Differential changes to splanchnic and peripheral protein metabolism during the diet-induced development of metabolic syndrome in rats.

Little is known about the effects of the development of metabolic syndrome (MS) on protein and amino acid (AA) metabolism. During this study, we took advantage of the variability in interindividual susceptibility to high fat diet-induced MS to study the relationships between MS, protein synthesis, and AA catabolism in multiple tissues in rats. After 4 mo of high-fat feeding, an MS score (ZMS) was calculated as the average of the z-scores for individual MS components [weight, adiposities, homeostasis model for the assessment of insulin resistance (HOMA-IR), and triglycerides]. In the small intestine, liver, plasma, kidneys, heart, and muscles, tissue protein synthesis was measured by 2H2O labeling, and we evaluated the proportion of tissue AA catabolism (relative to protein synthesis) and nutrient routing to nonindispensable AAs in tissue proteins using natural nitrogen and carbon isotopic distances between tissue proteins and nutrients (Δ15N and Δ13C), respectively. In the liver, protein mass and synthesis increased, whereas the proportion of AA catabolism decreased with ZMS. By contrast, in muscles, we found no association between ZMS and protein mass, protein synthesis (except for a weak positive association in the gastrocnemius muscle only), and proportion of AA catabolism. The development of MS was also associated with altered metabolic flexibility and fatty acid oxidation, as shown by less routing of dietary lipids to nonindispensable AA synthesis in liver and muscle. In conclusion, MS development is associated with a greater gain of both fat and protein masses, with higher protein anabolism that mainly occurs in the liver, whereas muscles probably develop anabolic resistance due to insulin resistance.

Characterization of dietary-induced hypercholesterolemia in the chicken.

The effect of 2% dietary cholesterol on the distribution of cholesterol among the plasma lipoproteins was studied in 2-week old male chickens. Very-low-, intermediate-, low- and high-density lipoproteins (VLDL, IDL, LDL and HDL) were separated from plasma by density gradient ultracentrifugation in order to determine their concentration and chemical composition. VLDL were furthermore characterized as concerned their size, mobility and protein content. The lipoprotein profile was quantitatively and qualitatively normal in the control group (n = 6) fed the diet without cholesterol, HDL representing the major lipoprotein class (5.06 +/- 0.36 g/l) and the main carrier of cholesterol. Birds fed the cholesterol containing diets for 5 weeks (n = 6) exhibited a dramatic hypercholesterolemia (1.60 +/- 0.89 g/l free cholesterol and 6.70 +/- 3.22 g/l cholesteryl esters) and a shift in their lipoprotein pattern, with an accumulation of beta-VLDL (6.08 +/- 4.21 g/l) and a marked decrease in HDL level (3.53 +/- 0.91 g/l). The decrease or absence of LDL was balanced by a considerable amount of beta-VLDL remnants (namely IDL), so that the concentration of IDL + LDL considered as a whole was not modified significantly (2.10 +/- 0.95 g/l compared to 1.66 +/- 1.13 g/l in controls). Chicken beta-VLDL, smaller in size (31.0 nm) than control VLDL (33.5 nm), were typically enriched in cholesterol (67%) but they lacked apoE. About 60% of plasma cholesterol was associated with beta-VLDL which therefore represented the main atherogenic lipoprotein class and were probably responsible for the greater amount of cholesterol found in the aorta in these chickens (2.44 +/- 0.99 mg/g aorta vs. 1.32 +/- 0.57 in controls). Since LDL were very reduced or absent, the cholesterol-fed chicken provides a suitable model in which to study the role of beta-VLDL in atherogenesis.

A density gradient study of the lipoprotein and apolipoprotein distribution in the chicken, Gallus domesticus.

Plasma lipoproteins from 5-week old male chickens were separated over the density range 1.006-1.172 g/ml into 22 subfractions by isopycnic density gradient ultracentrifugation, in order to establish the distribution of these particles and their constituent apolipoproteins as a function of density. Lipoprotein subfractions were characterized by electrophorectic, chemical and morphological analyses, and their protein moieties were defined according to net charge at alkaline pH, molecular weight and isoelectric point. These analyses have permitted us to reevaluate the density limits of the major chicken lipoprotein classes and to determine their main characteristics, which are as follows: (1) very-low-density lipoproteins (VLDL), isolated at d less than 1.016 g/ml, were present at low concentrations (less than 0.1 mg/ml) in fasted birds; their mean diameter determined by gradient gel electrophoresis and by electron microscopy was 20.5 and 31.4 nm respectively; (2) as the the density increased from VLDL to intermediate density lipoproteins (IDL), d 1.016-l.020 g/ml) and low-density lipoproteins (LDL, d 1.020-1.046 g/ml), the lipoprotein particles contained progressively less triacylglycerol and more protein, and their Stokes diameter decreased to 20.0 nm; (3) apolipoprotein B-100 was the major apolipoprotein in lipoproteins of d less than 1.046 g/ml, with an Mr of 350000; small amounts of apolipoprotein B-100 were detectable in HDL subfractions of d less than 1.076 g/ml; urea-soluble apolipoproteins were present in this density range as minor components of Mr 38000-39000, 27000-28000 (corresponding to apolipoprotein A-1) and Mr 11000-12000; (4) high density lipoprotein (HDL, d 1.052-1.130 g/ml) was isolated as a single band, whose protein content increased progressively with increase in density; the chemical composition of HDL resembled that of human HDL2, with apolipoprotein A-1 (M 27000-28000) as the major protein component, and a protein of Mr 11000-12000 as a minor component; (5) heterogeneity was observed in the particle size and apolipoprotein distribution of HDL subfractions: two lipoprotein bands which additional apolipoproteins of Mr 13000 and 15000 were detected. These studies illustrate the inadequacy in the chicken of the density limits applied to fractionate the lipoprotein spectrum, and particularly the inappropriateness of the 1.063 g/ml density limit as the cutoff for LDL and HDL particle populations in the species.

Effect of pravastatin, a HMG CoA reductase inhibitor, on blood lipids and aortic lipidosis in cholesterol-fed White Carneau pigeons.

The effect of pravastatin, an inhibitor of HMG CoA reductase, on blood lipids and aortic lipidosis was studied in young cholesterol-fed White Carneau pigeons. The birds were fed with normal ('N group', n = 20) or atherogenic diet (grains + 0.4% cholesterol + 4% lard) alone ('C group', n = 20) and in association with pravastatin ('P group', n = 20). Plasma lipids and aortic intima lipidosis were studied after 3-5 and 8-12 months of the diet. Compared to the N group, pigeons from C group exhibited hypercholesterolemia (TC = 1000 mg/dl) and hyperlipoproteinemia of which level was independent of the duration of the diet. Total VLDL (VLDL+LDL)-cholesterol and apolipoprotein-B levels rose significantly 15, 8 and 4 times, respectively, whereas HDL were increased two times (P < 0.01) in females only. Macroscopically visible intima lipidosis areas covered 40% and 80% of aortic surface after 3-5 and 8-12 months of the diet. In P group, the increase in plasma lipid values was significantly lower than in WC from C group: -40% for total cholesterol (600 mg/dl) (P < 0.01), -71% for VLDL (P < 0.001), -53% for (VLDL+LDL)-cholesterol (P < 0.01) and -54% for apo-B (P < 0.05). HDL remained as high as in C group. Consequently TC/HDL-C ratio was improved and atherogenic risk of cholesterol was reduced by 41% (P < 0.05). Intima lipidosis areas were lowered by 35% (P < 0.01). We conclude that pravastatin treatment involves (1) a decrease in hypercholesterolemia and hyperlipoproteinemia and (2) a lowering in extensiveness and severity of macroscopically visible aortic lipidosis in cholesterol-fed White Carneau pigeon.

Influence of orotic acid and estrogen on hepatic lipid storage and secretion in the goose susceptible to liver steatosis.

Fatty liver in the goose results from an increased hepatic lipogenesis in response to overfeeding, together with a deficient secretion of triacylglycerol as very-low-density lipoproteins (VLDL). Orotic acid and estrogen, which both modify lipid metabolism in the liver, were used in male geese as tools to understand the alterations of liver lipids and plasma lipoproteins during the induction of liver steatosis. Liver lipids were analyzed after solvent extraction and plasma lipoproteins after separation by density gradient ultracentrifugation. Contrary to what is known in the rat, orotic acid (1% in food for 2 weeks) failed to induce liver steatosis. In force-fed geese, liver weight increased from approximately 100 g to approximately 800 g in 2 weeks, as a consequence of a specific accumulation of triacylglycerol. In both groups, VLDL contained less triacylglycerol (35%) than normal. Such an uncoupling of triacylglycerol synthesis and secretion, of which the precise reason is still unknown, may facilitate their accumulation when force-feeding increases hepatic lipogenesis. As with force-feeding, triacylglycerol synthesis was enhanced by estrogen, but their secretion as VLDL was very efficient and prevented liver steatosis almost completely. Since HDL concentrations were considerably decreased by estrogen, VLDL were the main lipoprotein species, with 48 g/l and 62% triacylglycerol. Where estrogen-treated geese were force-fed concomitantly, VLDL concentration was even higher (62 g/l), but triacylglycerol secretion could not prevent liver steatosis (liver weight 640 g). The data are discussed in relation to in vitro studies showing that channelling of triacylglycerol towards secretion as VLDL or hepatic storage depends on their residence time in the different intracellular compartments.

Effects of the lipase inhibitors, Triton WR-1339 and tetrahydrolipstatin, on the synthesis and secretion of lipids by rat hepatocytes.

The lipase inhibitors, Triton WR-1339 and tetrahydrolipstatin, were incubated with rat hepatocytes. Triton WR-1339 increased the recovery of triacylglycerol in the hepatocytes and incubation medium by 31% and 38%, respectively. Tetrahydrolipstatin decreased the accumulation of newly synthesized, and of total triacylglycerol in the medium. This compound might be useful in determining mechanisms involved in intracellular triacylglycerol metabolism and the secretion of very low density lipoproteins.

Comparative study of hepatic VLDL secretion in vivo in the growing turkey (Meleagris gallopavo) and chicken (Gallus domesticus).

Hepatic secretion of VLDL was compared in young turkeys and chickens (8 and 4 weeks of age, respectively) and older birds (11 and 8 weeks of age, respectively) reared together under the same nutritional conditions. VLDL, VLDL-TG and total TG secretion rates were higher in chickens than in turkeys. The cholesteryl ester content of turkey VLDL was higher than that of chicken. Differences in the fatty acid composition of the VLDL lipids were observed between the species: the proportion of linoleic acid was greater in turkeys, whereas monounsaturated fatty acids were more abundant in chickens. These results are consistent with the hypothesis of a positive relationship between hepatic lipogenesis, delta-9-desaturation, VLDL secretion and fattening in turkeys and chickens.

Influence of a high ambient temperature on stearoyl-CoA-desaturase activity in the growing pig.

An experiment was conducted to determine the influence of a high ambient temperature on the stearoyl-CoA-desaturase activity and fatty acid composition of backfat, leaf fat, Longissimus dorsi muscle and liver, in the growing pig. Eighteen Large White X Landrace castrated pigs (20 kg body weight) were divided into three groups: I (31 degrees C, ad libitum), II (20 degrees C, pair-fed on the 31 degrees C group) and III (20 degrees C, ad libitum) until 35 kg body weight. At 20 degrees C, the level of feed intake had no effect on stearoyl-CoA-desaturase activity, whatever the tissue (groups II and III). At similar levels of feeding, (groups I and II), the stearoyl-CoA-desaturase activity was lower at 31 degrees C (P < 0.001) than at 20 degrees C, regardless of the tissue, with the exception of the hepatic stearoyl-CoA-desaturase activity, which was similar in all three groups. This reduction of the stearoyl-CoA-desaturase activity at 31 degrees C could be related to a decrease in the monounsaturated fatty acid percentage in all the tissues, in hot conditions. The present results show that changes in fatty acid composition caused by environmental temperature, in the pig, may be attributed at least in part to an alteration in the stearoyl-CoA-desaturase activity.

Role of hepatic lipogenesis in the susceptibility to fatty liver in the goose (Anser anser).

In response to overfeeding, the Landes goose develops a fatty liver that is twice as large as that of the Poland goose, despite similar food intake. The role of hepatic lipogenesis in the genetic susceptibility to fatty liver was assessed in male overfed geese of the two breeds. For a similar hepatic protein content, total activities of malic enzyme, glucose-6-phosphate dehydrogenase, acetyl-Coa-carboxylase and fatty acid synthase, and specific activity and mRNA level of malic enzyme were about two-fold higher in the Landes goose. In the Poland goose, the weight of the fatty liver was correlated positively with the specific activity of ME and the VLDL concentration, which was not the case in the Landes breed. These results show that: (1) hepatic lipogenesis remains very active until the end of the overfeeding period; (2) the pentose-phosphate pathway may function in birds, contrary to what is assumed usually; (3) the level of hepatic lipogenesis is a major factor in the susceptibility to hepatic steatosis in different breeds of geese; and (4) ME activity may be a limiting factor of lipid synthesis in the less susceptible Poland breed.

Plasma lipoprotein distribution in the turkey (Meleagris gallopavo).

The plasma lipoprotein profile has been determined in fasted 7-week-old male turkeys. Lipoprotein classes were subfractionated by density gradient ultracentrifugation. According to phospholipid concentration over the density gradient, an initial peak was visible in the usual LDL density range, whereas two peaks were detected in that of HDL. As density increased, the lipid composition of particles showed an increase in cholesteryl esters and decrease in triglycerides. VLDL were recovered in the first fraction (d<1.013) on the top of the gradient and IDL in fractions 2-5 (d=1.013-1.028 g/ml). The LDL and HDL populations in the density range 1.028-1.090 (fractions 6-12) differ from that found in the other bird species analyzed under the same experimental conditions. LDL predominated in fractions 6-8 with mostly beta-motility and apoB100 as the major protein component. HDL predominated in fractions 10-12 (d=1.055-1.090 g/ml) and corresponded to the first HDL peak (HDL-(A)), with mostly alpha-mobility and apoA-I as the major protein component. Both LDL- and HDL-like particle populations were present in fractions 6-12, making the separation between the two classes of lipoproteins difficult. The second peak in the HDL density range (HDL-(B), d=1.076-1.146 g/ml) contained only HDL-type particles above d=1.090 g/ml. This points out the specificity of the lipoprotein distribution in the turkey that is unique among animals. The density limit at d=1.048 g/ml is a good compromise for the separation of LDL from HDL; however, the presence of HDL-like particles in the LDL density range, and the existence of two, and even three HDL subclasses should be taken into account in the design of further metabolic studies.

Plasma lipoproteins and liver lipids in two breeds of geese with different susceptibility to hepatic steatosis: changes induced by development and force-feeding.

Susceptibility to fatty liver in the force-fed goose is partly under genetic control. However, the mechanisms leading to liver steatosis in this avian model are poorly understood, but may involve perturbation in hepatic lipoprotein synthesis. Plasma lipoproteins were fractionated by density gradient ultracentrifugation from plasma of geese differing in their susceptibility to liver steatosis (Landes breed, highly susceptible; Rhine breed, partly resistant). The concentrations and chemical compositions of the major lipoprotein classes (VLDL, IDL, LDL and HDL) were characterized at 8, 22 and 27 wk of age and compared to the lipid composition of the corresponding liver. In non-force-fed geese, the lipoprotein profile was typical of birds, with high-density lipoprotein (HDL) predominating (4-5 g/L). However, at 22 and 27 wk of age, very low-density lipoprotein (VLDL) levels were significantly lower in Landes geese suggesting that this breed may possess a lower ability to export liver lipids, which would explain its susceptibility to liver steatosis when overfed. The livers of force-fed geese were specifically enriched in triglyceride, and to a lesser extent, in cholesteryl esters and non-esterified fatty acids as compared to those of control geese of the same age (27 wk). This accumulation of lipids was more pronounced in the Landes breed and was responsible for the higher liver weight in that breed. In both breeds, liver steatosis was accompanied by an increase in plasma levels of HDL (11 g/L), whereas low-density lipoproteins were essentially absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in lipid content of fowl spermatozoa after liquid storage at 2 to 5 degrees C.

Quantitative and qualitative changes may occur in the lipids of spermatozoa during in vitro storage of gametes and may indicate possible degradations occurring within the cells under these conditions. The aim of the present study was to investigate such changes. The motility, viability, morphological integrity and lipid content were measured in fowl semen stored for 48 h at 2 to 5 degrees C and diluted 1:1 in Beltsville Poultry Semen Extender (BPSE) under aerobic agitation. The total lipid content of spermatozoa decreased (P < 0.05) from 820 to 620 micrograms/10(9) cells over 48 h. There was no significant evolution in the total lipid content of seminal plasma (1000 to 850 micrograms/10(9) cells). The proportion of phospholipids in spermatozoa decreased from 75 to 60% of the total lipids. Among the phospholipids, the proportions of phosphatidylcholine, phosphatidylethanolamine and sphingomyelin decreased (P < 0.05) from 58, 13 and 10% at 0 h to 42, 10 and 9% at 48 h, respectively. In contrast, lysophosphatidylcholine, which was marginally represented at 0 h (2%), increased considerably (24%) at 48 h. During the same period, the proportion of motile spermatozoa decreased from 87.5 to 46% and the proportion of viable and morphologically normal cells decreased from 84 to 48%. These results indicate the occurrence of lipid lysis, peroxidation and/or endogenous metabolism able to modify the structure of the spermatozoal membranes and to alter their metabolism and fusion abilities.

Reproductive period affects lipid composition and quality of fresh and stored spermatozoa in Turkeys.

Semen of Turkeys between 31 and 52 weeks of age was analyzed to investigate the cause of reduction in Turkey fertility at the end of the reproductive period. Sperm motility and viability, lipid concentration, fatty acid composition and lipid peroxides were evaluated on fresh spermatozoa or spermatozoa stored for 48h at 4 degrees C. Fertility of fresh semen was also evaluated. Fertility obtained with fresh semen decreased at 44-47 weeks of age. Ageing was also accompanied by a decrease in sperm viability (at 47 weeks) and later by a decrease in motility of spermatozoa (at 52 weeks). Polyunsaturated fatty acids (PUFAs) were the first lipids of fresh spermatozoa affected by age, especially n-3 and n-9 PUFAs. Changes in these PUFAs were followed by a 30% increase in lipid peroxidation at 47 and 52 weeks of age and a reduction in phospholipid content at 52 weeks. In vitro storage did not cause lipid peroxidation in sperm obtained during the first half of the reproductive period but malondialdehyde (MDA) levels significantly increased in sperm obtained during the second half of this period. In vitro storage also decreased phospholipid content of spermatozoa from 41 weeks of age, and viability and motility regardless of age. In conclusion, lipid alteration mainly originating from PUFAs peroxidation could partly explain the decrease in semen quality and fertility observed with ageing. In addition, lipid peroxidation was increased during in vitro storage of spermatozoa from older Turkeys.

Impact of changes in composition of storage medium on lipid content and quality of turkey spermatozoa.

Turkey semen quality is damaged by long term in vitro storage. The objective of the present study was to determine whether changes in energy substrates and antioxidants of semen extender could limit loss of quality and lipid content of turkey spermatozoa during storage. Spermatozoa were incubated in extenders based on Beltsville Poultry Semen Extender (BPSE) to which different energy substrates (acetate, pyruvate and hydroxybutyric acid) or antioxidant (Vitamin E) had been added. Semen was stored at 4 degrees C for 48 h and changes in quality, phospholipid and malondialdehyde (MDA) content of semen were evaluated. Among the different substrates studied, only acetate was able to limit the loss of motility and ATP content after 48 h in vitro storage. Losses of spermatozoal phospholipids were similar when gametes were incubated in an extender without any substrate or in normal BPSE (784-675nmol/10(9) spz versus 837-703 nmol/10(9) spz). However, motility and ATP content were significantly more affected after 48 h of storage in samples incubated without substrates than in BPSE (motility, 2.2 versus 0; ATP, 10 nmol/10(9) spz versus 3 nmol/10(9) spz). The addition of Vitamin E to the extender did not modify either the MDA or phospholipid content of fresh or stored spermatozoa, but increased the motility of stored semen. In conclusion, acetate is an essential substrate for in vitro storage. Spermatozoal phospholipids decreased during storage, but this did not seem to originate from metabolism of endogenous fatty acids. The positive effects of Vitamin E on semen storage did not originate from preservation of lipid oxidation.

Influence of a high ambient temperature on lipid metabolism in the growing pig.

Because pigs are fatter when they are heat-stressed, it was hypothesized that lipid metabolism is enhanced in heat-stressed pigs. To test this hypothesis, an experiment was conducted to determine the influence of a high ambient temperature on the level of plasma lipids, thyroid hormones, lipoprotein lipase activity, and on the composition of very low density lipoproteins (VLDL) and chylomicrons in the growing pig. Twelve Large White x Landrace castrated male pigs with an initial weight of 20 +/- 0.6 kg were allotted to one of the following treatments: 1) ambient temperature of 31 degrees C, with ad libitum access to feed or 2) ambient temperature of 20 degrees C and fed the amount consumed by those kept at 31 degrees C until 35 kg BW. Ambient temperature did not affect piglet performance. Compared to that in pigs kept at 20 degrees C, in pigs kept at 31 degrees C the lipid content of backfat was 26% higher and the proportion of flare fat was increased by more than twofold (P < 0.001). Lipoprotein lipase activity was increased more than twofold in backfat and nearly twofold in leaf fat at 31 vs 20 degrees C (P < 0.001). In warmth-exposed (31 degrees C), feed-restricted pigs, the plasma level of triiodothyronine was 30% lower than at 20 degrees C (P < 0.001), whereas VLDL-lipid concentration was more than fourfold higher, and plasma concentrations of NEFA and triglycerides were 2.6- and 3.6-fold higher, respectively (P < 0.001). In conclusion, the chronic exposure of growing pigs to a high ambient temperature enhances lipid metabolism in both the liver (VLDL production) and the adipose tissue (lipoprotein lipase activity). Consequently, plasma triglyceride uptake and storage are facilitated in the adipose tissue, which results in greater fatness.

Alterations in follicular function associated with selection on ovulation rate in Finn ewes.

Finn ewes have been selected on ovulation rate to produce three lines with approximate ovulation rates of 5 (High), 3 (Control), and 2.5 (Low). The associated alterations in follicular function were investigated in three experiments. The function of large estrogenic follicles (Exp. 1) was assessed by measuring in vitro output of steroids and inhibin after a 1-h culture period. Follicles from High line ewes contained fewer (P < .01) granulosa cells than follicles from Low line ewes. Estradiol output per granulosa cell and testosterone output per thecal cell were greater for High than for Low line follicles (P < .01 and < .05, respectively). In contrast, inhibin output, expressed per follicle or per granulosa cell, did not differ between lines. In Exp. 2, cell proliferation in small follicles from the three lines was assessed after incubation of follicles in the presence of [3H]thymidine and in the presence or absence of FSH. The slope of the linear regression relating labeling index of the granulosa cells and follicle size differed significantly between High and Low lines with a significant negative coefficient for High line and a nonsignificant positive slope in the Low line. In Exp. 3, follicular fluid and serum proteins were compared between High and Low lines with 2D PAGE. A line difference was detected for a serum protein (40 kDa, pI = 6). High line had one spot, whereas Low line had three spots on 2D PAGE. This protein was not apolipoprotein E. Furthermore, the pattern of lipoproteins (high-density and low-density lipoproteins) in serum was similar between High and Low line sheep. The results indicate that selection for High ovulation rate was associated with smaller follicles that contained fewer granulosa cells per thecal cell. Aspects of function of estrogenic follicles (estradiol but not inhibin production) were also changed by selection.

Relationships between storage and secretion of hepatic lipids in two breeds of geese with different susceptibility to liver steatosis.

Susceptibility to liver steatosis was studied in Landes and Poland geese, which are hyper- and hyporesponsive, respectively, to overfeeding. Plasma lipoproteins were characterized at different stages of the overfeeding process, whereas fatty liver composition was determined after completion of overfeeding and slaughtering. Before overfeeding, plasma lipoprotein profile was typical of birds in both breeds, except that very low density lipoproteins (VLDL) were low in triglyceride (approximately 30%). Moreover, high-density lipoprotein (HDL) concentration was higher in the Poland geese (6.44 vs 4.97 g/L). During overfeeding, hepatic lipogenesis was increased, and fatty liver resulted from accumulation of primarily triglyceride (approximately 95% of lipid content), but also of all other lipids. This accumulation was significantly greater in the Landes geese for all lipids but phospholipid. Thus, the liver weight was 100% higher in this breed (1,005 g vs 485 g), whereas lipid release during sterilization was twofold higher (26.3 vs 7.5%). Parallel, plasma concentration and triglyceride content of hepatic lipoproteins, VLDL and HDL, increased about one- to twofold, this effect being greater in the Poland geese. Therefore, channeling of triglyceride towards secretion rather than in situ storage may be responsible for the hyporesponsiveness of this breed to overfeeding. In both breeds, and especially in the Landes geese, a relative deficiency in phospholipid synthesis together with an enhanced secretion may be limiting factors of hepatocyte hypertrophia and, therefore, of steatosis.

Activity of phospholipases A and lysophospholipase in turkey semen and oviducal fluid.

Changes in lipid composition of turkey semen have previously been reported to occur during in vitro storage and may be mediated by endogenous hydrolysis of phospholipids. To investigate the presence of phospholipases able to initiate such degradation, phospholipaseA2 (PLA2), phospholipase A1 (PLA1), and lysophospholipase (LPLase) activities were measured in turkey spermatozoa and seminal plasma. These enzymes were also measured in the oviductal fluid because they may be involved in the process prior to fertilization in the female. In spermatozoa and seminal plasma, the major PLA2 was a calcium-dependent and sodium deoxycholate (DOC) stimulated enzyme. However, calcium-independent PLA2 activities were also detected with different characteristics in spermatozoa (DOC inhibited enzyme) and seminal plasma (DOC stimulated enzyme). Additionally, PLA1 activity and high LPLase activity were present in spermatozoa and seminal plasma. In vitro storage of semen for 48 h did not affect PLA2 and LPLase activities. By contrast, PLA1 was the major phospholipase activity detected in oviductal fluid. A PLA2 activity stimulated by calcium or DOC and LPLase activity were also detected, but both were low relative to PLA1. These results showed that turkey semen had several enzymatic activities able to hydrolyze phospholipids. In addition, the phospholipase activities described here in the oviductal fluid could be involved in membrane destabilization prior to fertilization.

Differential channelling of liver lipids in relation to susceptibility to hepatic steatosis in the goose.

In response to overfeeding for the production of "foie gras," the Poland goose differs from the Landes goose by a lesser susceptibility to hepatic steatosis, resulting in a lower accumulation of hepatic triacylglycerol (TG), together with a greater exportation of hepatic phospholipid (PL) in very low density lipoproteins (VLDL) and high density lipoproteins (HDL) (Fournier et al., 1997). A study was designed 1) to compare the liver composition in overfed and nonoverfed geese of the two breeds of geese and 2) to determine whether the differential channelling of lipids in response to overfeeding is reflected in the PL and fatty acid profiles of the different hepatic lipids, whether stored or secreted. In nonoverfed geese, there were no breed-related differences in liver weight (approximately 90 to 100 g), hepatic lipid content (3 to 4%), and lipid and PL composition. However, plasma VLDL and HDL of the Landes breed contained a higher phosphatidylcholine (PC) to phosphatidylethanolamine (PE) ratio than those of the Poland breed (20.7 and 33.8 vs 12.6 and 25.6 in VLDL and HDL, respectively). After 14 d of overfeeding, hepatic PL profiles were identical in the two breeds and similar to that in control livers; choline-containing PL accounted for 95% of total PL. In contrast, plasma HDL concentrations of the Landes geese were lower than those of the Poland geese (9.4 vs 12.9 g/L) and their PC:PE (13.6%) and PL-polyunsaturated fatty acids (PUFA) content (25%) were decreased compared with the Poland geese (21.2 and 30%). It is likely that the higher susceptibility to fatty liver of the Landes breed involves a differential channelling of PL, resulting in a greater hepatic retention of PC and PUFA that are necessary for plasma membrane growth and cell hypertrophy.

N-3 fatty acids improve body composition and insulin sensitivity during energy restriction in the rat.

The hypothesis that n-3 polyunsaturated fatty acids (PUFA) could contribute to maintain muscle mass during energy restriction aiming to weight loss was tested in the rat, with special attention paid to insulin signalling. After 10 weeks on a diet rich in lipids and sucrose, male rats were energy restricted and fed diets rich in 18:1 n-9 (OLE), 18:3 n-3 (ALA) or n-3 long-chain (LC, >18 carbons) PUFA. After 4 weeks, they were killed after an insulin injection. Red blood cells, liver, and Gastrocnemius muscle were enriched in ALA in the ALA group, and in LC-PUFA in the ALA and LC groups. The LC diet resulted in a higher weight loss, without negative impact on the muscle weight. In parallel, hepatic phosphorylation of insulin receptor and IRS1 was the highest in this group. This suggests that the trend we observed in the preservation of protein homeostasis in the LC group is mediated, at least partly, by an enhancement of the early steps of insulin signalling resulting from cell membrane enrichment in n-3 PUFA.