Abnormality in fatty acid composition of gastric mucosal phospholipids in patients with liver cirrhosis and its correction with a polyunsaturated fatty acid-enriched soft oil capsule

The abnormal composition of the fatty acids in gastric mucosal phospholipids was examined in 11 patients with non-alcoholic liver cirrhosis accompanied by gastritis and in 10 healthy subjects without liver disease and gastritis. The cases positive for serum anti-Helicobacter pylori immunoglobulin G antibody were excluded. The arachidonic acid (AA, C20:4n-6) contents of the two main components of phospholipid, the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) fractions, in gastric biopsy specimens were significantly lower in the cirrhosis group, although PC and PE contents in gastric biopsy specimens were not altered. In the cirrhosis group, AA contents of the PC fractions in gastric biopsy specimens were significantly correlated with AA contents of plasma PC fractions and serum albumin levels. Soft oil capsules containing polyunsaturated fatty acid (PUFA) such as AA, eicosapentanoic acid (EPA, C20:5n-3) and docosahexanoic acid (DHA, C20:6n-3) were administered after each meal daily for 4 weeks to six cirrhotic patients and four control subjects, who were randomly selected from the patients and control subjects. After administration of PUFA-enriched oil capsules, gastric mucosal AA contents of PC and PE fractions were significantly improved almost to the control levels. In three cirrhotic patients with severe or mild gastritis whose gastric mucosal lesions were endoscopically shown to have responded to PUFA-enriched oil capsules, AA contents of plasma PC and PE fractions before administration were much lower than in the remaining three cirrhotics that did not respond to the PUFA-enriched oil capsules, but significantly improved to the control levels after administration of oil capsules. The results demonstrate that administration of PUFA-enriched soft oil capsules increased AA contents of the phospholipids in gastric mucosa and thus improved gastric mucosal lesions endoscopically in cirrhotic patients with gastritis.     

Infarct sizing with technetium-99m stannous pyrophosphate scintigraphy in dogs and man; relationship between scintigraphic and praecordial mapping estimates of infarct size in patients

The dynamics of changes in serum lipids (free fatty acids, free glycerol, triglycerides, total cholesterol, and phospholipids) were studied in male Wistar rats irradiated in an open experimental field with a daily dose of 15.48 mC.kg.--1 (60 R) up to a total exposure of 774.0 mC. kg.--1 (3,000 R). The resulting changes occurred in several periods. Initial period of 0--7 days included a drop in triglyceride level and a rise in free glycerol, total cholesterol, and phospholipids in both control and irradiated rats. The period of 14--25 days marked the appearance of serum hyperlipaemia. Between 25--50 days, the levels of the different fractions oscillated and existing changes became more pronounced. The general level of serum lipids during continuous gamma-irradiation exceeded that found in controls. Changes in control animals from experimental field reflected the influence of a changed environment. The modifying factor affecting both irradiated and control rats was night fasting prior to sacrificing the animals and, probably, also the presence of an infradian rhythm in some serum lipid fractions.     

Effects of oxidative stress on glycerolipid acyl turnover in rat hepatocytes

Lipid peroxidation was induced in freshly isolated rat hepatocytes by incubation in the presence of Fe3+, resulting in accumulation of thiobarbituric acid reactive substances. Analysis of lipid classes revealed that the levels and fatty acid compositions of the two major phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE), remained unchanged but the levels of triacylglycerols (TAG) were significantly reduced, and some of their polyunsaturated fatty acids were selectively lost as the result of oxidant treatment. Acyl turnover in PC and PE as determined by 18O incorporation from H2 (18)O-containing media remained largely unchanged during oxidant treatment, while some increased turnover of the saturated fatty acids in TAG was observed. We hypothesize that constitutive recycling of membrane phospholipids rather than selective in situ repair eliminates peroxidized species of PC and PE. TAG could serve as an expendable fatty acid reserve, providing a limited but very dynamic pool of polyunsaturated fatty acids for the resynthesis of phospholipids.     

Studies on phospholipids of different mutants of Salmonella minnesota

Lipid composition of the cells of smooth (S form) and core-defective rough mutants (Ra, Rb & Re) of Salmonella minnesota has been studied. The readily-extractable lipids (RELs), acid-extractable lipids, and polar and nonpolar phospholipids have been analysed. Fatty acid composition of the different fractions containing phospholipids and other neutral lipids have been determined by GLC and GC-MS techniques. Phosphatidyl glycerol (PG), phosphatidylethanolamine (PE) and diphosphatidyl glycerol (DPG) were the major phospholipids present in all the strains. The major saturated fatty acid found was C16:0, and unsaturated fatty acids were, C16:1 and C18:1. Cyclopropane fatty acids, C17cy and C19cy, were also present in small amounts. Increased amounts of REL and unsaturated fatty acids were found in the mutants compared with the smooth strain. The amount of PG and PE decreased and DPG increased in the mutant strains.     

Acute modulation of rat hepatic lipid metabolism by sulphur-substituted fatty acid analogues

A single oral dose of two 3-thia (3-thiadicarboxylic and tetradecylthioacetic acids) and of 4-thia (tetradecylthiopropionic acid) fatty acids were administered to normolipidemic rats and their effects on lipid metabolism over a 24 hr period were studied. All three thia fatty acids could be detected in plasma 2 hr after treatment. Tetradecylthioacetic and tetradecylthiopropionic acids were detected in different hepatic lipid fractions but were incorporated mainly into hepatic phospholipids. Two hours after administration hepatic mitochondrial beta-oxidation and the total liver level of long-chain fatty acyl-CoA increased with a concomitant decrease in saturated fatty acids, total hepatic malonyl-CoA and plasma triacylglycerol levels in the 3-thia fatty acid groups. Tetradecylthiopropionic acid administration caused a decrease in mitochondrial beta-oxidation and an increase in plasma triacylglycerol at 24 hr. The activities of key lipogenic enzymes were unaffected in all treatment groups. Plasma cholesterol level was reduced only at 8 hr in 3-thiadicarboxylic acid treated rats although 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase was suppressed already at 2, 4, 8 and 12 hr. The results show that thia fatty acids are rapidly absorbed and are systemically available after oral administration but the 3-thia fatty acids reached systemic circulation more slowly and less completely than the 4-thia fatty acid. Very low levels of the thia fatty acids are detected in plasma 24 hr after a single administration. They are incorporated into all hepatic lipid classes, especially phospholipids. Rapid incorporation of a non beta-oxidizable thia fatty acid into hepatic lipids may cause a diversion of other fatty acids from glycerolipid biosynthesis to mitochondrial beta-oxidation. Stimulation of mitochondrial beta-oxidation and suppression of HMG-CoA reductase are primary events, occurring within hours, after 3-thia fatty acid administration. The hypotriglyceridemic effect of the 3-thia fatty acids observed at 2-4 hr is independent of the activities of key lipogenic and triacylglycerol synthesising enzymes.     

Incorporation in vivo of 1-14C-palmitic acid into placental and fetal liver lipids of the rabbit

The incorporation of free fatty acid into the placental and fetal liver lipids of rabbits was studied after fetal injections of albumin-bound 1-14C-palmitic acid. The fetuses were killed either 5--10 or 10--20 min after the injection. The placentas and livers were extracted for lipids and the specific activities of triglycerides (TG), phospholipids (PL), free fatty acids (FFA), monoglycerides (MG) and diglycerides (DG) measured. The lipids of the liver and placenta took up 17.0 and 3.6% of the dose, respectively, and of that liver TG accounted for 74% and the placental TG 34% of the label in each tissue. Most of the remaining counts were in the PL fraction with the rest more or less evely distributed between the FFA, DG and MG fractions. No activity was recorded in the cholesterol esters. The placental TG, PL, DG and MG specific activities reached the same level as that of the placental FFA, while in the liver these esters had higher specific activities (than the liver FFA). The liver TG, DG and PL had higher specific activities when compared with those of the placenta. The specific activity of the placental FFA was lower at 10--20 min than at 5--10 min; the opposite was seen for the placental TG. No time-related changes were seen in the liver lipids. It is concluded that (i) both placenta and fetal liver incorporate FFA into glycerides and PL; (ii) the liver incorporates FFA more rapidly and to a greater extent than the placenta; (iii) most of the FFA is incorporated into TG and to a lesser extent (PL; (iv) in both organs hydrolysis of PL or TG occurs. These results are discussed with reference to placental transport of FFA and fetal fat metabolism.     

AIDS patients in Italian prisons: a burning issue with no easy solution

Administration of sodium metavanadate (3 mg/kg) to adult female Sprague Dawley rats for 5 consecutive days by intreaeritoneal route resulted in major alterations in lipid profiles and protein concentration in all the brain regions. Sodium metavanadate exposure displayed phospholipids, cholesterol and cerebrosides, and protein, but ganglioside concentration was significantly increased in various areas of the brain. Loss of body weight observed in this study could be attributed to the loss of appetite; loss of nutrients and wasting of tissues. It is likely that large amount of body water was lost through diarrhoea. Gas liquid chromatography has revealed that oleic acid, linoleic acid, linolenic acid, and archidonic acid were preferentially lost in the brain of vanadium-exposed rats. Thin layer chromatography further proved degradation of individual lipids. Sphingomyelin was substantially decreased followed by phosphatidyl choline and phosphatidyl ethanolamine, but phosphatidyl serine and phosphatidyl inositol were slightly affected. Our recent work has demonstrated vanadium-induced stimulation of lipid peroxidation in the various regions of the rat brain. It is speculative that deterioration of myelin sheath by vanadium exposure contributed to preferential lipid loss but lesser loss of protein. These studies also indicate that vanadium-induced stimulation of lipid peroxidation is characterized by a selective loss of brain polyunsaturated fatty acids and thus comprehensive degradation of lipids in the different regions of the rat brain. However, the mechanism involved in the elevation of ganglioside levels is not yet fully understood. It is concluded that these perturbations produced damage to the associated physiological functions leading to CNS dysfunctions.     

Optical activity of a nucleotide-sensitive tryptophan in myosin subfragment 1 during ATP hydrolysis

Male rats of the Wistar strain were divided 4 groups, and give a liquid diet of control feed, bezafibrate (150 mg/kg), ethanol, and ethanol plus bezafibrate for 5 week. The effect of bezafibrate supplementation on rats fed ethanol was examined in terms of the fatty acid composition of the phospholipids in the erythrocyte membrane. In the phospholipids profiles of erythrocyte membranes, PI was significantly decreased. The decrease in PI caused by bezafibrate appeared to substantially affect the membrane and consequently lead to changes in the membrane anchor. In the fatty acid composition of the PC, C20: 4 was significantly decreased in the group receiving alcohol (p < 0.05) but increased in the groups receiving bezafibrate (p < 0.05). In the fatty acid composition of the PE, C16: 0 was significantly increased in the three groups when compared with the control, and C20: 4 was decreased in the alcohol group (p < 0.05). In the fatty acid of SM and PI, C20: 4 was decreased and C18: 0 increased in the alcohol group. In the PS, C14: 0 was increased in the alcohol group, and decreased in the alcohol plus bezafibrate group (p < 0.01). The levels of arachidonic acid in the total fatty acids that constituted the membrane phospholipids were decreased in the rats given ethanol (p < 0.05). However, arachidonic acid in the group of bezafibrate supplementation on rats fed ethanol were elevated in comparison with the alcohol group (p < 0.05). With decreasing arachidonic acid as a marker of alcohol tissue injury following chronic alcohol intake, the effects of bezafibrate supplementation appear to contribute to membrane fluidity by altering the biochemical flexibility of the membrane.     

Lipids in total parenteral nutrition solutions differentially modify lipids in piglet intestinal brush border and microsomal membranes

BACKGROUND: Fats in the diet modify the lipid composition and function of the intestinal brush border membrane (BBM) as well as the enterocyte microsomal membrane (EMM). METHODS: This study was undertaken in pigs to establish the effect of 3 weeks of total parenteral nutrition (TPN) on the fatty acids in the major phospholipids, (phosphatidylcholine [PC] and phosphatidylethenolamine [PE] in the jejunal and ileal BBM and EMM. RESULTS: In a comparison of 21-day-old milk-fed piglets and newborn animals, there were differences in the major fatty acids (palmitic, 16:0; stearic, 18:0; oleic, 18:1 omega 9, and linoleic acid, 18:2 omega 6) in PC and PE in BBM and EMM. Age-matched (3-week-old) animals fed a lipid-free glucose-containing TPN solution had different membrane fatty acids than did milk-fed piglets, or animals given a soybean oil-containing TPN solution for 21 days. Substituting fish oil or fish oil plus soybean oil altered BBM and EMM fatty acids, compared with the soybean oil-based TPN solutions. These changes varied between the class of phospholipids (PC vs PE), between intestinal site (jejunum vs ileum), and between the type of membrane (BBM vs EMM). CONCLUSIONS: The jejunum and ileum have distinctive control mechanisms for varying their membrane lipids in response to TPN. There is some postmicrosomal modification of lipids between the EMM and BBM. It remains to be established whether the lipid content of the membranes of other organs, and therefore their function, is modified by the lipid composition of parenterally infused lipids.     

The clinico-biochemical aspects of the pathogenesis of gestoses

The content of lipids and fatty acids was measured in lung tissue of intact rats and animals with lung edema caused by nitrogen oxide or adrenaline. Lung edema was found to involve disagreement between the phospholipid and fatty acid spectra and to increase the permeability of membranes. The toxic and adrenaline-induced edemas were found identical as regards the type of changes in the ratio of fractions of neutral lipids, phospholipids, and fatty acid spectrum, that is, these shifts represent a nonspecific reaction of lung tissue to aggression.     

Phospholipid requirement of epididymal testosterone 5 alpha-reductase and phospholipid composition of epididymal microsomes

We have investigated phospholipid requirement for testosterone 5 alpha-reductase solubilized from microsomal and nuclear fractions of rat epididymis. The 5 alpha-reductase from microsomal fraction was stimulated by phosphatidylcholine (PC) with long acyl-chain lengths, but inhibited by short chain PC. The nuclear enzyme activity was weakly activated by PC with various acyl-chain lengths tested. Synthetic phosphatidylserine (PS), such as dioleoylPS, most strongly stimulated the microsomal enzyme activity, but did not exhibit any activation of the nuclear enzyme activity. Endogenous phospholipids, such as PC, PS, and phosphatidylethanolamine (PE) separated from bovine epididymal microsomes were tested for their stimulatory effects on microsomal and nuclear enzymes. Among these endogenous phospholipids, PS most greatly stimulated the microsomal 5 alpha-reductase activity, whereas both PC and PE weakly activated the enzyme activity. On the other hand, endogenous PC and PS had no ability to support the nuclear enzyme activity. The fatty acid compositions of PC and PS from bovine epididymal microsomes were determined, in order to elucidate the relationship between 5 alpha-reductase activation by these phospholipids and the structure of their acyl chains. The relative content of fatty acids in PC, in a decreasing order, was palmitate > linoleate > oleate; that in PS was stearate > oleate > palmitate. Based on these observations, the roles of microsomal PS and PC in epididymal 5 alpha-reductase reaction will be discussed.     

The effect of silymarin-N-methylglucamine salt and silybin-dihemisuccinate on (1-14C)-acetate incorporation in rat liver lipids (author''s transl)

60 min after i.v. application of 140.5 mg silymarin-N-methylglucamine salt/kg body weight dissolved in 4% polyvinylpyrrolidone solution, and 30 min after i.p. administration [1-14C]-acetate, compared to rats treated with solvent only, a statistically significant increase of specific radioactivities in total lipids, triglycerides, total phospholipids as well as in the phosphatidylcholine fraction and a decrease of specific activities in the free cholesterol fraction of the liver can be determined. 70 min after i.p. application of 140.5 mg silybin-dihemisuccinate/kg body weight dissolved in phosphate buffer, and 10 min after i.v. administration of [1-14C]-acetate in comparison with rats treated with solvent only, a statistically significant enhancement of specific activities of total liver lipids, free hepatic cholesterol, liver triglycerides, total liver phospholipids, and the hepatic fraction of phosphatidyl ethanolamine can be measured. Silybin also produces an increased specific radioactivity of the serum triglyceride fraction.     

Different degrees of moderate iron deficiency modulate lipid metabolism of rats

Severe iron deficiency affects lipid metabolism. To investigate whether moderate iron depletion also alters lipid variables-including lipid levels in serum and liver, hepatic lipogenesis, and fatty acid composition indicative of an impaired desaturation-we carried out experiments with rats fed 9, 13, and 18 mg iron/kg diet over a total of 5 wk. The study also included three pair-fed control groups and an ad libitum control group, fed with 50 mg iron/kg diet. The iron-depleted rats were classified as iron-deficient on the basis of reduced serum iron, hemoglobin concentration, and hematocrit. All moderately iron-deficient rats had significantly lower cholesterol concentrations in liver and serum lipoproteins than their pair-fed controls. Rats with the lowest dietary iron supply had higher concentrations of hepatic phosphatidylcholine (PC) and phosphatidylethanolamine (PE), lower activities of glucose-6-phosphate dehydrogenase, malic enzyme and fatty acid synthase, and higher triacylglycerol concentrations in serum lipoproteins than the corresponding pair-fed control rats. Moderate iron deficiency also depressed the serum phospholipid level. Moreover, several consistent significant differences in fatty acid composition of hepatic PC and PE occurred within moderate iron deficiency, which indicate impaired desaturation by delta-9 and delta-6 desaturases of saturated and essential fatty acids. We conclude that lipid variables, including cholesterol in liver and serum lipoproteins as well as fatty acid desaturation, reflect the gradations of iron status best and can be used as an indicator of the degree of moderate iron deficiency.     

Incorporation of polyunsaturated fatty acids into phospholipids of hemocytes from the tobacco hornworm, Manduca sexta

We examined the incorporation of four radioactive fatty acids, 18:1n-9, 18:2n-6, 20:4n-6 and 20:5n-3, into cellular lipids of hemocytes from tobacco hornworms, Manduca sexta. Most of the radioactivity associated with 18:1n-9 was recovered from triacylglycerols (TGs), and the radioactivity associated with 18:2n-6 was heavily incorporated into phospholipids (PLs) and TGs. Most of the radioactivity associated with the two eicosanoid-precursor polyunsaturated fatty acids (PUFAs), 20:4n-6 and 20:5n-3, was incorporated into PLs. The incorporated fatty acids were redistributed among the lipid classes during 2 h incubations. The two C20 PUFAs were moved from PLs to TGs. While 18:2n-6 underwent little change, 18:1n-9 was redistributed from TGs to PLs. Within PLs, each of the fatty acids were incorporated into phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylglycerol (PtG) and phosphatidylserine/inositol (PS/PI). The incorporation patterns changed over time, indicating that the incorporated fatty acids were redistributed among the four PL fractions. The radioactivity associated with 18:1n-9 was mostly recovered from the sn-1 position of PC (59%) and PE (83%). Most of the radioactivity associated with 18:2n-6 was found in the sn-2 position of PC (88%) and PE (67%). Over 90% of the radioactivity associated with 20:5n-3 was recovered from the sn-2 position of PC and PE. Incorporation of 20:4n-6 differed from 20:5n-3 because more radioactivity was recovered from the sn-2 position of PC (93%) than PE (69%). These findings are in line with the general background of lipid biochemistry, from which incorporation of 20:4n-6 into PE marks a notable departure: 31% of the radioactivity associated with this acid was recovered from the sn-1 position of PE. These findings indicate that hemocytes from the tobacco hornworm elaborate a fatty acid incorporation system, which exhibits specificity with respect to fatty acid structure and lipid class.     

Potential use of cytokine therapy in poultry

The time course of incorporation of [14C]arachidonic acid and [3H]docosahexaenoic acid into various lipid fractions in placental choriocarcinoma (BeWo) cells was investigated. BeWo cells were found to rapidly incorporate exogenous [14C]arachidonic acid and [3H] docosahexaenoic acid into the total cellular lipid pool. The extent of docosahexaenoic acid esterification was more rapid than for arachidonic acid, although this difference abated with time to leave only a small percentage of the fatty acids in their unesterified form. Furthermore, uptake was found to be saturable. In the cellular lipids these fatty acids were mainly esterified into the phospholipid (PL) and the triacyglycerol (TAG) fractions. Smaller amounts were also detected in the diacylglycerol and cholesterol ester fractions. Almost 60% of the total amount of [3H]Docosahexaenoic acid taken up by the cells was esterified into TAG whereas 37% was in PL fractions. For arachidonic acid the reverse was true, 60% of the total uptake was incorporated into PL fractions whereas less than 35% was in TAG. Marked differences were also found in the distribution of the fatty acids into individual phospholipid classes. The higher incorporation of docosahexaenoic acid and arachidonic acid was found in PC and PE, respectively. The greater cellular uptake of docosahexaenoic acid and its preferential incorporation in TAG suggests that both uptake and transport modes of this fatty acid by the placenta to fetus is different from that of arachidonic acid.     

Brain phospholipids and fatty acids in Friedreich's ataxia and spinocerebellar atrophy type-1

Previous studies of patients with spinocerebellar atrophy type 1 (SCA-1) and Friedreich's ataxia (FA) have suggested the occurrence of membrane disturbances in both disorders. We measured concentrations of phosphatidylcholine (PC), diacyl and plasmalogen phosphatidylethanolamine (PE), and phosphatidylserine (PS), along with their fatty acid profiles, in the brains of eight patients with Friedreich's ataxia (FA) and nine patients with dominantly inherited spinocerebellar atrophy type 1 (SCA-1). Compared with the controls, levels of all phospholipid types (PE, PS, and PC) were reduced in the cerebellar but not occipital cortex of SCA-1 patients. In contrast, in the FA group, levels of PS and PE, but not PC, were reduced in both cerebellar and occipital cortices. The fatty acid composition of individual brain phospholipids was altered in both FA and SCA-1 patients, most markedly in the plasmalogen PE and PS classes of cerebellar phospholipids. Given the neuropathologic characteristics of each disorder, it is likely that altered fatty acid composition and phospholipid levels in SCA-1 cerebellar cortex occur as a consequence of pronounced cerebellar degeneration. In contrast, reduced phospholipid levels in FA cerebellar and occipital cortex, areas characterized by, at most, minimal neuronal loss in FA, may represent a widespread alteration in cellular phospholipid metabolism occurring in response to the specific gene defect in the disorder.     

Relationship between lipid composition and antibiotic-resistance to isoniazid, streptomycin, p-aminosalicylic acid, ethambutol, rifampicin in mycobacteria

The content of neutral lipids, peptido-glycolipids and phospholipids, separated by solvent extractions and TLC, was investigated and compared in various strains of Mycobacterium tuberculosis and in Mycobacterium avium. The examined strains could be divided into two groups: (i) those possessing a stable INH-resistance with a chromosomal location for the resistance genes, in which the content of total lipids and the distribution of lipid subfractions were modified with respect to the control strain H37Rv; (ii) those strains, such as the mutants resistant to streptomycin (Sm), ethambutol (EM), p-aminosalicylic acid (PAS) and rifampicin (R/AMP), uncorrelated drugs with different genetic location of the antibiotic-resistance, in which a disturbance of the lipid metabolism does not appeared to be significant. TLC and chemical analysis of INH-mutants suggested that the decrease of the cell lipids was associated with the peptidoglyco-phospholipid fraction, while the neutral lipids were characterized by a most elevated amount of both menaquinone-9 and free fatty acids, and by comparable levels of both glycerides and total fatty acids with respect to the sensitive strain. In the pattern of fatty acid shorter than C26 of all the fractions studied, no significant differences were observed between the H37Rv strain and the other resistant strains, including the M. avium. In the course of the lipid analysis no unusual phospholipids in addition to CL, PE and phosphatidylinositol-oligo-mannoside (PIM) were detected. Reasoning in a speculative way, the dramatic fall of the complex lipid elaboration in the INH-resistant mycobacteria, may underline a role for these substances in the envelope of the mycobacterial cell that defends itself from the selecting attack of the antibiotic molecule and that keeps this phenotypic expression of INH-resistance in the mutants.     

Regulatory factors in the development of fatty infiltration of the liver during gram-negative sepsis

To further understand the development of fatty liver during gram-negative sepsis, we measured fatty acid uptake in addition to esterification and secretion of lipids by freshly isolated hepatocytes from fasted and fed control and Escherichia coli-treated rats. Rats were made septic by intravenous (IV) injection of 8 x 10(7) live E coli colonies per 100 g body weight. For the fasted groups, food was removed after E coli injection. Fed rats received a nutritionally adequate diet intragastrically for 5 days before and 24 hours after inducing sepsis. Twenty-four hours after E coli injection, the esterification of newly synthesized fatty acids, as measured by 3H2O incorporation, and the esterification of exogenous fatty acids, measured from 14C-palmitate incorporation, into triglyceride (TG), total cholesterol, and total phospholipid phosphorus were significantly greater in hepatocytes from fasted septic rats compared with their control rats. In fed septic rats, esterification of 14C-palmitate into TG was fourfold greater than in the fed control rats. The increased rates of esterification in hepatocytes from fasted and fed septic rats were not accompanied by an increase in the labeled TG in the medium. This inability to secrete the additional TG that the hepatocytes produce resulted in a higher concentration of cellular TG in fasted and fed septic rats than in their controls. The enzymes glycerol-3-phosphate acyltransferase (GPAT) and phosphatidate phosphohydrolase (PPH) do not appear to be factors contributing to the increased TG synthesis, since the increase in enzyme activity was not accompanied by a similar increase in TG synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Surface-specific electrical occlusal caries diagnosis: reproducibility, correlation with histological lesion depth, and tooth type dependence

We investigated the lipid metabolism in primary cultured hepatocytes to elucidate the causes of hyperlipidemia, increased cholesteryl esters, and decreased triglyceride levels in the livers of daunomycin-nephrotic rats. The incorporation of 14C-palmitate into phospholipids and triglycerides in primary cultured hepatocytes and medium was similar in daunomycin-nephrotic and control rats. The incorporation of 14C-acetate into phospholipids, triglycerides, cholesterol, cholesteryl esters, and total fatty acids in primary cultured hepatocytes was increased in daunomycin-nephrotic rats. The radioactivity of phospholipids, triglycerides, cholesterol, cholesteryl esters, and very-low-density lipoprotein lipids in medium was increased in the hepatocytes of daunomycin-nephrotic rats using 14C-acetate as a precursor. The increased cholesterogenesis and the increased secretion of triglycerides synthesized from acetate by hepatocytes may be due to an increased cholesteryl ester content and a decreased triglyceride content in the livers of daunomycin-nephrotic rats. The increased secretion of lipids synthesized from acetate by hepatocytes may be due to increased accumulation of lipids in serum and very-low-density lipoprotein in daunomycin-nephrotic rats.     

Linoleic and alpha-linolenic acids differently modify the effects of elaidic acid on polyunsaturated fatty acid metabolism and some immune indices in rats

To explore whether the metabolic responses to trans, compared with cis, fatty acids depend on the source of dietary polyunsaturated fatty acids (PUFA), male Sprague-Dawley rats, 5 weeks old, were fed on diets containing 30 g oleic (cis) or elaidic (trans) acids/kg in combination with either 70 g perilla oil (alpha-linolenic acid) or safflowerseed oil (linoleic acid)/kg for 3 weeks in separate experiments. The dietary fats were adjusted to have the same level of total PUFA. The dietary manipulation did not influence the growth indices, but spleen weight was greater when the dietary PUFA source was perilla oil. The incorporation of trans fatty acid into liver phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine and adipose tissue lipids, particularly phospholipids, was significantly higher when rats were fed on safflowerseed oil compared with perilla oil. However, only limited differences were observed in the effects of cis and trans fatty acids on the proportions of PUFA in liver phospholipids. Splenic production of prostaglandin E2 was reduced by trans fatty acid when safflowerseed oil was the PUFA source, but no trans effect was observed on leukotriene C4 production. Dietary PUFA significantly influenced the concentration of plasma immunoglobulins (Ig) but the effect of geometry was only seen in IgG which was increased by trans acid. Dietary trans fatty acid increased the CD4+:CD8+ T-lymphocyte ratio in the spleen, reflecting a decreasing trend of the proportion of CD8+, when combined with perilla oil. These observations indicate that the type of PUFA simultaneously ingested specifically influences the effect that trans acid exerts on PUFA metabolism, eicosanoid production and some immune indices.