Effect of dietary fat sources on fatty acid deposition and lipid metabolism in broiler chickens.

The hypothesis tested was that dietary vegetable fats rich in saturated fatty acids, when compared with a vegetable oil rich in linoleic acid, increase fat deposition in broiler chickens and affect synthesis or oxidation, or both, of individual fatty acids. Diets with native sunflower oil (SO), a 50:50 mix of hydrogenated and native SO, palm oil, and randomized palm oil were fed to broiler chickens. Intake of digestible fat and fatty acids, whole body fatty acid deposition, hepatic fatty acid profile, and hepatic enzyme activities involved in fatty acid oxidation and synthesis were measured. The fat deposition:digestible fat intake ratio was significantly lower for the SO group in comparison with the groups fed the vegetable fats rich in saturated fatty acids. The difference between digestible intake and deposition of C18:2, reflecting its maximum disappearance rate, was highest for the SO group and lowest for the palm oil- and randomized palm oil-fed birds. The calculated minimal rate of de novo synthesis of monounsaturated fatty acids (MUFA), calculated as deposition minus digestible intake, was more than 50% lower for the SO group than for the other 3 dietary groups. Based on the fatty acid profiles in the liver, it would appear that increasing contents of C18:2 decrease the desaturation of saturated fatty acids into MUFA. It is concluded that a diet rich in C18:2 in comparison with different kinds of vegetable saturated fatty acids decreases the deposition of fat, especially of MUFA. It appears to be caused by a higher ß-oxidation and a reduced de novo synthesis of MUFA, but this conclusion is not fully supported by the measured activities of enzymes involved in fatty acid synthesis and oxidation.

Fatty acid digestion and deposition in broiler chickens fed diets containing either native or randomized palm oil.

The hypothesis tested was that randomization of palm oil would increase its digestibility, especially that of its palmitic acid (C16:0) component, with subsequent changes in the fatty acid composition in body tissues. Broiler chickens were fed diets containing either native or randomized palm oil. Diets with either native or a 50/50 mix of native and hydrogenated sunflower oil were also fed. Randomization of palm oil raised the fraction of C16:0 at the sn-2 position of the glycerol molecule from 14 to 32%. Hydrogenation of sunflower oil reduced fat and total saturated fatty acid digestibility, whereas no change in digestibility of total unsaturated fatty acids was found. Randomization of palm oil raised the group mean apparent digestibility of C16:0 by 2.6 and 5.8% units during the starter and grower-finisher phase, respectively. On the basis of the observed digestibilities in the grower-finisher period, it was calculated that the digestibility for C16:0 at the sn-2 and sn-1,3 position was 90 and 51%, respectively. The feeding of randomized instead of native palm oil significantly raised the palmitic acid content of breast meat and abdominal fat and lowered the ratio of unsaturated to saturated fatty acids. It is concluded that randomized palm oil may be used as vegetable oil in broiler nutrition with positive effect on saturated fatty acid digestibility when compared with native palm oil and positive effect on firmness of meat when compared with vegetable oils rich in unsaturated fatty acids.

Body composition and heat expenditure in broiler chickens fed diets with or without trans fatty acids.

The effect of a diet containing trans fatty acids (TFA) on the fatty acid composition and fat accumulation was investigated in broiler chickens. Female broilers were fed a control or a TFA-containing diet. The difference between the diets was that a part of cis 18:1 in the control diet was replaced by the TFA. Body composition, energy balance and the fatty acid composition were examined. Over the time-period studied (15 days), the body fat content and the protein content did not differ significantly between the TFA-fed group and the control. In energy balance studies, total energy intake, energy loss in excreta, energy expenditure and energy storage did not differ between the treatments. Compared to the control diet, the TFA diet resulted in significantly higher amounts of 14:0 and 18:1n-7 and lower amounts of 18:1n-9 and 20:4n-6 in the body. In conclusion, the data suggest that feeding TFA for 15 days to female broilers had no effect on energy retention, energy expenditure and energy loss in excreta or in body composition in terms of fat and protein. Only the fatty acid composition in the body was affected by the treatment with TFA. In addition, 50% of ingested TFA was incorporated into the body fat. This may have a negative effect on the dietetic value of chicken meat.

Body composition and selected blood parameters in mice fed a combination of fibre and conjugated linoleic acid.

Feeding mice conjugated linoleic acid (CLA) reduces body fat. Soluble fibre decreases apparent lipid digestibility. The objective of the present study was to examine whether a combination of dietary CLA and soluble fibre would further decrease the proportion of body fat than a diet with CLA alone. Therefore, we fed mice diets with CLA and different amounts of Nutrim, containing 10% soluble fibre. CLA was added to the control diet at the expense of high oleic acid sunflower oil (HOSF) component and Nutrim was added at the expense of an isoenergetic combination of starch, dextrose and cellulose. The diets were fed for 28 days. Weight gain after 28 days was less in CLA-fed animals than in HOSF-fed animals. Both CLA and Nutrim increased the body water content. CLA reduced total body fat and epidydymal fat but Nutrim did not. No interaction of CLA and fibre was detected. We, therefore, must conclude that under the present experimental conditions dietary CLA and fibre do not interact to reduce body fat deposition.

The influence of dietary linoleic and alpha-linolenic acid on body composition and the activities of key enzymes of hepatic lipogenesis and fatty acid oxidation in mice.

We have recently suggested that feeding the C18 polyunsaturated fatty acid, alpha-linolenic acid (ALA), instead of linoleic acid (LA) reduced body fat in mice. However, the difference in body fat did not reach statistical significance, which prompted us to carry out this study using more animals and diets with higher contents of ALA and LA so that the contrast would be greater. The diets contained either 12% (w/w) LA and 3% ALA or 12% ALA and 4% LA. A low-fat diet was used as control. The diets were fed for 35 days. The proportion of body fat was not influenced by the type of dietary fatty acid. Plasma total cholesterol and phospholipids were significantly lower in ALA-fed mice than in mice fed LA. Activities of enzymes in the fatty acid oxidation pathway were significantly raised by these two diets when compared with the control diet. alpha-Linolenic acid vs. LA did not affect fatty acid oxidation enzymes. In mice fed the diet with LA activities of enzymes of de novo fatty acid synthesis were significantly decreased when compared with mice fed the control diet. alpha-Linolenic acid vs. LA feeding did not influence lipogenic enzymes. It is concluded that feeding mice for 35 days with diets either rich in LA or ALA did not significantly influence body composition.

Studies on hepatic lipidosis and coinciding health and fertility problems of high-producing dairy cows using the "Utrecht fatty liver model of dairy cows". A review.

Fatty liver or hepatic lipidosis is a major metabolic disorder of high-producing dairy cows that occurs rather frequently in early lactation and is associated with decreased health, production and fertility. A background section of the review explores reasons why high-producing dairy cows are prone to develop fatty liver post partum. Hepatic lipidosis and coinciding health and fertility problems seriously endanger profitability and longevity of the dairy cow. Results from a great number of earlier epidemiological and clinical studies made it clear that a different approach was needed for elucidation of pathogenesis and etiology of this complex of health problems. There was a need for an adequate animal model in which hepatic lipidosis and production, health and fertility problems could be provoked under controlled conditions. It was hypothesized that overconditioning ante partum and feed restriction post partum might induce lipolysis in adipose tissue and triacylglycerol accumulation in the liver following calving. This consideration formed the basis for the experiments, which resulted in the "Utrecht fatty liver model of dairy cows". In this model, post partum triacylglycerol-lipidosis as well as the whole complex of health and fertility problems are induced under well-controlled conditions. The experimental protocol based on this hypothesis produced in all cases (10 feeding trials with over 150 dairy cattle) the intended result, i.e. all experimental cows developed post partum higher hepatic triacylglycerol concentrations than did control cows. The model was evaluated in biochemical, clinical pathology, immunological, clinical and fertility terms. It turned out that in this model, post partum triacylglycerol-lipidosis as well as the whole complex of health and fertility problems were induced under well-controlled conditions.

Unrestricted feed intake during the dry period impairs the postpartum oxidation and synthesis of fatty acids in the liver of dairy cows.

The purpose of this study was to determine the activities of key hepatic enzymes of fatty acid synthesis and oxidation in cows that had excessive body fat at parturition. Dairy cows were allocated to either an experimental group or a control group. All cows were offered a total mixed ration with an energy content of 6.6 MJ of net energy for lactation per kilogram of dry matter and consisting of corn silage, beet pulp, rapeseed meal, and soybean meal. Control cows were restricted to 6.8 kg/dry matter of the mixed ration in the dry period. Experimental cows had unrestricted access to the mixed ration during the dry period to increase body fat and induce fatty liver postpartum. Blood and liver samples were collected 1 wk before and 1, 2, and 4 wk after parturition. Before parturition, neither the serum nonesterifled fatty acids nor the hepatic triacylglycerol concentrations differed between experimental and control cows. After parturition, the values for these variables were greater in experimental cows than in control cows. Plasma 3-hydroxybutyrate increased sharply after parturition in the experimental group. In liver, the activity of acetyl-CoA carboxylase was already significantly lower in the experimental group before parturition. After parturition, the activities of acetyl-CoA carboxylase and fatty acid synthase dropped in the experimental group. The activity of 3-hydroxy-acyl-CoA dehydrogenase in liver was less in experimental cows following parturition. Hepatic citrate synthase activity increased only in the control group after parturition. Unrestricted feed intake before parturition reduces de novo fatty acid synthesis as well as fatty acid oxidation after parturition. The reduction in fatty acid oxidation following parturition may contribute to postpartum accumulation of triacylglycerol in the livers of cows with unrestricted access to feed during the dry period.

High fat intake lowers hepatic fatty acid synthesis and raises fatty acid oxidation in aerobic muscle in Shetland ponies.

The metabolic effects of feeding soyabean oil instead of an isoenergetic amount of maize starch plus glucose were studied in ponies. Twelve adult Shetland ponies were given a control diet (15 g fat/kg DM) or a high-fat diet (118 g fat/kg DM) according to a parallel design. The diets were fed for 45 d. Plasma triacylglycerol (TAG) concentrations decreased by 55 % following fat supplementation. Fat feeding also reduced glycogen concentrations significantly by up to 65 % in masseter, gluteus and semitendinosus muscles (P < 0.05 and P < 0.01 and P < 0.01 respectively). The high-fat diet significantly increased the TAG content of semitendinosus muscle by 80 % (P < 0.05). Hepatic acetyl-CoA carboxylase and fatty acid synthase activities were 53 % (P < 0.01) and 56 % (P < 0.01) lower respectively in the high-fat group, but diacylglycerol acyltransferase activity was unaffected. Although carnitine palmitoyltransferase-I (CPT-I) activity in liver mitochondria was not influenced, fat supplementation did render CPT-I less sensitive to inhibition by malonyl-CoA. There was no significant effect of diet on the activity of phosphofructokinase in the different muscles. The activity of citrate synthase was raised significantly (by 25 %; P < 0.05) in the masseter muscle of fat-fed ponies, as was CPT-I activity (by 46 %; P < 0.01). We conclude that fat feeding enhances both the transport of fatty acids through the mitochondrial inner membrane and the oxidative capacity of highly-aerobic muscles. The higher oxidative ability together with the depressed rate of de novo fatty acid synthesis in liver may contribute to the dietary fat-induced decrease in plasma TAG concentrations in equines.

The AMP-activated protein kinase prevents ceramide synthesis de novo and apoptosis in astrocytes.

Fatty acids induce apoptosis in primary astrocytes by enhancing ceramide synthesis de novo. The possible role of the AMP-activated protein kinase (AMPK) in the control of apoptosis was studied in this model. Long-term stimulation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) prevented apoptosis. AICAR blunted fatty acid-mediated induction of serine palmitoyltransferase and ceramide synthesis de novo, without affecting fatty acid synthesis and oxidation. Prevention of ceramide accumulation by AICAR led to a concomitant blockade of the Raf-1/extracellular signal-regulated kinase cascade, which selectively mediates fatty acid-induced apoptosis. Data indicate that AMPK may protect cells from apoptosis induced by stress stimuli.

Consumption of olive oil has opposite effects on plasma total cholesterol and sphingomyelin concentrations in rats.

The hypothesis that olive-oil consumption alters plasma sphingomyelin concentrations and hepatic sphingomyelin metabolism was tested. Rats were fed on purified, high-cholesterol diets with either coconut fat or olive-oil (180 g/kg). In accordance with previous work, olive-oil v. coconut-fat consumption significantly elevated hepatic and total plasma cholesterol concentrations. During the course of the experiment, the concentration of plasma sphingomyelin rose in the coconut-fat group and remained constant in the olive-oil group. When compared with the coconut-fat-fed group, the plasma sphingomyelin levels were significantly lower in the olive-oil-fed group after 14 and 21 d of treatment. Dietary olive oil raised the amounts of cholesterol and sphingomyelin in the VLDL density region, and this change was associated with a reduction in the cholesterol and sphingomyelin contents of the LDL and HDL density ranges. Olive-oil consumption reduced the activity of serine palmitoyltransferase, while the activities of phosphatidylcholine:ceramide cholinephosphotransferase and phosphatidylethanolamine:ceramide ethanolaminephosphotransferase were left unchanged. Dietary olive oil also enhanced the activity of acidic sphingomyelinase, but not that of neutral sphingomyelinase. The present data indicate that dietary olive oil v. coconut fat has opposite effects on total plasma cholesterol and sphingomyelin concentrations. The lower plasma sphingomyelin levels observed in olive-oil-fed, as compared with coconut-fat-fed rats, may be explained by a simultaneous elevation and reduction in sphingomyelin catabolism and synthesis respectively, as based on the measured enzyme activities.

Lipid metabolism in equines fed a fat-rich diet.

The hypothesis tested was that dietary fat, when compared with an isoenergetic amount of non-structural carbohydrates, stimulates lipolysis in adipose tissue and also stimulates the fatty-acid oxidative capacity in skeletal muscle from horses. Six adult horses were fed a high-fat, glucose or starch containing diet according to a 3 x 3 Latin square design with feeding periods of three weeks. The diets were formulated so that the intake of soybean oil versus either glucose or corn starch were the only variables. In accordance with previous work, whole plasma triacylglycerol (TAG) concentration decreased significantly by 58% following fat supplementation. This fat effect was accompanied by a 247% increase in lipoprotein lipase (LPL) activity in post-heparin plasma. The dietary variables did neither significantly affect the basal in vitro lipolytic rate nor the lipolytic rate after adding noradrenaline. There was no significant diet effect on the activities of hexokinase and phosphofructokinase as indicators of glycolytic flux and citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase as indicators of fatty-acid oxidative capacity. The concentrations of muscle glycogen and TAG were not affected by fat supplementation. It is concluded that our hypothesis is not supported by the present results.

Do cytoskeletal components control fatty acid translocation into liver mitochondria?

For two decades it has been assumed that inhibition of carnitine palmitoyltransferase I (CPT-I) by malonyl-CoA represents the main regulatory mechanism of liver ketogenesis. However, recent evidence indicates that CPT-I activity is also controlled by interactions between mitochondria and cytoskeletal components. This newly recognized mechanism emphasizes the emerging role of the cytoskeleton in the regulation of metabolic pathways.

Interrelation of fatty acid composition in adipose tissue, serum, and liver of dairy cows during the development of fatty liver postpartum.

We investigated the composition of fatty acids in adipose tissue, serum, and liver of cows that were fed at restricted energy intake or were overfed during the dry period. Overfed cows had higher concentrations of serum nonesterified fatty acids and consequently accumulated greater amounts of triacylglycerols in the liver than did cows that were fed at restricted energy intake. The percentages of the different fatty acids present in adipose tissue were similar for both groups and did not change during sampling intervals. Before parturition, concentrations of the individual fatty acids present in serum were similar between groups. After parturition, concentrations of major fatty acids in serum, including palmitic, stearic, oleic, and linoleic acids significantly increased in both groups and were higher in overfed cows than in cows that were fed at restricted energy intake. The shift of concentrations of the different fatty acids present in the liver--as a result of increased lipolysis-was observed in palmitic, oleic, and linoleic acids but not stearic acid, suggesting that stearic acid is used by the liver (i.e., oxidation) or is considerably secreted through the milk, thereby not increasing in accumulation in the liver. In conclusion, different feeding regimens during the dry period do not influence the composition of fatty acids in adipose tissue. More intensive lipolysis results in increased concentrations of palmitic, stearic, oleic, and linoleic acids in the blood; subsequently, these fatty acids, excluding stearic acid, greatly accumulated in the liver.

Consumption of casein instead of soybean protein produces a transient rise in the concentration of sphingomyelin in VLDL in rats.

In rats fed cholesterol-rich diets, dietary casein vs. soybean protein raises VLDL cholesterol concentrations. Because sphingomyelin may be an essential, structural component of VLDL, we tested whether casein feeding would raise VLDL-sphingomyelin. Rats were fed cholesterol-rich semipurified diets containing either soybean protein (35 g/100 g) or casein for up to 21 d. Consistent with previous work, casein consumption increased hepatic and VLDL cholesterol concentrations. Dietary casein also significantly raised the amount of sphingomyelin in the VLDL fraction, but this effect was transient. Casein feeding transiently lowered LDL- and HDL-2-sphingomyelin concentrations. We suggest that an increase in hepatic VLDL secretion after casein consumption imposed an increased demand for sphingomyelin in the liver. The activity of key enzymes of sphingomyelin synthesis, i.e., serine palmitoyltransferase, phosphatidylcholine:ceramide phosphocholinetransferase and phosphatidylethanolamine:ceramide phosphoethanolaminetransferase and sphingomyelin degradation, i.e., acid sphingomyelinase, were enhanced and depressed, respectively, by casein consumption. Again these effects were transient. Thus, these data indicate that the extra sphingomyelin needed after short-term casein feeding came about through enhanced rates of biosynthesis and reduced rates of degradation in the liver. In addition, plasma transfer of sphingomyelin from HDL-2 to VLDL might have contributed to the increase in VLDL sphingomyelin in the casein-fed rats. This study shows that dietary casein vs. soybean protein transiently influences sphingomyelin metabolism in rats.

Cloning and expression of CTP:phosphoethanolamine cytidylyltransferase cDNA from rat liver.

CTP:phosphoethanolamine cytidylyltransferase (ET) is a key regulatory enzyme in the CDP-ethanolamine pathway for phosphatidylethanolamine synthesis. As a first step in the elucidation of the structure-function relationship and the regulation of ET, an ET cDNA was cloned from rat liver. The cloned cDNA encodes a protein of 404 amino acid residues with a calculated molecular mass of 45.2 kDa. The deduced amino acid sequence is very similar to that of human ET (89% identity). Furthermore, it shows less, but significant, similarity to yeast ET as well as to other cytidylyltransferases, including rat CTP:phosphocholine cytidylyltransferase and Bacillus subtilis glycerol-3-phosphate cytidylyltransferase. Like human and yeast ET, rat ET has a large repetitive internal sequence in the N- and C-terminal halves of the protein. Both parts of the repeat contain the HXGH motif, the most conserved region in the N-terminal active domain of other cytidylyltransferases, indicating the existence of two catalytic domains in ET. The hydropathy profile revealed that rat ET is largely hydrophilic and lacks a hydrophobic stretch long enough to span a bilayer membrane. There was no prediction for an amphipathic alpha-helix. Transfection of COS cells with the cDNA clone resulted in an 11-fold increase in ET activity, corresponding to an increase in the amount of ET protein as detected on a Western blot. Determination of the ET activity during liver development showed a 2. 5-fold increase between day 17 of gestation and birth (day 22) and the amount of ET protein changed accordingly. Northern blot analysis showed that this was accompanied by an increase in the amount of ET mRNA. Between day 17 of gestation and birth, the amount of mRNA in fetal rat liver increased approx. 6-fold, suggesting the regulation of ET at both pretranslational and post-translational levels during rat liver development.

Metabolism of trans fatty acids by hepatocytes.

The present work was undertaken to study the metabolism of fatty acids with trans double bonds by rat hepatocytes. In liver mitochondria, elaidoyl-CoA was a poorer substrate for carnitine palmitoyltransferase I (CPT-I) than oleoyl-CoA. Likewise, incubation of hepatocytes with oleic acid produced a more pronounced stimulation of CPT-I than incubation with trans fatty acids. This was not due to a differential effect of cis and trans fatty acids on acetyl-CoA carboxylase (ACC) activity and malonyl-CoA levels. Elaidic acid was metabolized by hepatocytes at a higher rate than oleic acid. Surprisingly, compared to oleic acid, elaidic acid was a better substrate for mitochondrial and, especially, peroxisomal oxidation, but a poorer substrate for cellular and very low density lipoprotein triacylglycerol synthesis. Results thus show that trans fatty acids are preferentially oxidized by hepatic peroxisomes, and that the ACC/malonyl-CoA/CPT-I system for coordinate control of fatty acid metabolism is not responsible for the distinct hepatic utilization of cis and trans fatty acids.

Inhibition of phosphatidylcholine and phosphatidylethanolamine biosynthesis in rat-2 fibroblasts by cell-permeable ceramides.

Phospholipids and sphingolipids are important precursors of lipid-derived second messengers such as diacylglycerol and ceramide, which participate in several signal transduction pathways and in that way mediate the effects of various agonists. The cross-talk between glycerophospholipid and sphingolipid metabolism was investigated by examining the effects of cell-permeable ceramides on phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) synthesis in Rat-2 fibroblasts. Addition of short-chain C6-ceramide to the cells resulted in a dose- and time-dependent inhibition of the CDP-pathways for PtdCho and PtdEtn synthesis. Treatment of cells for 4 h with 50 microM C6-ceramide caused an 83% and a 56% decrease in incorporation of radiolabelled choline and ethanolamine into PtdCho and PtdEtn, respectively. Exposure of the cells for longer time-periods (>/= 16 h) to 50 microM C6-ceramide resulted in apoptosis. The structural analogue dihydro-C6-ceramide did not affect PtdCho and PtdEtn synthesis. In pulse-chase experiments, radioactive choline and ethanolamine accumulated in CDP-choline and CDP-ethanolamine under the influence of C6-ceramide, suggesting that synthesis of both PtdCho and PtdEtn were inhibited at the final step in the CDP-pathways. Indeed, cholinephosphotransferase and ethanolaminephosphotransferase activities in membrane fractions from C6-ceramide-treated cells were reduced by 64% and 43%, respectively, when compared with control cells. No changes in diacylglycerol mass levels or synthesis of diacylglycerol from radiolabelled palmitate were observed. It was concluded that C6-ceramide affected glycerophospholipid synthesis predominantly by inhibition of the step in the CDP-pathways catalysed by cholinephosphotransferase and ethanolaminephosphotransferase.

Effect of overfeeding during the dry period on the rate of esterification in adipose tissue of dairy cows during the periparturient period.

The in vitro rate of esterification of fatty acids in adipose tissue was compared between cows that were fed at restricted energy intake and cows that were overfed during the dry period. Subcutaneous adipose tissue was biopsied at -1, 0.5, 1, and 3 wk from parturition. The basal in vitro rate of esterification was quantified, as well as the rate of esterification after the addition of glucose or glucose plus insulin. The basal rate in adipose tissue from overfed cows at -1 wk was higher than in adipose tissue from cows that were fed at restricted energy intake and indicated enhanced storage of triacylglycerols in adipose tissue of overfed cows at that time. The rate of esterification after the addition of glucose or glucose plus insulin was increased in both groups at each sampling time, but the mean rates, expressed as a percentage of the basal rates, were lower for overfed cows than for cows that were fed at restricted energy intake at 0.5 and 1 wk. Although the addition of glucose or glucose plus insulin increased esterification rates in adipose tissue from both groups of cows, adipose tissue from overfed cows was less sensitive to the addition of these compounds. In conclusion, overfeeding during the dry period predisposed cows to accumulate fat in adipose tissue during the prepartum period. The smaller increase in esterification rate after the addition of glucose or glucose plus insulin in adipose tissue of overfed cows indicates a lower ability of the adipose tissue to esterify circulating fatty acids or to reesterify mobilized fatty acids, which, combined with higher rates of lipolysis postpartum, contributes to continuously elevated concentrations of circulating nonesterified fatty acids postpartum, leading to a more severe hepatic lipidosis in overfed cows.

Effect of fatty liver on hepatic gluconeogenesis in periparturient dairy cows.

The purpose of this study was to compare the hepatic enzyme activities of gluconeogenesis between control cows and experimental cows that had been overfed during the dry period to induce fatty liver postpartum. Blood and liver samples were collected 1 wk before and 0.5, 1, 2, and 3 wk after parturition. Before parturition, neither the serum nonesterified fatty acid nor the liver triacylglycerol concentration differed between the two groups. After parturition, these variables were higher in experimental cows than in control cows. Liver glycogen was higher at 1 wk before parturition in experimental cows; sharply decreased after parturition in both groups; and, at 1 wk after parturition, was lower in experimental cows than in control cows. In the liver, activities of phosphoenolpyruvate carboxykinase were significantly lower at 1 wk before and at 0.5 and 2 wk after parturition in experimental cows; in addition, the activities tended to be lower at 1 wk after parturition. Activities of fructose 1,6-bisphosphatase tended to be lower, but activities of glucose 6-phosphatase tended to be higher, at 0.5 wk after parturition in experimental cows than in control cows. Our results suggest that, in fatty infiltrated liver, the rate of gluconeogenesis is not optimal, which results in prolongation of lipolysis, particularly during the first weeks after parturition.

Dietary pectin lowers sphingomyelin concentration in VLDL and raises hepatic sphingomyelinase activity in rats.

There is evidence that cholesterol and sphingomyelin metabolism are interrelated, and thus the hypothesis tested was that dietary pectin, because it can alter hepatic cholesterol metabolism, would also alter hepatic sphingomyelin metabolism. For that purpose, 4-wk-old female Wistar rats were fed a diet without or with pectin (20 g/100 g) up to 21 d. In accordance with previous work, pectin consumption caused a significant (P < 0.001) reduction in hepatic (65%), whole plasma (37%), and VLDL (80%) cholesterol levels. Pectin also significantly reduced VLDL sphingomyelin concentrations (57%), but raised the amount of sphingomyelin in the high density lipoproteins (HDL)-2 fractions (58%), so that the level of sphingomyelin in whole plasma remained unaffected. Pectin did not affect the sphingomyelin concentration in the liver. Pectin consumption did not affect the hepatic sphingomyelin synthesizing enzymes, serine palmitoyltransferase, phosphatidylcholine:ceramide phosphocholine transferase, or phosphatidylethanolamine:ceramide phosphoethanolamine transferase. In contrast, dietary pectin activated both lysosomal (28%) and plasma membrane (26%) sphingomyelinase and thus may have enhanced sphingomyelin degradation. An attempt was made to describe the effects of dietary pectin on sphingomyelin metabolism in terms of altered fluxes through liver and plasma, with whole liver and whole plasma concentrations of sphingomyelin remaining unaffected.