Lipoprotein lipase activity in skeletal muscle and brown adipose tissue of pregnant and lactating rats

Changes in lipoprotein lipase (LPL) activity during pregnancy and lactation were followed in skeletal muscles and interscapular brown adipose tissue (BAT) of rats fed two diets differing in energy density (high carbohydrate or high fat). Rats were decapitated after 7, 19 or 21 d of pregnancy or after 3 or 12 d of lactation. Virgin rats and females separated from their litter just after delivery were used as nonpregnant and nonlactating controls, respectively. Blood was collected for determination of plasma glucose, triglycerides (TG) and nonesterified fatty acids (NEFA). Soleus, extensor digitorum longus (EDL), diaphragm and interscapular BAT were rapidly removed and frozen in liquid nitrogen for LPL activity measurement. LPL activity was not significantly higher in muscles and BAT of virgin rats fed the high fat diet than in those of rats fed the high carbohydrate diet. No significant change of skeletal muscle LPL activity was observed during pregnancy, regardless of the diet fed. Although BAT exhibited a transitory hypertrophy during pregnancy, its LPL activity was not significantly altered; during lactation BAT lost weight and its LPL activity dropped sharply when either diet was fed, leaving more TG available for milk production.     

Lipoprotein lipase and the disposition of dietary fatty acids

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.     

Unusual metabolic characteristics in skeletal muscles of transgenic rabbits for human lipoprotein lipase

Background

The lipoprotein lipase (LPL) hydrolyses circulating triacylglycerol-rich lipoproteins. Thereby, LPL acts as a metabolic gate-keeper for fatty acids partitioning between adipose tissue for storage and skeletal muscle primarily for energy use. Transgenic mice that markedly over-express LPL exclusively in muscle, show increases not only in LPL activity, but also in oxidative enzyme activities and in number of mitochondria, together with an impaired glucose tolerance. However, the role of LPL in intracellular nutrient pathways remains uncertain. To examine differences in muscle nutrient uptake and fatty acid oxidative pattern, transgenic rabbits harboring a DNA fragment of the human LPL gene (hLPL) and their wild-type littermates were compared for two muscles of different metabolic type, and for perirenal fat.

Results

Analyses of skeletal muscles and adipose tissue showed the expression of the hLPL DNA fragment in tissues of the hLPL group only. Unexpectedly, the activity level of LPL in both tissues was similar in the two groups. Nevertheless, mitochondrial fatty acid oxidation rate, measured ex vivo using [1-¹⁴C]oleate as substrate, was lower in hLPL rabbits than in wild-type rabbits for the two muscles under study. Both insulin-sensitive glucose transporter GLUT4 and muscle fatty acid binding protein (H-FABP) contents were higher in hLPL rabbits than in wild-type littermates for the pure oxidative semimembranosus proprius muscle, but differences between groups did not reach significance when considering the fast-twitch glycolytic longissimus muscle. Variations in both glucose uptake potential, intra-cytoplasmic binding of fatty acids, and lipid oxidation rate observed in hLPL rabbits compared with their wild-type littermates, were not followed by any modifications in tissue lipid content, body fat, and plasma levels in energy-yielding metabolites.

Conclusions

Expression of intracellular binding proteins for both fatty acids and glucose, and their following oxidation rates in skeletal muscles of hLPL rabbits were not fully consistent with the physiology rules. The modifications observed in muscle metabolic properties might not be directly associated with any LPL-linked pathways, but resulted likely of transgene random insertion into rabbit organism close to any regulatory genes. Our findings enlighten the risks for undesirable phenotypic modifications in micro-injected animals and difficulties of biotechnology in mammals larger than mice.

     

Short-term intake of conjugated linoleic acid inhibits lipoprotein lipase and glucose metabolism but does not enhance lipolysis in mouse adipose tissue

Feeding diets supplemented with t10c12 conjugated linoleic acid (CLA) to growing mice reduces body fat mass. The effects are evident after 1 wk and maximal by 3 wk and are accompanied by reductions in fat cell size. This may complicate direct comparisons with adipocytes from control mice. Accordingly, we investigated the early biochemical events that occur within adipocytes during the first week of CLA feeding, before changes in the size of adipocytes have occurred. Female ICR mice were fed a control diet or a diet supplemented with 0.5 g/100 g of CLA for 4 d, at which time there were no differences in body weight, fat mass or adipocyte size (except that CLA-fed mice had fewer adipocytes >90 micro m in diameter). Parametrial adipose tissue from the CLA-fed mice had significantly reduced heparin-releasable lipoprotein lipase (LPL) and intracellular LPL activities and significantly reduced glucose incorporation into CO(2), fatty acid and glycerol. There were no differences between adipose tissues from CLA-fed or control mice in the ratios of 16:0 to 16:1 and 18:0 to 18:1 fatty acids or in norepinephrine-stimulated lipolysis. Serum insulin levels in food-deprived mice, measured at 4 d and 7 wk, did not differ between groups nor did the concentration of free fatty acids in serum of food-deprived or fed mice measured at the same time points. In mice, CLA-induced inhibition of heparin-releasable LPL and glucose metabolism may be the most important early steps leading to subsequent body fat reduction. In addition, CLA does not appear to enhance lipolysis in mouse adipose tissue in vivo.     

Purified chickpea or lentil proteins impair VLDL metabolism and lipoprotein lipase activity in epididymal fat,but not in muscle,compared to casein,in growing rats

Background  It is well known that the legume proteins have a lowering effect on plasma cholesterol and triacylglycerols (TG) concentrations compared to animal proteins. The protein itself, as well as non-protein constituents, naturally present in legumes may be implicated. Aim of the study  The effects of various dietary purified legumes proteins compared to casein, were determined on plasma TG level, VLDL concentration and composition. Moreover, lipoprotein lipase (LPL) activity in epididymal fat, gastrocnemius and heart was investigated to evaluate in these tissues their capacity to release free fatty acids from their TG substrate and the liver capacity to stock the TG. Methods  Weaning male Wistar rats were fed ad libitum one of the following diets: 200 g/kg diet of purified proteins of lentil (L), or chickpea (CP) or casein (CAS). At day 28, VLDL were isolated from plasma sample by a single ultracentrifugation flotation. Hepatic lipase and LPL activity in epididymal fat, gastrocnemius and heart were measured by using glycerol tri [9–10(n)-³H] oleate emulsion as substrate. Results  Compared with CAS diet, the CP and L protein diets exhibited similar cholesterolemia, but lower triglyceridemia (1.9-fold and 2.5-fold) and VLDL particle number, as measured by their reduced contents of TG and apolipoproteins. CP and L protein diets reduced liver TG and cholesterol by 31 and 45%, respectively compared to CAS diet. Furthermore, LPL activity in adipose tissue of rats fed CP or L was 1.6-fold lower than that of rats fed CAS. There was no significant difference in heart and gastrocnemius LPL activities with the three proteins. In contrast, hepatic lipase activity was higher in rats fed CP and L diets. Conclusion  The low food efficiency ratio of purified CP and L proteins related to CAS is associated with decreased plasma VLDL and adipose tissue LPL activity. The low liver TG concomitant with reduced TG and apolipoproteins contents of VLDL confirm that hypotriglyceridemia is essentially due to impaired synthesis, exportation and transport of TG by VLDL which prevent lipid storage in adipose tissue.     

A high dietary lipid intake during pregnancy and lactation enhances mammary gland lipid uptake and lipoprotein lipase activity in rats.

Rats fed a diet with high fat concentration produce larger amounts of milk with a higher lipid concentration than rats fed a lower fat diet. This investigation was designed to study the relationship between dietary fat intake, mammary gland lipid uptake and lipogenesis in rat dams fed, during pregnancy and lactation, one of two purified diets, with equal energy density, containing 2.5 (LL) or 20 g fat/100 g diet (HL). Milk lipid concentration and fatty acid composition were determined at d 14 of lactation. Mammary gland lipogenesis, lipoprotein lipase (LPL) activity and the uptake of [1-(14)C]triolein by the mammary gland and its transfer to the pups was measured. The intestinal absorption of oral (14)C-lipid, (14)CO(2) production and the amount of (14)C-lipid transferred to the pups (milk clot + pups carcass) were significantly higher in the HL group than in the LL group (P < 0.05). Mammary gland lipogenesis was 75% lower and LPL activity was 30% higher in the HL group (P < 0.05). Medium-chain fatty acids (C6-C14) excretion was 46% lower and that of long-chain fatty acids was 142% (P < 0.001) higher in the HL group than in the LL group. The higher milk lipid excretion in the rats fed a high-fat diet resulted from a larger uptake of dietary lipid by the mammary gland, indicated by a larger transfer of (14)C-lipid to the pups and by a higher LPL activity in the mammary gland.     

Acyl pattern of adipose tissue triglycerides, plasma free fatty acids, and diet of a group of men participating in a primary coronary prevention program (the Oslo Study)

The acyl pattern of adipose tissue triglycerides and of plasma free fatty acids were determined after 7 yr of diet intervention on elevated plasma cholesterol in 42 men taking part in the smoking-lipid trial of the Oslo Study. Twenty-two of the men were advised to change dietary habits (mainly reduce saturated fat) whereas the remaining 20 were controls. The adipose tissue from men in the intervention group contained relatively more linoleic and linolenic acids and relatively less saturated and monounsaturated fatty acids compared to men in the control group. There were strong correlations between the relative content of several fatty acids in adipose tissue triglycerides and plasma free fatty acid. Furthermore, there was a close correlation between the intake of polyunsaturated fatty acids found in a dietary survey done 2 to 3 yr before this study and the relative content of polyunsaturated fatty acids in adipose tissue.     

Metabolic adaptations in pregnancy and their implications for the availability of substrates to the fetus

During the first two-thirds of gestation, the mother is in an anabolic condition, increasing her fat depots thanks to both hyperphagia and enhanced lipogenesis. During the last third of gestation, the mother switches to a catabolic condition. Glucose is the most abundant nutrient crossing the placenta, which causes maternal hypoglycemia despite an increase in the gluconeogenetic activity. Adipose tissue lipolytic activity becomes enhanced, increasing plasma levels of FFA and glycerol that reach the liver; consequently there is an enhanced production of triglycerides that return to the circulation in the form of very low density lipoproteins (VLDL). Glycerol is also used as a preferential gluconeogenetic substrate, saving other more essential substrates, like amino acids, for the fetus. Under fasting conditions, fatty acids are converted into ketone bodies throughout the beta-oxidation pathway, and these compounds easily cross the placental barrier and are metabolized by the fetus. An enhanced liver production of VLDL-triglycerides together with a decrease in adipose tissue lipoprotein lipase (LPL) and an increase in plasma activity of cholesterol ester transfer protein causes both an intense increment in these lipoproteins and a proportional enrichment of triglycerides in both low and high density lipoproteins. Maternal triglycerides do not cross the placenta, but the presence of LPL and other lipases allows their hydrolysis, releasing fatty acids to the fetus. Under fasting conditions, the maternal liver uses circulating triglycerides as ketogenic substrates. Around parturition there is an induction of LPL activity in the mammary glands, driving circulating triglycerides to this organ for milk synthesis, allowing essential fatty acids derived from the mother's diet to become available to the suckling newborn.     

The carbon pathway for lipogenesis in isolated adipocytes from rat, guinea pig, and human adipose tissue.

The synthesis of fatty acids from a variety of labeled substrates by isolated adipocytes of the rat, guinea pig, and human was investigated. The incorporation of radioactive glucose and pyruvate into triglyceride fatty acids was considerably lower in human than either rat or guinea pig adipose tissue. By contrast, the incorporation of palmitate into adipose tissue triglycerides was approximately the same in all three species. End carbon analysis of fatty acids isolated from adipocytes incubated with pyruvate-U-14C indicated that although the synthesis of fatty acids in human adipose tissue was extremely low compared to that of the rat and guinea pig, it represented de novo biosynthesis rather than chain elongation of existing fatty acids. It is suggested that in the human, fatty acids are synthetised de novo primarily in the liver. In adipose tissue, lipogenesis consists essentially of the esterification of fatty acids, obtained from plasma, into triglycerides.     

Effects of high-fat diet intake on glucose uptake in central and peripheral tissues of non-obese rats

We previously demonstrated that plasma glucose concentration was higher while plasma insulin concentration was lower in rats fed a high-fat diet. In the present study, we examined the effects of high-fat diet on glucose uptake in central and peripheral tissues in non-obese rats. Forty male Sprague-Dawley rats were fed high- or low-fat diets for 4 wk. Body weight and body fat accumulation were not different between the two diet groups after 4 wk. Glucose uptake in the skeletal muscles and adipose tissues, estimated by the 2-deoxy-D-glucose method, was lower in the rats fed the high-fat diet than that in the rats fed the low-fat diet, whereas uptake in the liver and pancreas did not differ between the two groups. Glucose uptake in the hypothalamus and cortex was higher in the high-fat diet group as compared with that in the low-fat diet group. These results suggest that increased plasma glucose levels in rats fed the high-fat diet were caused by a decrease in glucose uptake in the skeletal muscles and adipose tissues. Reduced plasma insulin level in the high fat diet group with no difference in glucose uptake in the pancreas may be due to increased sympathetic activity in the pancreas resulting from the increased glucose uptake in the brain regions involved in autonomic functions.     

Comparative changes of fat digestibility and fat accumulation by the carbon chain length of dietary glycerol tri-homogenous fatty acids in rats

The present study was undertaken to investigate the influence of the carbon chain length of dietary glycerol tri-homogenous fatty acid on fat digestibility and body fat accumulation in rats. Thirty-six Wistar male rats were divided into six groups and fed the semipurified C8, C10, C12, C14, C16, C18 triglyceride diets, respectively. Body weight was significantly lower (p<0.05) in rats fed the C14, C16 and C18 diets than in rats fed the C8, C10 and C12 diets. Weights of adipose tissues and apparent fat digestibility were markedly low in the C16 and C18 fed rats. In these groups, fat content of whole-body carcass was significantly lower (p<0.05), but moisture, ash and protein contents were significantly greater (p<0.05) than those of the other groups. Fatty acid profile of epididymal adipose tissue revealed that dietary C8:0 was not directly incorporated into adipose tissues, and only a small amount of dietary C10:0 was directly deposited as body triglycerides. Meanwhile, dietary C12:0 was extensively incorporated into adipose tissues when compared to those of C8 and C10 rats. The present study indicated that apparent fat and energy digestibilities of dietary glycerol tripalmitin and glycerol tristearin were remarkably lower than the glycerol tricaprylin, tricaprin, trilaurin and trimyristin, which results in lower fat accumulation in the C16 and C18 fed rats.     

Effects of ethanol intake on lipid metabolism in the lactating rat

Female rats receiving alcohol (20%) in drinking water during lactation (AL) were compared to pair-fed animals (PF) and normal controls (C) fed ad lib. All animals were killed on the 12th day of lactation. When compared to C rats, food intake decreased in both AL and PF groups, and this effect was followed by a lower body weight and mammary gland (MG), liver, and parametrial adipose tissue weights. Mammary glands triacylglyceride concentration (TG) was much lower in PF than in AL, although in the latter, values did not reach those of C, and had higher liver TG concentration than any of the other groups. Both PF and AL rats had lower plasma TG, glycerol, and free fatty acid concentrations and higher β;-hydroxybutyrate concentration than C rats. When compared to C rats, the rate of lipogenesis in MG was higher in both PF and AL rats, whereas in liver it was higher in PF and lower in AL rats, and in adipose tissue it was higher in PF and unchanged in AL rats. The appearance of ¹⁴C lipids 4 h after oral [¹⁴] triolein in both MG and liver was lower in AL and PF rats and only lower in adipose tissue of AL rats as compared to the C rats. Lipoprotein lipase and hormone-sensitive lipase activities were lower in MG in both PF and AL rats than in C, whereas in adipose tissue the activity of lipoprotein lipase did not differ between AL and C rats and the activity of HSL was lower in the former. These findings therefore show that in spite of reduced uptake of orally administered triglycerides due to decreased LPL activity, maternal alcohol feeding during lactation in the rat preserves the mammary gland triglyceride content thanks to enhanced lipogenetic activity. On the other hand, it causes liver triglycerides accumulation, probably as a result of the decreased rate of triglycerides released into circulation, and these changes are not caused by the reduced food intake of the animals.     

Weaning affects lipoprotein lipase activity and gene expression in adipose tissues and in masseter but not in other muscles of the calf

The nutritional and physiological modifications that occur during the weaning period induce adaptations of tissue metabolism in all mammal species. Among the adaptations due to weaning in ruminants, the regulation of lipoprotein lipase (LPL) activity, one of the rate-limiting steps of fatty acid utilization by tissues, was still unknown. The present study aimed at comparing LPL activity and gene expression in the heart, seven skeletal muscles and three adipose tissue sites between two groups of seven preruminant (PR) or ruminant (R) calves having a similar age (170 d), similar empty body weight (194 kg) at slaughter, and similar net energy intake from birth onwards. Triacylglycerol content of adipose tissues was 16 % lower in R than in PR calves, This could be partly the result from a lower LPL activity (-57 %, ). LPL mRNA levels were also lower in R calves (-48 % to -68 %, ) suggesting a pretranslational regulation of LPL activity. Activity and mRNA levels of LPL did not differ significantly in the heart and skeletal muscles except in the masseter in which LPL activity and mRNA levels were higher (+50 % and +120 % respectively, ) in the R calves. Regulation of LPL in masseter could be explained by the high contractile activity of this muscle after weaning due to solid food chewing. In conclusion, weaning in the calf affects LPL activity and expression in adipose tissues, but not in skeletal muscles except the masseter.     

Dietary (n-3) polyunsaturated fatty acids up-regulate plasma leptin in insulin-resistant rats

The study was designed to evaluate the chronic regulation of plasma leptin by dietary (n-3) polyunsaturated fatty acids (PUFA) in insulin-resistant, sucrose-fed rats. Male Sprague-Dawley rats were randomly assigned to consume for 3 or 6 wk a diet containing 57.5% (g/100 g) sucrose and 14% lipids as either fish oil (SF) or control oils (SC). After 3 and 6 wk of consuming the SF diet, plasma leptin was 70% (P < 0.001) and 75% (P < 0.05) greater, respectively, than in rats fed the SC diet. The same result was found when plasma leptin was adjusted by total fat mass, as measured by dual-energy X-ray absorptiometry. Despite high leptin levels, food intake of rats fed the SF diet was greater than in SC-fed rats without any difference in body weight or total fat mass. After 3 wk, accumulated leptin in epididymal and retroperitoneal adipose tissue was higher in the SF-fed rats than in the SC-fed rats. However, after 6 wk, tissue leptin in the SF-fed rats did not differ from that of the SC-fed rats. The SF diet increased adipose tissue glucose transporter-4 protein quantity and prevented the sucrose-induced elevations in plasma triglycerides and free fatty acids. When all SC- and SF-fed rats (both diets and feeding durations) were considered, plasma leptin levels were positively correlated with body weight (r = 0.5, P < 0.0001) and with total fat mass (r = 0.5, P < 0.0005). These results suggest that plasma leptin at a given time could be inappropriately high for a given fat mass in insulin-sensitive rats fed (n-3) PUFA.     

The influence of dietary medium and long chain triglycerides on growth performances and fat deposition in growing rats.

The present study was undertaken to investigate the effects of dietary medium and long chain triglycerides (MCT and LCT) on fat deposition and fatty acid composition of adipose tissues of rats. Twenty-seven Wistar strain male rats were divided into three groups and fed semisynthetic experimental diets: Basal (AIN 76), MCT (basal+C8:0 10%), LCT (basal+corn oil 10%). Feed intake was measured every day and body weight was measured once a week. At the beginning, 4th and 8th week of experimental feeding, 3, 12, 12 rats were slaughtered, respectively. Liver, perirenal and epididymal adipose tissue pads were weighted and their fatty acid composition was determined. Chemical composition of wholebody carcass was measured. Body weight gain was greater in rats fed the LCT diet than in rats fed the basal and MCT diets. Feed intakes were decreased in rats fed the MCT and LCT diets compared to that of the basal group. Subsequently, when compared to the basal group rats, feed efficiencies in rats fed the MCT and LCT diets were improved at the level of 6 and 14% for 4 weeks, and then 17 and 24% for 8 weeks, respectively. The weight of perirenal and epididymal adipose tissue pads tended to be larger in rats fed the MCT and LCT diets than in the basal group, although not significant. There were not significant differences in wholebody composition among the three groups. But it appeared that in rats fed the MCT diet, moisture content tended to be decreased and crude protein content increased compared to the LCT group rats. Fatty acid composition of the rats fed the LCT diet showed a good reflection of dietary fatty acid composition. Unlike LCT, little of medium chain fatty acid (MCFA) itself were incorporated into liver or adipose tissues. However, it seems that fat deposition of the MCT group was accomplished not by incorporation of dietary fatty acids but by de novo fatty acids synthesis.     

Lipoprotein metabolism in a rat model of diet-induced adiposity

Obesity in humans is associated with decreased plasma levels of high density lipoprotein (HDL), but the mechanisms effecting this relationship have not been established. Four treatment groups were used to develop a range of moderate adiposity: rat pups were raised in litters of 4 or 14 and fed from weaning diets of 6 or 24% fat (wt/wt) for 15-17 wk. Lipoproteins from plasma and from a recirculating in situ liver perfusion system were then separated and analyzed, lipoprotein lipase (LPL) activity was assayed in samples of adipose tissue and skeletal muscle and body composition and cholesterol concentrations of various tissues were determined. There was little effect of the diet or litter size treatments on plasma lipids or lipoprotein profiles. Compared to the marked changes in lipid and lipoprotein metabolism that have been observed in severely obese animal models, there was generally little effect of the treatments used to produce this model of moderate diet-induced adiposity. Adiposity was unrelated to plasma total cholesterol and triglycerides. While fatness was positively, although weakly, correlated with plasma levels of several HDL components, including HDL cholesterol, there were no consistent treatment effects on these measures. Plasma HDL levels and adiposity were unrelated to hepatic HDL production or tissue LPL activities. A review of the literature suggests that differences in plasma HDL responses to adiposity in humans and in experimental animals may be due to inherent species differences in lipoprotein metabolism.     

Body fat accumulation is greater in rats fed a beef tallow diet than in rats fed a safflower or soybean oil diet

The effects of dietary fats , consisting of different fatty acids, on body fat accumulation and uncoupling protein (UCP) in interscapular brown adipose tissue were studied in rats. Metabolisable energy in experimental diets based on safflower oil, soybean oil or beef tallow was measured strictly (experiment 1). Male Wistar rats were then meal-fed an isoenergetic diet for 8 weeks (experiment 2). Each group of rats showed the same weight gain during the 8-week experimental period. Carcass fat content was greater in rats fed the beef tallow diet than in those fed the with the safflower or soybean oil diets, whereas the weight of abdominal adipose tissue was the same for all three dietary groups. Gene expression of UCP1 and the UCP content of the interscapular brown adipose tissue was lower in the beef tallow diet group than in the other dietary groups. A negative correlation was observed between carcass fat content and n-6 unsaturated fatty acid content in dietary fats. These results suggest that the greater body fat accumulation in rats fed the beef tallow diet results from lower expression of UCP1 mRNA and lower UCP content in brown adipose tissue. n-6 Polyunsaturated fatty acids may be the most effective fatty acids in limiting body fat.     

Effect of dietary seal and fish oils on triacylglycerol metabolism in rats

Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were distributed mainly in the sn-1 and 3 positions of seal oil triacylglycerol and in the sn-2 position of fish oil triacylglycerol. Seal oil or fish oil-rich fats having constant polyunsaturated/monounsaturated/saturated fatty acids and n-6/n-3 polyunsaturated fatty acid (PUFA) ratios were fed to rats for 3 wk. Control rats were fed on a fat containing linoleic acid as the sole PUFA. Seal oil more effectively lowered serum and liver triacylglycerol concentrations than fish oil. The activities of fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH) and hepatic triacylglycerol lipase (HTGL) were significantly lower in the seal oil group than in the control group, whereas the activity of HTGL was significantly lower and the hepatic peroxisomal beta-oxidation and activity of lipoprotein lipase (LPL) in adipose tissue were significantly higher in the fish oil group than in the control group. These observations suggest that the predominant hypotriacylglycerolemic effect of seal oil is caused by the suppression of fatty acid synthesis.     

Dietary fish oil increases lipid mobilization but does not decrease lipid storage-related enzyme activities in adipose tissue of insulin-resistant,sucrose-fed rats

Fish oil feeding has been shown to limit visceral fat accumulation in insulin-resistant rats. Our goal was to determine whether this finding is due to increased fat mobilization or decreased lipid storage. Adipocytes were isolated from rats fed for 3 wk a diet containing 57.5 g/100 g sucrose and 14 g/100 g lipids as either fish oil (SF) or a mixture of standard oils (SC); there was also a reference group (R). Substituting fish oil for standard oils protected rats from visceral fat hypertrophy, hypertriglyceridemia and hyperglycemia. The stimulation of lipolysis was greater in adipocytes isolated from SF-fed rats than in those from SC-fed rats. Fatty acid synthase (FAS) activity was markedly lower in the liver but not in the adipose tissues of rats fed SF. Lipoprotein lipase (LPL) activity was 2.2-fold higher in the adipose tissues but not in the muscle in rats fed the SF diet than in those fed the SC diet. The decrease in visceral fat in rats fed fish oil could be attributed to decreased plasma triacylglycerol concentration and/or increased lipid mobilization rather than to reduced lipid storage.     

Maternal and early dietary fatty acid intake: changes in lipid metabolism and liver enzymes in adult rats

Over the last decade, much evidence has emerged to suggest that alterations in maternal nutrition during pregnancy may irreversibly affect aspects of physiological and biochemical functions in the fetus. This study was designed to determine the mechanisms involved in these alterations. Our hypothesis was that the type of maternal dietary fat received in early life could determine the level of lipoprotein lipase (LPL; EC 3.1.1.34) activity and gene expression which would be maintained into later life. A diet high in (n-3) polyunsaturated fatty acids was predicted to be associated with higher levels of lipoprotein lipase (LPL) activity and expression and lower levels of plasma triglyceride after a high fat meal challenge. Using a 2x2 factorial design, Wistar Albino rats were pair-fed either a fish oil diet (50 g/kg) or a mixed oil diet (50 g/kg) for the last 2 wk of gestation, during lactation and pups were fed these diets until 5 wk of age. After 5 wk, the rats were fed nonpurified diet. The rats were killed at 5 wk (young) or 10 wk (adult) of age after a mixed oil (50 g/kg) test meal. There were significant age effects on plasma triglyceride (P<0.02), cholesterol (P<0.001), glucose-dependent insulinotrophic polypeptide (GIP) (P<0.001) and liver glutathione reductase activity (P<0.05) which were all higher in the young rats compared to the adults. There were significant effects of diet on triglyceride (P<0.001), cholesterol (P<0.001) and LPL mRNA levels (P<0.001). GIP and triglyceride levels were significantly correlated (r = 0.66; P<0.001). Omental adipose tissue LPL activity as significantly higher in the fish-oil fed groups compared to the other groups (P<0.001), whereas Epididymal adipose tissue LPL mRNA was significantly higher in the mixed oil-fed adults compared to the other groups (P<0.001). The latter result suggested an imprinting effect of fatty acid composition in early life on LPL gene expression. Liver superoxide dismutase activity was affected by age and diet and was higher in the young than in the adults and higher in the fish oil-fed young than in those fed the mixed oil-fed (P<0.005). Catalase activity was also affected by age (P<0.001) and diet (P<0.001), and there was a significant interaction between age and diet (P<0.001). Catalase activity was higher in rats fed fish oils at both stages of development, suggesting that feeding fish oils to rats in early life raises oxidative stress throughout life. The majority of the significant differences shown were between the age groups and not between the two dietary groups, suggesting that postprandial handling of a standard fat meal is affected more by age than by early dietary fatty acid composition. However, the mechanisms of biological imprinting of fatty acids on LPL expression and on enzymes related to oxidative stress requires more investigation.