Changes in the composition of fatty acids in blood plasma lipids and in various organs in traumatic shock

The composition of fatty acids of the total lipids of the myocardium, lungs, liver, intestine, adipose tissue, and blood plasma was studied during traumatic shock reproduced in dogs by crush of soft tissues of the hip. The formation of the shock process was accompanied by a rise in the percentage content of linoleic and arachidonic acids in the blood plasma and some organs; a close correlation existed between the linoleic acid content in the adipose tissue and the blood. Oleic acid deficiency was revealed in the lipids of the organs under study.     

Expression of mRNAs for alpha-fetoprotein (AFP) and albumin and incorporation of AFP and docosahexaenoic acid in baboon fetuses.

alpha-Fetoprotein and albumin, two members of a multigene family, reversibly bind fatty acids with high affinity. The origin of alpha-fetoprotein (AFP) and albumin present in fetal tissues other than the liver and yolk sac is a subject of controversy. In this work, we have searched for the presence of the albumin and AFP mRNA molecules in different fetal organs of the baboon (Papio cinocephalus), using a highly sensitive gel-blot hybridization assay with human albumin and AFP cDNA probes. Large amounts of albumin and AFP mRNA molecules were found in the fetal liver; significant quantities were also present in the gastrointestinal tract and in the kidney. No detectable levels were found in the other tissues examined (brain, skin, spleen, pancreas, muscle, heart, thymus, placenta, and amnion). After injection of radiolabeled AFP into pregnant baboons, all fetal tissues took up the protein. White adipose tissue, kidney, intestine, lung, liver, and cerebral cortex showed a great uptake of exogenous AFP. [14C]Docosahexaenoic acid (22:6, n-3), injected at the same time, was actively transferred from the maternal compartment across the placenta and incorporated into cellular lipids by all fetal tissues and particularly by liver (around 70% of total incorporation). The levels of [14C]docosahexaenoic acid per gram of tissue increased in the order: maternal blood less than placenta less than fetal liver, indicating a selective accumulation of this fatty acid by the fetus. These results indicate that intracellular AFP in non-hepatic tissues of the developing baboon is, for the most part, of plasma origin.     

The transfer of fatty acids across the sheep placenta

Maternal and fetal plasma concentrations of free fatty acids, triacylglycerols and phospholipids and the profile of their fatty acids were measured in three catheterized and unanaesthetized sheep. Fetal concentrations of all three lipid fractions were low and did not correlate with maternal concentrations. There were no measurable umbilical venous-arterial differences. Linoleic acid concentrations were low in both mother and fetus. The fatty acid composition of fetal adipose tissue, liver, lung and cerebellum of five animals was analysed. Again linoleic acid levels were very low, but phospholipids contained 2-8% arachidonic acid. [14C] linoleic acid and [3H] palmitic acid were infused intravenously into three ewes. Only trace amounts of labelled fatty acids were found in fetal plasma and these were confined to the free fatty acids. 14C-label was incorporated into fetal tissue lipids, but most of this probably was due to fetal lipid synthesis from [14C] acetate or other water-soluble products of maternal [14C] linoleic acid catabolism. It is concluded that only trace amounts of fatty acids cross the sheep placenta. They are derived mainly from the maternal plasma free fatty acids and might just be sufficient to be the source of the small amounts of essential fatty acids found in the lamb fetus, but are insignificant in terms of energy supply or lipid storage.     

Metabolism of [1-(14)C]arachidonic acid in ruminant tissues during the pre- and postnatal periods of development under in vitro conditions]

After in vitro incubation of liver, skeletal muscle and adipose tissues from the fetuses and adult cattle as well as of placenta tissue with [1-14C]arachidonic acid, about 90% of the radioactive label was found in the lipids, 10%-in the prostaglandins, and 0.1%-in 14CO2. Arachidonic acid was utilized for the synthesis of lipids and prostaglandins in the majority of fetal tissues in a much greater degree, whereas that in energy-linked process--in a smaller degree compared with adult cattle tissues. [1-14C]arachidonic acid metabolism in the placenta and liver of the given species proceeds much more intensely than that in the skeletal muscles and adipose tissue. In tissues of adult animals [1-14C]arachidonic acid is predominantly utilized for the synthesis of phospholipids, whereas that in fetal tissues is utilized for the synthesis of phospholipids, cholesterol, esters and triglycerides.     

Characterization and metabolism of ovine foetal lipids

1. Total phospholipid concentrations in liver, kidney and brain of the 140-day ovine foetus were only half of those in comparable maternal tissues. 2. Phosphatidylcholine was the predominant phospholipid in all foetal tissues examined. The most striking difference between foetal and maternal tissues in individual phospholipids was in the heart; foetal heart contained more ethanolamine plasmalogen than choline plasmalogen, whereas in adult tissue the concentration of these was reversed. Sphingomyelin content of foetal brain was only one-sixth of that of maternal brain tissue. 3. Oleic acid (18:1) was the predominant acid in the phospholipid extracted from foetal tissues, except in brain where palmitic acid (16:0) was slightly higher. In phospholipids from adult tissues there was a higher proportion of unsaturated fatty acids (linoleic acid, 18:2, and linolenic acid, 18:3) and a correspondingly lower proportion of oleic acid (18:1). The distribution of fatty acids in the neutral lipid fraction of foetal and maternal tissues was very similar; oleic acid (18:1) was generally the principal component. 4. (14)C derived from [U-(14)C]-glucose and [U-(14)C]fructose infused into the foetal circulation in utero was incorporated into the neutral lipids and phospholipids of heart, liver, kidney, brain and adipose tissue. 5. Phospholipid analysis revealed that the specific activity of phosphatidic acid was higher in liver than in other tissues. The specific activity of phosphatidylethanolamine was less than that of phosphatidylcholine in heart, but in other tissues they were about the same. The specific activities of phosphatidylinositol and phosphatidic acid in brain were very similar and were higher than the other components. The specific activity of phosphatidylserine was highest in liver and brown fat. 6. The pattern of incorporation of (14)C derived from [(14)C]glucose and [(14)C]fructose into foetal neutral lipids was similar. Diglyceride accounted for most of the radioactivity in brain, whereas triglyceride had more label in heart, liver, kidney and fat.     

Dietary fat impacts fetal growth and metabolism: uptake of chylomicron remnant core lipids by the placenta

The fetus requires significant energy for growth and development. Although glucose is a major source of energy for the fetus, other maternal nutrients also appear to promote growth. Thus, the goal of these studies was to determine whether triglyceride-rich remnants are taken up by the placenta and whether maternal dietary lipids, independently of adiposity, can impact fetal growth. To accomplish our first goal, chylomicron particles were duallly labeled with cholesteryl ester and triglycerides. The placenta took up remnant particles/core lipids at rates greater than adipose tissue and skeletal muscle but less than the liver. Although the placenta expresses apoE receptors, uptake of chylomicron remnants and/or core lipids can occur independently of apoE. To determine the impact of dietary lipid on fetal growth, independent of maternal adiposity, females were fed high-fat diets (HFD) for 1 mo; there was no change in adiposity or leptin levels prior to or during pregnancy of dams fed HFD. Fetal masses were greater in dams fed HFD, and mRNA levels of proteins involved in fatty acid oxidation (CPT I, PPARα), but not glucose oxidation (pyruvate kinase) or other regulatory processes (HNF-4α, LXR), were increased with maternal dietary fat. There was also no change in mRNA levels of proteins involved in placental glucose and fatty acid transport, and GLUT1 protein levels in microvillous membranes were similar in placentas of dams fed either diet. Thus, the ability of the placenta to take up chylomicron remnant core lipids likely contributes to accelerated fetal growth in females fed high fat diets.     

Gestational hyperlipidemia in the rat is characterized by accumulation of n - 6 and n - 3 fatty acids, especially docosahexaenoic acid.

We have evaluated the relative and quantitative changes in long-chain fatty acids in maternal liver, serum, carcass and conceptus (fetuses plus placentae) during pregnancy in the rat, to ascertain whether previous concern over lower proportions of n - 6 and n - 3 fatty acids in maternal serum could be indicative of suboptimal n - 6 or n - 3 fatty acid status. Gestational hyperlipidemia was characterized by proportional decreases in linoleic, stearic and arachidonic acids but increases in palmitic and docosahexaenoic acids. However, the quantitative amount (microgram/ml) of linoleic, arachidonic and docosahexaenoic acids in serum lipids actually increased 2-5-fold from mid-pregnancy to term. Compared to non-pregnant rats, gestational hyperlipidemia was also associated with a lower proportion but similar quantity of linoleic acid in maternal carcass and adipose stores. We conclude that gestational hyperlipidemia in the rat is characterized by a relative but not quantitative decrease in whole-body stores of n - 6 fatty acids and a marked proportional and quantitative increase in docosahexaenoic acid in maternal organs and in the conceptus.     

Comparison of the fatty acid component in structural lipids from dolphins, zebra and giraffe: possible evolutionary implications

Essential fatty acid compositional data on the structural lipids of mammals which predominantly eat n-3 fatty acids suggests preferential incorporation of n-6 essential fatty acids.
The structural lipids of liver, muscle and brain of five species of dolphin (Tursiops truncatus, Stenella allenuata, Steno bredanesis, Delphinus delphis and Lagenorhynchus obliquidens) , obtained from the wild, contained substantial amounts of arachidonic acid and other n-6 long chain derivatives of linoleic acid. The n-6 to n-3 ratio was approximately 1:1.
Data for two species of leaf-eating land mammals, the zebra, Equus burchelli Gray and giraffe, Giraffa camelopardalis L., indicate that tissue phosphoglycerides were dominated by n-6 fatty acids.     

Effect of docosahexaenoic acid on tissue targeting and metabolism of plasma lipoproteins

We examined the effect of the docosahexaenoic acid (DHA) content of lipoproteins on their metabolism in vivo by a radioisotope labeling and tracking method. Purified HDL and LDL were labeled with (3)H-cholesteryl oleate tracer. To mimic dietary-related changes in fatty acid composition of lipoproteins, we incorporated lipids acylated with either DHA, arachidonic (AA) or oleic (OA) acid to phosphatidylcholine (didocosahexaenoylphosphatidylcholine (di22:6-PC), diarachidonoylphosphatidylcholine (di20:4-PC) and dioleoylphosphatidylcholine (di18:0-PC), respectively) into the purified particles. The lipids, at the amount added, did not cause detectable alterations in the morphology of the lipoproteins. Levels of radiotracers in blood and in several target tissues such as brain, heart, liver, muscle and adipose were determined at 1.5, 3 and 24h after intravenous injection into C57Bl/6J mice. No statistically significant differences were detected in the tissue distribution of tracers introduced into HDL enriched in DHA, compared to particles enriched with OA. In contrast, we found a significantly higher proportion of radiolabel associated with LDL enriched in DHA in heart, brown adipose and brain tissues. The uptake of labels associated with DHA containing LDL nearly doubled for heart and brown adipose tissues at 1.5 and 3h, and it was 30% higher for brain tissues at 24h. The tissue distribution of labels from the same particles enriched in AA or OA did not show a statistically significant difference from unaltered control lipoproteins. These findings point to the possible role of DHA in the regulation of LDL metabolism and involvement of the lipoproteins in transport of n-3 PUFA to target organs.     

Essential fatty acid interconversion during gestation in the rat

The synthesis of arachidonic acid has been investigated in fetal and pregnant rat liver microsomes in the course of the gestation. The delta 5-desaturase activity decreased 2-3 times in rat liver between the 19th and 22nd day of the pregnancy. During this period the delta 5-desaturate activity increased 3-fold in the fetal liver, exceeding the activity of the maternal liver. In contrast, the activity of the fetal delta 6-desaturase was in the same range as in pregnant rat liver and the liver of control animals and did not change between these two stages of the gestation. The elongation rate of linoleic acid in fetal liver was 2-3 times lower than in maternal liver but this increased during the pregnancy. The fatty acid activate rate was always higher than the activity of the desaturases. At the 19th day, the activity of the delta 5-desaturase was apparently the rate limiting step of arachidonic acid synthesis in fetal liver. We did not find any delta 5- and delta 6-desaturase activities or linoleic acid elongation in the placenta microsomes.     

Influence of sex and gonadal hormones on rat-liver and carcass lipids during the development of an essential fatty acid deficiency

1. Groups of intact male and female rats and castrated rats injected with oestradiol or testosterone were given a diet containing hydrogenated coconut oil for 9 weeks, and at intervals the amounts and fatty acid compositions of the carcass and liver lipids were determined. 2. Male rats grew faster and larger, and exhibited typical external essential fatty acid deficiency symptoms sooner than did females. Testosterone-treated castrated male rats were similar to males, and oestradiol-injected castrated male rats resembled females. 3. Intact females maintained a higher linoleic acid concentration in their carcass than did males. Total amounts of carcass linoleic acid remained similar for all groups, only 200mg. being removed in 9 weeks regardless of body size. 4. The amounts of total cholesteryl esters were independent of liver size. They were higher in males and testosterone-treated castrated male rats than in females and oestrogen-treated castrated male rats. 5. Phospholipids represented about 80% of the liver lipids. The total amounts of the phospholipid linoleic acid and arachidonic acid were similar for all groups regardless of liver size, and were not affected appreciably by the deficiency. Females and oestrogen-treated castrated male rats maintained a higher proportion of phospholipid arachidonic acid for longer periods than did their male counterparts. Both the total amounts and the proportions of eicosatrienoic acid and palmitic acid were higher in males than in females. 6. Supplementation of the essential fatty acid-deficient diet with linoleic acid caused a rapid loss of eicosatrienoic acid and palmitic acid with a concomitant increase in stearic acid and arachidonic acid. 7. There were no obvious differences in the way that the essential fatty acids were metabolized or mobilized from adipose tissue of male or female rats during essential fatty acid deficiency. 8. The results indicated that the greater growth rate of the male rats caused them to require and synthesize more phospholipids than did the females. In the absence of adequate amounts of arachidonic acid, eicosatrienoic acid was substituted into the additional phospholipid. The earlier symptoms of essential fatty acid deficiency in the male rat could therefore be ascribed to the higher tissue concentrations of this unnatural phospholipid and its inability to perform the normal metabolic functions of phospholipids.     

The fatty acid composition of the tissues of streptozotocin-diabetic rats

The authors studied acute changes in the fatty acid composition of the tissues of streptozotocin-diabetic rats. They found that streptozotocin diabetes led to changes in the total lipids fatty acid spectrum in serum and in tissues (liver, adipose tissue, renal cortex diaphragm). After only 7 days' diabetes there was an increase in the percentual proportion of saturated fatty acids and a decrease in the amount of polyene fatty acids in the serum and in all the above tissue of diabetic animals. Palmitic acid (16:0) participated in the increase in the proportion of saturated fatty acids in all the given tissues, while stearic acid (18:0) played a role in the increase in the renal cortex and the serum. Among the monoene acids, there was a drop in the proportion of palmitoleic acid (16:1) in the adipose tissue and serum and in the amount of oleic acid (18:1) in the renal cortex, liver and muscle. Linoleic acid (18:2) played a role in the decrease in the proportion of polyene acids in all the given tissues and the serum, while arachidonic acid (20:4) was involved in the drop in the renal cortex, liver and muscle. The results show that diabetes leads to changes in the fatty acid composition of the renal cortex and muscle, as well as of the liver and adipose tissue. At present it is not yet clear whether there is an absolute decrease in the proportion of essential fatty acids, or whether diabetes is characterized by an increase in the amount of lipids in both serum and tissues.     

Linoleic acid kinetics and conversion to arachidonic acid in the pregnant and fetal baboon.

Linoleic acid plasma kinetics in pregnant baboons and its conversion to long chain polyunsaturates (LCP) in fetal organs is characterized over a 29-day period using stable isotope tracers. Pregnant baboons consumed an LCP-free diet and received [U-13C]linoleic acid (18:2*) in their third trimester of gestation. In maternal plasma, 18:2* dropped to near baseline by 14 days post-dose, while labeled arachidonic acid (20:4*) plateaued at 10 days at about 70% of total labeled fatty acids. After 2;-5 days, total tracer fatty acids decreased in visceral organs, but increased in the fetal brain. Maximal fetal incorporation of 18:2* was 1;-2 days post-dose; thereafter it dropped while 20:4* increased reciprocally. Labeled 20:4 replaced 18:2* in neural tissues by 5 days post-dose. In liver, kidney, and lung, 20:4* became dominant by 12 days, but in heart the crossover was >29 days. Fetal brain 20:4* plateaued by 21 days at 0. 025% of dose, while fetal liver 20:4* was constant from 1 to 29 days at 0.006% of dose. Under these dietary conditions we estimate that the fetus derives about 50% its 20:4 requirement from conversion of dietary 18:2, with the balance from maternal stores, and conclude that 1) fetal organs accumulate 18:2 within a day of a maternal dose and convert much of it to 20:4 within weeks, 2) modest dietary 18:2 levels may support fetal brain requirements for 20:4, and 3) the brain retains n;-6 fatty acids uniquely compared with major visceral organs.     

Differences in tissue-specific lipid composition between embryos of wild and captive breeding alligators (Alligator mississippiensis)

Fertile eggs obtained from alligators reared in captivity typically exhibit high rates of embryonic mortality. Also, the fatty acid composition of the yolk lipid of the captive eggs is markedly different from that observed in eggs from wild alligators, possibly as a result of differences in maternal diet in the two situations. The fatty acid compositions of tissue lipids during the embryonic development of wild and captive alligators were compared. The lipids of liver, adipose tissue and heart of the two types of embryo displayed fatty acid profiles which generally reflected the acyl compositions of the respective yolks. Thus the lipids from these tissues of the captive embryos contained markedly higher proportionate levels of linoleic and linolenic acids, lower levels of palmitoleic acid, and, in general, lower levels of docosahexaenoic acid and other C20 and C22 polyunsaturates, in comparison to the values for the wild embryos. In contrast, the fatty acid composition of the brain phosphoglycerides was very similar in the two types of embryo. Thus, at least in those embryos which had survived during the developmental period studied, the brain was able to maintain a relatively constant fatty acid composition, in spite of major differences between the wild and captive eggs in the proportions of the various fatty acids supplied from the yolk. It is suggested that a major cause of embryonic mortality in the captive embryos could be a failure to maintain an adequate level of docosahexaenoic acid in the developing brain.     

Plasma concentrations of estradiol 17beta and PGF2alpha metabolite and placental fatty acid composition and antioxidant enzyme activity in cows with and without retained fetal membranes

Fetal membrane retention is one of the most common problems in Holstein cattle after parturition. To investigate mechanisms involved, the following parameters were studied in the peri-parturition period: plasmatic concentrations of estradiol-17beta (E2) and PGFM (PGF2alpha metabolite), activity of antioxidant enzymes (superoxide dismutase-SOD, catalase-CAT and glutathione peroxidase-GSH-Px), thiobarbituric acid reagent substances (TBAR) concentrations and fatty acid composition of the placentae. E2 at parturition in the NPR group (control cows, n = 10) was higher than in PR cows (placental retention, n = 10) (P < 0.05). Activity of SOD in fetal tissue of NPR animals was higher than that of the PR group. In contrast, there was no difference between the two groups in activity of GSH-Px and CAT and the TBAR content of placental tissues. PR maternal tissues had proportionally more arachidonic and linoleic acid than tissues from NPR cows. Therefore, a complex of sequential events may cause placenta retention, starting with an unbalance of antioxidant capacity of the placenta, followed by a decrease in production of estrogen, which leads to the accumulation of arachidonic and linoleic acid in placental tissues.     

Tissue specific differences in the fatty acid composition of the marmoset monkey (Callithrix jacchus)

1. The possible relationship between the fatty acid composition of the adipose tissue of the marmoset monkey (Callithrix jacchus) and its dietary lipid intake was examined after a long-term feeding trial. 2. Only the proportions of stearic and linoleic acid in the adipose tissue were similar to those in the diet. The proportions of all other saturated and unsaturated fatty acid components were significantly different thus greatly reducing the potential value of this relationship in the marmoset. 3. The phospholipid fatty acid profiles of cardiac and skeletal muscle, aortae, kidney, liver, lung and brain were also compared to those of the plasma, platelets or red blood cells. 4. With the exception of the liver where the fatty acid profile is similar to that of the plasma, no clear relationships were found between the fatty acid profiles of these tissues and the components of the blood. 5. The fatty acid composition of skeletal muscle was very similar to that of the cardiac muscle of the marmoset, suggesting that muscle biopsy might be useful as an index of cardiac muscle composition.     

Origin of hepatic triglyceride fatty acids: quantitative estimation of the relative contributions of linoleic acid by diet and adipose tissue in normal and ethanol-fed rats

The present study demonstrates that the rat liver obtains most of its triglyceride fatty acids from dietary sources. The dietary and adipose tissue contributions of linoleic acid for hepatic triglyceride esterification were shown to be 50.42 and 13.85 micro moles, respectively, during a 4-day period. When ethanol provided 40% of the caloric intake, fatty liver developed and hepatic triglyceride content increased threefold. Under these conditions, the dietary and adipose tissue contributions of linoleic acid were estimated at 192.85 and 10.73 micro moles, respectively. This increase in dietary fatty acid utilization was sufficient to account for the entire increase in esterified hepatic linoleic acid. Any explanation of these observations must include the high dietary fatty acid utilization in both control and ethanol-treated animals. One possibility is that most dietary lipids first enter a rapidly turning over pool in adipose tissue from which most hepatic triglyceride fatty acids are derived. Another is that dietary fatty acids, incorporated into chylomicrons, are stored separately and used preferentially by the liver as compared with lipids derived from adipose tissue and bound to albumin. The pros and cons of these possibilities are discussed.     

The fatty acid composition of glycerolipids in nerve,brain, and other tissues of the streptozotocin diabetic rat

The fatty acid composition of individual glycerolipids in brain and sciatic nerve of rats made diabetic with streptozotocin and sacrificed 8 weeks later was determined and compared to the alterations that occurred in liver and kidney glycerlipids. A substantial decrease in the proportion of arachidonic acid and increases in the relative content of linoleic and docosahexenoic (22∶6n3) acids occurred in the phosphoglycerides of visceral tissues from diabetic animals as reported by others. In contrast, except for a small rise in the percentage of linoleic acid, no consistent changes in fatty acid composition of phosphatidylcholine, phosphatidylethanolamine, ethanolamine plasmalogen, phosphatidylinositol or phosphatidylerrine from brain or nerve were detected. The fatty acids of triacylglycerol associated with nerve exhibited alterations similar to those characteristic of liver. The differences which developed as a result of diabetes were completely prevented if animals were maintained continuously on insulin commencing shortly after administration of streptozotocin. It is concluded that the fatty acid composition of brain and nerve phosphoglycerides are unusually resistant to alteration in the diabetic animal and that consequently, changes in bulk membrane fluidity are unlikely to contribute to functional abnormalities displayed by diabetic peripheral nerve. Special Issue dedicated to Dr. Eugene Kreps.     

Soybean Oil Supplementation Improves Growth and Prevents Docosapentaenoic Acid (22: 5n–6) Accumulation in Tissues of Rats Fed on Palm Oil Diet

Effects of soybean oil supplementation as a source of linoleic and α-linolenic acids in a palm oil diet on growth and docosapentaenoic acid (22: 5n–6) levels in tissue lipids in male Sprague–Dawley rats were studied. The rats fed for two months with the diets containing soybean oil (10–50%) in palm oil showed significantly higher weight gain than that in rats fed a diet containing only palm oil as a fat source. The highest weight gain was observed in rats fed 50% soybean oil blended in palm oil. Such performance was also better than those observed in rats received diets containing soybean oil alone or canola oil alone. Addition of soybean oil to the palm oil diet prevented 22: 5n–6 accumulation in plasma, red blood cells, liver, heart, and retinal lipids with a compensative increase of docosahexaenoic acid (22:6n–3). Poly-unsaturated fatty acid profiles of brain were not affected by the addition of soybean oil. Changes in arachidonic acid contents in organs were not observed. The results indicated that soybean oil supplementation increases the weight gain and prevents the accumulation of 22: 5n–6 in the tissues which were observed in the rats fed a diet containing palm oil alone.     

Genesis of fatty liver and hyperlipemia in the fetal guinea pig.

10 to 20% of [1-14C] palmitate injected into pregnant guinea pigs was recovered in lipids of their fetuses. From these data and the rate of transport of palmitate in maternal blood, it appears that placental transport of free fatty acids can account for the accumulation of lipids in late gestational fetuses. About 80% of the labeled palmitate in the fetus appeared initially in lipids of the liver. 14C appeared in plasma triglyceride fatty acids after a few minutes and subsequently accumulated in lipids of white and brown adipose tissue, suggesting that much of the palmitate deposited in adipose tissue were derived from hepatogenous triglyceride fatty acids. By contrast, 14C was usually maximal in heart and carcass lipids before it appeared in plasma triglyceride fatty acids. Lipoprotein lipase activity in fetal adipose tissue was low, and activity of cofactor protein of lipoprotein lipase in fetal blood plasma was much lower than that observed in other mammalian species. On the basis of these and earlier observations, it is concluded that the accumulation of triglycerides in liver and blood plasma of fetal guinea pigs during late gestation is at least partly the result of the large uptake of maternally derived free fatty acids by the fetal liver accompanied by rapid synthesis and secretion of triglyceride-rich very low density lipoproteins into the blood. However, limited uptake of triglyceride fatty acids in adipose tissue may contribute to the fatty liver and hyperlipemia.