantly decreased cholesterol and phospholipids of serum, liver, aorta, and heart. The phospholipids of epididymal fat and brain were also significantly lowered. The triglyceride levels in serum, liver, and epididymal fat were significantly decreased. The maximal hypolipidemic effect of HMG was observed in serum. U.S. Patent No. 3629449, dated December 21, 1971, on “Process of combatting hypercholesterolemia.” A part of the work submitted to Aligarh Muslim University for Ph.D. degree.     

Effect of the nature and amount of dietary energy on lipid composition of rat bone marrow

The effect of the nature and amount of dietary calories on the lipid composition of bone marrow of rats was studied. Male weanling rats were fed 3 isocaloric diets, containing high carbohydrate, normal protein, and high protein, and a fourth high fat diet for 49 days. Feeding of the high carbohydrate, high protein, and high fat diets caused a significant increase in the level of total lipids compared to the normal protein diet. This increase of total lipids was due primarily to the increase in the level of triglycerides. There was no significant difference in fatty acid composition of either nonpolar or polar lipids of bone marrow among rats fed high carbohydrate diet and those fed normal protein diet. A comparison of fatty acid compositions between bone marrow lipids of rats fed high protein diet and the other 2 isocaloric diets revealed that the proportion of palmitic acid was higher and the proportion of oleic acid was lower in animals fed high protein diet than in animals fed the other 2 diets. Compared to the 3 isocaloric low fat diets, dietary feeding of high fat diet caused a decrease in the proportion of palmitic and palmitoleic acids and an increase in the proportion of oleic and linoleic acids in total fatty acids of both nonpolar and polar lipids.     

Interaction between dietary proteins and lipids in the regulation of serum and liver lipids in the rabbit. Effect of fish protein

Purified diets varying in dietary protein, namely casein (CA), soy protein (SP), fish protein (FP), and lipid origin (corn oil (CN), coconut oil (CO)) were fed to rabbits to evaluate the effects of protein and fat source, as well as protein-lipid interactions, on serum total, lipoprotein and hepatic lipid levels. Dietary proteins and lipids exerted a separate effect on serum total cholesterol (C), very low-density lipoprotein cholesterol (VLDL-C), and low-density lipoprotein cholesterol to high density lipoprotein cholesterol (LDL-C/HDL-C) ratio. Hence, CA increased serum cholesterol compared to SP, while coconut oil enhanced serum and VLDL-C, and decreased LDL-C/HDL-C compared to corn oil. Dietary proteins interacted with dietary lipids to modulate HDL-C levels. Thus, FP maintained a high level of HDL-C regardless of lipid origin, compared to CA and SP whose HDL-C levels were decreased by corn oil, compared to coconut oil. A dietary protein-lipid interaction was also observed in the regulation of liver cholesterol levels. Coconut oil, compared to corn oil, decreased liver cholesterol in rabbits fed FP, whereas hepatic cholesterol concentration was unaltered by dietary lipid source in CA- and SP-fed rabbits. These results demonstrate that dietary proteins act synergistically with dietary lipids to regulate cholesterol metabolism in the rabbit. This work was presented in part at the 74th Annual FASEB meeting held in Washington, D.C., April 1–5, 1990.     

Dietary protein deficiency affects n−3 and n−6 polyunsaturated fatty acids hepatic storage and very low density lipoprotein transport in rats on different diets

Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition. The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, or hydrogenated coconut, oil poor in EFA. Animals were divided into six groups, SOC (20% casein +5% soybean oil), SOd (2% casein +5% soybean oil), COC (20% casein +5% hydrogenated coconut oil), COd (2% casein + 5% hydrogenated coconut oil), SAC (20% casein +5% salmon oil) and SAd (2% casein +5% salmon oil). After 28 d, liver steatosis and reduced VLDL-phospholipid contents (P<0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein levels, DHA levels remained higher in rats fed salmon oil diets. While in rats fed the hydrogenated coconut oil-fed diets the amount of 22∶5n−6 was lower in liver, it was higher in VLDL lipids at low protein levels. Both EPA and arachidonic acid are precursors of eicosanoids and their diminution may be related to certain clinical symptoms seen in infants suffering from kwashiorkor.     

Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) (“coconut oil diet”) or linseed oil (80 g/kg) (“linseed oil diet”) as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver. The concentrations of serum lipids were elevated in zinc-deficient rats fed either type of dietary fat. These results demonstrate that fatty liver in zinc-deficient rats on the coconut oil diet is caused by elevated activities of lipogenic enzymes, and not by disturbed lipid secretion from liver. Dietary linseed oil prevents both the elevation of lipogenic enzyme activity and fatty liver in zinc-deficient rats.     

Stimulation of lipid absorption in young rats by cholesterol: Early time changes and effects on pentobarbital sleeping time

Four groups of young male and female rats were fed a chow diet (0), chow plus 10% corn oil (F), chow plus 1% cholesterol (C), or chow plus 1% cholesterol plus 10% corn oil (CF) for 1, 2, 4 and 8 days. After 2 dats, male F, C and CF rats exhibited a shorter anesthesia period (−20 to −30%) when given pentobarbital. By 4 days, male F and C rats had pentobarbital sleeping times (PB-ST) 20% less than 0 rats. These effects were additive and CF rats had 40% shorter PB-ST. Reduction of PB-ST by cholesterol and corn oil was similar but slightly less in female rats. Liver lipid content doubled in 4 days in CF rats, and liver cholesterol was 4 times that of 0 rats. These changes and the increases in metabolism of barbiturate suggested changes in liver microsomal enzyme activities. Serum glutamic oxaloacetic and glutamic pyruvic transaminase, two enzymes reflective of liver damage, did not increase after 8 days on C, F or CF diets. Our results suggest that consumption of an animal sterol and a high lipid diet by laboratory rats, normally consuming a diet low in fat (3–4%), increases the ability of the animal to detoxify a barbiturate. Storage of absorbed dietary cholesterol in the liver may represent a major mechanism for maintaining extra hepatic cholesterol homeostasis.     

Nutritional and toxicological evaluation of mango kernel oil

Mango-kernel fat is a solid fat at room temperature and has a melting point of ca. 35 C. The fat was analyzed for its physico-chemical properties. It is rich in equal amounts of stearic and oleic acids (42%). Nutritional and toxicological evaluation of this fat was carried out by multigeneration breeding studies in weanling albino rats, feeding them mango-kernel fat or groundnut oil (GNO) at a 10% level in a 20% protein diet that was adequate in vitamins and minerals. The feed-efficiency ratio and growth rate of rats fed mango-kernel fat were comparable with the control group. Studies of calcium, phosphorous and nitrogen balance showed that the retention of these nutrients was not adversely affected by the mango-fat intake. The apparent digestibility of mango fat was comparable with GNO when fed to rats. Toxicological evaluation of the fat showed a comparable reproductive performance with the GNO-fed animals. Liver serum total cholesterol, triglycerides and total lipids were found to be within normal levels. The organ weights of the various tissues of the animals of both groups in the last generation were comparable. Histopathological studies of various organs revealed no abnormalities. These studies indicate that mangokernel fat can substitute for any solid fat without adverse effect.     

Lipid composition of the placenta of rats with protein restriction and deficiency of essential fatty acids

The influence of diet restriction and EFA deficiency during pregnancy in the rat on the lipid and phospholipids composition of the placenta was investigated. Female virgin albino Wistar rats weighing 130 +/- 4 g, were assigned to three equivalent groups. Prior mating and during pregnancy each group of rats received the following regimen: Animals in the Control Group (C) were fed a 25% casein diet in ad libitum quantities; the dietary Restricted Group (D) received the same control diet in amounts calculated to approximate 50% (g/100 g rat) of the intake of group C; the Deficient and Restricted Group (DD) rats were fed a restricted amount of EFA deficient diet. On the 21st day of gestation pregnant animals were sacrificed. The foetuses and placentae obtained by caesarium section were isolated and weighed. A 50% food restriction before and during pregnancy resulted in a significant decrease in phospholipid contents (p less than 0.05); severe EFA deficiency superimposed to 50% food restriction, moreover induced significant changes in the fatty acid pattern of phospholipids, decreasing n3 and n6 fatty acids and increasing eicosatrienoic acid. There was an accumulation of triglycerides in the placenta of rats fed on the EFA deficient diet. In the two restricted groups fetal weight was reduced, but although in the DD group, placental weight was not affected, litter size was dramatically reduced.     

Cholesterol vehicle in experimental atherosclerosis. III. Effects of absence or presence of fatty vehicle

Three separate experiments show that cholesterol administered to rabbits in the absence of added fat is more atherogenic than cholesterol fed together with corn oil. When cholesterol is dissolved in the corn oil (by heating) prior to mixing with the diet, it is more atherogenic than when it is suspended in the oil. In every case the lowest serum and liver cholesterol levels were observed in the group not receiving corn oil. Gas chromatography of the fatty acids of the serum cholesterol esters of pooled sera suggest that there are smaller amounts of unsaturated C₁₈ fatty acids in the cholesterol-no fat group. Deficiency in these unsaturated acids may be the cause of the high atherogenicity of the cholesterol-no fat diet. There is also a lower proportion of unsaturated fatty acids in the triglycerides of this group. Heating of corn oil 10 min, at 160–200(°C.) causes an increase of titratable fatty acid in the oil (0.005 m-equiv./g. to 0.088 m-equiv./g. or 0.14% FFA to 2.5% FFA). The relatively large amounts of free unsaturated fatty acids in the heated oil may be the cause of the greater atherogenicity of the solution, as compared to the suspension, of cholesterol in corn oil. Presented at the 33rd Fall Meeting, American Oil Chemists’ So ciety, Los Angeles, Calif., September 28–30, 1959. This work was supported by grants from the National Institutes of Health (H-3299 and A-2131), The Nutrition Foundation Inc., and The John A. Hart-ford Foundation Inc.