Liver Lipid Fractions Research Articles

Lipogenesis and Lipolysis in Fed and Fasted Chicks from High and Low Body Weight Lines

Lipogenic and lipolytic capacities were examined in fasted and nonfasted 28-day-old chicks from high-weight (HW) and low-weight (LW) selected lines. Lipogenesis was assessed in liver and bone (sternum) tissues through the activities of malic enzyme (EC 1.1.1.40), citrate cleavage enzyme (EC 4.1.3.8), and acetyl coenzyme A carboxylase (EC 6.4.1.2), as well as through the in vitro incorporation of acetate-1-14C into liver and bone lipid fractions. Lipolysis was estimated through the in vitro release of free fatty acids (FFA) from abdominal adipose tissue and through plasma FFA.Fasting depressed lipogenesis and increased lipolysis. Regardless of the feeding state, LW chicks exhibited higher lipogenic and lipolytic capacities than their HW counterparts, suggesting that lipid degradation may be relatively more important than synthesis in determining net fat deposition. In addition, the incorporation of radioactive acetate into bone lipid was associated with detectable activity of lipogenic enzymes, providing further evidence that the skeleton is an important site of lipogenesis in the chicken.

Nutritional Effects of Fresh, Laboratory Heated, and Pressure Deep‐Fry Fats

ABSTRACTCooking fats from a pressure deep‐fat frying operation producing fried chicken, were compared with laboratory heated and fresh fats in the diets of animals. Included were corn oil (CO), peanut oil (PO), and partially hydrogenated soybean oil (HSBO). Weanling rats were fed diets containing 15% fat for 28 days. Laboratory heating reduced absorption of CO and PO, but not that of HSBO. Pressure deep‐frying increased absorption of HSBO. Animals derived less metabolizable energy from diets containing heated or hydrogenated fats relative to fresh oil. Polar lipid fractions of liver changed due to heating. Pressure deep‐frying with fats resulted in less deterioration than with laboratory heating, as shown by chemical analyses, coefficient of digestibility, and metabolizable energy studies.

Lipid metabolism in polychlorinated biphenyl-poisoned rats

To clarify the metabolism of lipids in polychlorinated biphenyl (PCB)-poisoned rats, in vivo and in vitro experiments were carried out. Male Wistar rats were separated into two groups, to one group a commercial flour diet was given and to the other group 500 ppm of PCB (Kanechlor-500) supplemented diet was given for 35 days. These animals were used for the following in vivo and in vitro experiments. (1) In vivo experiment: [ 14C] Acetate or [ 14C]glucose was administered to these rats and respiratory 14CO 2 and incorporation of 14C into the various lipid fractions in liver were determined. It was observed that the conversion into cholesterol from acetate or glucose was significantly accelerated in PCB-poisoned rats. However, no significant change was observed regarding respiratory 14CO 2 content between control and PCB-poisoned rats 90 min after administration of [ 14C]acetate or [ 14C]glucose. (2) In vitro experiment: Liver slices from control rats or PCB-poisoned rats were incubated with [ 14C]acetate or [ 14C]glucose for 90 min at 37°C and incorporation of 14C into various lipid fractions was investigated. In liver slices from PCB-treated rats, conversion into the [ 14C]sterol fraction from [ 14C]acetate and [ 14C]glucose was significantly accelerated.

Fatty Liver due to Disproportionally Added Methionine to a Low Soybean Diet and Lipotropic Action of Phosphatides in Rats

Young female rats of the Wistar strain were fed a 20% soybean diet (approximately 8% soybean protein) with or without the supply of 0.3% methionine. Methionine supply caused an accumulation of triglycerides in the liver. In vitro incorporation of acetate-1-14C into the liver lipid fraction and its incorporation ratios of triglyceride/phospholipid were higher in the livers from rats fed the methionine-supplemented diet (Met diet) than in those of animals fed the 20% soybean diet (basal diet). In vivo incorporation of 32P into the phospholipid fraction was lower in the livers of rats fed the Met diet than in those of rats fed the basal diet. Injection of phospholipid (lecithin) through a tail vein increased the plasma level of esterified fatty acids in rats fed the Met diet only and not in those fed the basal diet. Injection of an apolipoprotein fraction produced no effect on the plasma esterified fatty acid levels. The effect of phospholipids in increasing triglyceride transport was confirmed in liver perfusion experiments. These results indicate that supplying methionine to the low soybean protein diet induced disproportionation of synthesis and transport of triglycerides by the shortage of phospholipids.

The incorporation of orally administered radiolabeled dihomo gamma-linolenic acid (20 : 3 omega 6) into rat tissue lipids and its conversion of arachidonic acid.

Radioactivity from orally administered radiolabeled dihomo-gamma-linolenic acid (20 : 3 omega 6) was recovered from the liver, plasma and brain lipid fractions. After administration the fatty acid was metabolized to arachidonic acid, the 22 carbon chain length fatty acid, and was also beta-oxidized. However, 22 hr after administration of [1-14C] 20 : 3 between one-third and one-half of the recovered radioactivity was still associated with dihomo-gamma-linolenic acid in the liver and plasma lipid fractions. Orally administered dihomo-gamma-linolenic acid is incorporated into lipid fractions and is, therefore, available in the metabolic pool for PGE1 synthesis.

Studies on the metabolic role of myo-inositol. Distribution of radioactive myo-inositol in the male rat

Radioactive myo-inositol was injected intraperitoneally into nephrectomized rats. The radioactive material present in liver, spleen, brain, heart, diaphragm, seminal vesicle, coagulating gland, prostate, epididymis, vas deferens and testis was shown to consist exclusively of myo-inositol and its derivatives, as shown by paper chromatography of hydrolysates and trichloroacetic acid extracts of these tissues. Radioactive myo-inositol was accumulated rapidly within 1 h by the thyroid, coagulating gland and seminal vesicle. Other tissues, such as the pituitary, prostate gland, liver and spleen, concentrated myo-inositol less actively. The muscle tissues studied (diaphragm and heart) concentrated little inositol, whereas brain, testis, and epididymal fat-pad did not concentrate it at all. The lipid fraction of liver contained most of the radio-labelled myo-inositol. In the other organs most of the radioactivity was found in the aqueous trichloroacetic acid extract, largely as free myo-inositol.

Dietary factors and aflatoxin toxicity: I. comparison of the effect of two diets supplemented with aflatoxin B1 upon two different strains of rats

AbstractPrevious studies in this laboratory with rats fed low levels of aflatoxin as a component of peanut discards, suggested either a strain tolerance for aflatoxin or a possible protective factor present in the diets used. In this study, two strains of rats, the Charles‐River strain and the former USC strain, were used to test the effect of 1.7 ppm purified aflatoxin B1 included for 3 months in two different diets; one previously used in this laboratory and one used by other investigators in aflatoxin studies. After an experimental period of either 12 or 18 months, growth, mortality, gross pathology, and organ wt were measured, and histopathological examination and biochemical analyses were performed. Plasma and liver cholesterol levels, total liver lipids, and fatty acids in the various lipid fractions of plasma, liver, and liver tumor lipids were measured. Both strains of rats proved to be susceptible to aflatoxin toxicity at this level as manifested by the appearance of hepatomas; however, liver involvement was more extensive in the Charles‐River rats. The diet used by other investigators produced symptoms similar to those observed as a result of essential fatty acid deficiency and also affected the response to aflatoxin through an aggravation of symptoms, i.e. an inhibition of growth and increased size and severity of the liver tumors.

Effect on dietary sucrose and fructose on the metabolism and lipid fractions in liver in the rat.

Male and female weanling rats were fed one of the following diets for 26 weeks: 60% (w/w) starch as control (59% of energy content); 20 (20), 40 (39) or 60% (59%) sucrose; or 20% (20%) fructose. With increasing levels of dietary sucrose the livers of male rats but not those of females, were progressively heavier. Livers of rats of both sexes showed progressively higher total lipid levels mainly as a result of high triglyceride levels. The 20% fructose diet produced the same effect as the 40% sucrose diet. The incorporation of 14C-glucose into liver lipids in vitro, and the production of 14CO2 were both depressed by sucrose and fructose feeding in both sexes.

Propylene Glycol Interference in Determination of Serum and Liver Triglycerides

Abstract Single intraperitoneal injections (of 0.5, 1.0, and 2.0 ml per kilogram body weight) of a solution of sodium pentobarbital (50 mg/ml, in propylene glycol, 40 ml/100 ml) elevated rat serum triglyceride values obtained by the semi-automated fluorometric method of Kessler and Lederer. Increases of 267, 619, and 813%, respectively, were noted within 5 min. Liver triglycerides and other major lipid fractions in serum and liver were unaffected. The solution added directly to pooled rat sera in vitro also elevated the apparent triglyceride concentrations, propylene glycol being the responsible agent. Essentially all of the propylene glycol was recovered as apparent triglyceride. This type of chemically induced artifact can be corrected for by determining a blank on each unknown (i.e., the hydrolysis step is omitted from the procedure). Subtraction of the blank concentration from the total triglyceride concentration yields the true triglyceride concentration. Extraction of the unknown by the Folch procedure also eliminates interference from propylene glycol.

Effect of heated fat upon metabolism of 1- 14 C-acetate in the rat.

AbstractGroups of rats were prefed for 18 weeks with fresh or heated corn oil (≈5% nonurea adduct) at 10, 20 and 30% protein levels and at 10% protein+2% cellulose; 1‐14C‐sodium acetate was injected intraperitonially into each animal and the radioactivity was measured in expelled CO2 and also in the lipid fractions of liver. In the groups of rats fed 10% protein, one‐half of the administered radioactivity was found 50 min after acetate injection into rats fed fresh oil, whereas 90 min were required to reach the same level in rats fed heated oil. The same trend was found in all the groups of rats receiving different protein levels. The conversion of acetate to CO2 was significantly higher at a 10% dietary protein level than at the 20 or 30%, but there appeared to be no significant difference in the conversions at the 20 and 30% protein levels. However addition of 2% cellulose to the 10% dietary protein level significantly increased the conversion of the acetate to CO2 in rats fed heated oil. The livers of animals receiving heated fat diets had a higher lipid content, mainly triglyceride. When the liver lipids from rats fed fresh corn oil were separated by argentation thin layer chromatography, the bulk of the radioactivity was found in the saturated fractions. Monoene, diene and triene fractions from the liver lipid of rats fed heated oil had almost twice the radioactivity of those from fresh oil, suggesting the preferential utilization of acetate in the synthesis of these unsaturated fatty acids.

The metabolism of liver and plasma lipids after partial hepatectomy in the rat

The concentration and fatty acid composition of plasma and liver lipids and the metabolism of intravenously administered [ 3H]oleic acid complexed to albumin was studied in partially hepatectomized or laparotomized rats. 1. 1. Partial hepatectomy induced significant elevations of the hepatic concentrations of glyceride and esterified cholesterol. In contrast, the concentrations of free cholesterol and phospholipid remained essentially unchanged. The main change in the fatty acid composition of liver lipids was increased percentages of mono- and diunsaturated fatty acids. A specific feature of the phospholipid fraction was a decrease in the percentage of arachidonic acid. 2. 2. Partial hepatectomy brought about an increase in the concentration of plasma triglyceride and a decrease in the ratio esterified/free cholesterol. The fatty acid composition of the plasma lipid fractions showed changes similar to those which occurred in the corresponding liver lipid fractions. 3. 3. The fractional turnover rate of plasma free fatty acids was lower in partially hepatectomized rats at 4 h but not at 51 h after operation. The flux of free fatty acids through the plasma was, however, not altered by partial hepatectomy. The incorporation of intravenously injected [ 3H]oleic acid into liver lipids was increased at 4 h but not at 51 h after partial hepatectomy compared to laparotomy. The data presented support the hypothesis that the fatty liver that ensues after partial liver resection is essentially the result of an increased incorporation of plasma free fatty acids into liver triglycerides.

Effect of Dietary Lipids and Cholesterol on the Levels and Synthesis of Some Hepatic Lipid Components of Young Chickens

INTRODUCTIONSEVERAL workers (Ridout et al., 1952; Klein, 1958; Morin et al., 1962; Diller et al., 1961) have reported that dietary cholesterol increased liver glyceride, cholesteryl ester and to a lesser extent, free cholesterol. Liver cholesterol increased to the same extent when cholesterol was consumed with unsaturated or saturated fat (Homer et al., 1960). Unsaturated fat stimulated the incoporation of labeled acetate into liver (Wood and Migicovsky, 1958; Weiss et al., 1967), whereas triglyceride radioactivity decreased and with no change in cholesteryl ester (Weiss et al., 1967).This study is concerned with the changes in the levels and synthesis of lipid fractions of liver of young chickens on a saturated or unsaturated diet with or without cholesterol. The results obtained demonstrate that chicken liver responds to the ingestion of cholesterol differently, depending on the type of fat consumed.MATERIALS AND METHODSA total of 45 newly-hatched New Hampshire chickens, from…

THE INFLUENCE OF GONADAL HORMONES ON THE UPTAKE OF [14C]ACETATE BY LIVER LIPID FRACTIONS IN THE IMMATURE MALE CHICK

SUMMARY Six-week-old cockerels with an equalized food intake and receiving by injection oestrogen, androgen or progesterone were used in an investigation on the influence of the gonadal hormones on the rate of uptake of [14C]acetate into liver lipid fractions. The results obtained indicate that oestrogen was the only one of these hormones that affected the overall lipid composition of the liver significantly. However, although in all these treatments most of the label was incorporated into the triglyceride fraction, both testosterone and progesterone showed incorporation-time patterns which differed substantially from those obtained in control and oestrogen-treated birds. There was a very rapid incorporation of label into the liver lipids of the testosterone and progesterone-treated birds and the amount incorporated was greater than the maximum incorporation obtained at a later time in the control or oestrogen-treated birds. It is possible that a different biosynthetic pathway is utilized in the formation of triglycerides in testosterone and progesterone-treated birds than in oestrogen-treated birds. The results indicate also that although testosterone and progesterone do not influence the overall lipid composition of the liver, they exert a significant influence on metabolic processes involving the synthesis and degradation of liver lipids.

Fatty Acid Changes in Liver Fractions of Pigeons After Lethal-Dose Radiation and Therapy

INTRODUCTIONIN A previous study (Chung et al., 1966) delayed heterologous bone marrow and thymus transplantation resulted in decreased stearic acid content and increased palmitic, oleic, linoleic, and arachidonic acid content in liver tissues of pigeons. Irradiation has been known to decrease palmitic acid and to decrease polyunsaturated fatty acids (Hansen et al., 1965; Notario et al., 1965).To further explain these fatty acid changes we attempted to study the fatty acid changes in the liver lipid fractions of pigeons after lethal-dose radiation and delayed heterologous bone marrow, thymus, and spleen transplantation.MATERIALS AND METHODSNon-inbred sexually mature pigeons, 6–10 months of age, and descendants from the White King colony were purchased commercially. Each bird was exposed to 2,500 rads total-body roentgen irradiation with a cobalt-60 radiation source at the Oak Ridge Associated Universities Medical Center. Dose response curves were established previously (Shaw and Vermund, 1961) and showed that .

Effects of Dietary Fat Level on Pantothenate Depletion and Liver Fatty Acid Composition in the Rat

Weanling male rats were fed a 6% or an 18% cottonseed oil diet, lacking pantothenate or supplemented with graded levels of pantothenate, to determine whether a high fat diet would accelerate the development of pantothenate deficiency or increase the pantothenate requirement for growth. The fatty acid composition of liver lipid fractions was also determined. Increasing the level of fat did not increase the pantothenate requirement for maximal growth or accelerate the development of the deficiency as indicated by body weight, adrenal weight, or onset and incidence of greying. Pantothenate deficiency with either the 6% fat or the 18% fat diet significantly lowered the relative proportions of phospholipid arachidonate and stearate. Liver CoA values in both the control and deficient groups fed the 18% fat diet were significantly lower than in the rats fed the 6% fat diet.

The influence of gonadal hormones and biotin nutrition on the incorporation of sodium 2- 14C-acetate into the liver lipids of the female chick

An investigation was carried out into the effects of gonadal hormones and biotin nutrition on the incorporation of 14C-acetate into the liver lipid fractions of female chicks. Results suggest that there is a vast difference in liver lipid metabolism between hormone and non-hormone treated chicks. Biotin deficiency reduced the total incorporation of acetate into liver lipids. All treatment groups showed the same incorporation patterns with time in the case of the liver triglyceride and phospholipid fractions. Evidence suggested that the phospholipids were derived from the triglyceride fraction by some mechanism of trans-esterification. Results also indicate that abnormal synthesis of cholesterol occurs in biotin deficiency, and the possibility exists that the hormone treatment was able to offset the effects of biotin deficiency with respect to cholesterol synthesis. Liveweight gains showed that the hormone treatment considerably improved the growth responses of biotin-deficient chicks over the treatment period studied.

Fatty acid changes in liver and plasma lipid fractions after safflower oil was fed to rats deficient in essential fatty acids.

1. Fatty acid patterns of liver and plasma triglycerides, phospholipids and cholesteryl esters were determined at intervals during 24hr. after essential fatty acid-deficient rats were given one feeding of linoleate (as safflower oil). 2. Liver triglyceride, phospholipid and cholesteryl ester fatty acid compositions did not change up to 7hr. after feeding. Between 7 and 10hr., linoleic acid began to increase in all fractions, but arachidonic acid did not begin to rise in the phospholipid until 14-19hr. after feeding. 3. Oleic acid and eicosatrienoic acid in liver phospholipid began to decline at about the time that linoleic acid increased, i.e. about 9hr. before arachidonic acid began to increase. 4. Changes in linoleic acid, arachidonic acid and eicosatrienoic acid in phosphatidylcholine resembled those of the total phospholipid. Phosphatidylethanolamine had a higher percentage content of arachidonic acid before the linoleate was given than did phosphatidylcholine, and after the linoleate was given the fatty acid composition of this fraction was little changed. 5. The behaviour of the plasma lipid fatty acids was similar to that of the liver lipids, with changes in linoleic acid, eicosatrienoic acid and arachidonic acid appearing at the same times as they occurred in the liver. 6. The results indicated that linoleic acid was preferentially incorporated into the liver phospholipid at the expense of eicosatrienoic acid and oleic acid. The decline in these fatty acids apparently resulted from their competition with linoleic acid for available sites in the phospholipids rather than from any direct replacement by arachidonic acid.

Effect of Diethylstilbestrol and Cholesterol on the Fatty Acid Composition of Liver Lipid Fractions in Cockerels

INTRODUCTIONTHE fattening action of diethylstilbestrol (DES) has been extensively studied by several workers (Lorenz, 1944, 1945a, b; Sykes et al., 1945; Gassner and Wilgus, 1948; Umberger et al., 1959; and Herbert and Brunson, 1957). DES administration will increase liver lipids (Riddle and Opdyke, 1941) partly due to the increased phospholipid synthesis (Taurog et al., 1944). There is little doubt that increased lipid synthesis in the liver is the source of DES-induced lipemia (Ranney and Chaikoff, 1951) and the DES-induced lipemia does not depend on dietary fat (Lorenz, 1954). The consequence of the increased lipid synthesis in the liver on the fatty acid composition of the liver lipid fractions has been little explored. Blomstrand and Christensen (1961, 1963) reported that oleic acid increased significantly after DES treatment. Stearic acid of the cholesterol ester and triglyceride fractions decreased while the stearic acid of the phospholipid fraction and the linoleic acid of …

Influence of diets containing different natural oils on the incorporation of [1-14C] acetate in the various lipid fractions of rat liver.

1. A comparative study was undertaken with rats on the effect of various diets (normal stock, fat-free, palm oil and olive oil) on the in vitro incorporation of [14C]acetate by the liver into cholesterol and into the fatty acids of phospholipids and neutral fats. 2. The total lipids extracted from the incubation mixtures were fractionated into acetone-precipitable and digi- tonin-precipitable portions and also into the fatty acids of neutral lipids. 3. The incorporation of [14C]acetate into the acetone-precipitable fraction and into fatty acids of neutral fats was greatest in livers of rats given the fat-free diet, followed by those of the groups given olive oil, the normal stock diet, and palm oil. Livers from the group given the fat-free diet also exhibited the highest percentage of14C activity in the digitonin-precipitable fraction and were closely followed by the group on the normal stock diet. Compared with those of the other two groups, the livers of the groups given olive oil and palm oil showed much less activity in the digitonin- precipitable fraction. 4. The greater the amount of a specific type of fatty acid in the diet, the less was the14C activity incorporated into that type of fattyacid in the ncutral fats of liver slices, hut this was not so with the fatty acids obtained froin the acetone-precipitahlc fraction of the lipids.

The role of microbial flora in the hepatotoxicity of chlortetracycline in vivo: A study with germfree mice

Studies with germfree mice have revealed that chlortetracycline (CTC) hepatotoxicity does not depend on secondary effects related to modification of the indigenous microflora but that it is the consequence of a direct drug action. Germfree (GF) and conventionalized (CONV) mice, injected intraperitoneally with large doses of CTC, both developed signs of hepatotoxicity: liver weight, total lipids, and lipid fractions (glycerides, cholesterol, phospholipids) increased, while liver water and protein decreased; activity of the liver enzymes (glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, glutamic dehydrogenase, urea cleavage enzyme, and arginase) all decreased, even below that of liver protein concentration. In general, the effect of CTC on the GF mouse was more severe than on the CONV: lipids rose higher, while protein fell lower. In each type of mouse, the concentration of liver glycerides increased most. Fasting exacerbated all these effects especially in the CONV mouse. There were no significant differences between the livers of GF and CONV untreated mice in any of the parameters measured, except for total lipids and glycerides, which were lower in the GF liver. Thus, the presence of an indigenous flora appears not only to attenuate the lipogenic response of the liver to CTC but also to influence the liver lipi composition of the untreated mouse. Our results are consistent with the hypothesis that CTC interferes with protein metabolism of the liver in at least two broad ways: by exerting a catabolic or antianabolic affect, in that liver protein, in general, is decreased after CTC; and by interfering with metalloenzyme action by chelation with metal cofactors, leaving those enzymes relatively unaffected which require no metal cofactors.