The main aim of this work was to assess factors affecting the secretion of carotenoids in cows' milk. Our objectives were 1) to determine the kinetics of the decrease in carotenoids in plasma, milk, and adipose tissues following a switch from a high- to a low- carotenoid diet; and 2) to specify whether, during lipomobilization, the restitution of these compounds stored in the adipose tissues is sufficient to modify their secretion in milk. During the preexperimental period, 32 cows in midlactation were fed a grass silage-based diet, and were then assigned to 4 groups; 2 groups were maintained on the grass silage diet and 2 were switched to a late hay diet. For each forage diet, one group was fed according to net energy for lactation and nitrogen requirements, and the other was submitted to an energetic underfeeding, with similar forage and carotenoid intake between groups. Variations in concentration of carotenoids and color index (CI) of plasma and milk were monitored over 8 wk. Other components of nutritional interest; i.e., vitamin E (VE), vitamin A, and fatty acids, were also measured. The switch from grass silage to hay diet induced a rapid decrease in concentration of betal-carotene (BC) and VE and in the CI of plasma and milk during the first 2 wk. Pools of BC in adipose tissues also decreased by 40%. Concentrations of BC at the end of the experiment for silage and hay groups were 5.10 and 1.71 microg/mL in plasma and 0.17 and 0.07 microg/mL in milk, respectively. The energetic underfeeding did not affect BC concentration in plasma and induced a small increase in milk BC concentration, related to a decreased milk yield. In the silage group, the energetic underfeeding after 3 to 4 wk induced a decrease in CI and VE of plasma, but not of milk. The fatty acid profile in milk was modified by the change from grass silage to hay diet (C10 to C14 and linoleic acid increased; stearic and linolenic acid percentages decreased) and by underfeeding (oleic, vaccenic, and rumenic acid percentages increased). This study shows that BC and VE levels persist in midlactation cows' plasma and milk for about 2 wk. The results could not confirm a release of BC by bovine adipose tissue, but the level of underfeeding was moderate in this trial. The concentration of BC explained 58 and 40% of variation in CI of plasma and milk, respectively. These CI appear to be valuable tools for diet traceability (i.e., silage vs. hay).

Summary ― The production of very low density lipoproteins (VLDL) by the liver results from very complex processes that involve coordinated mechanisms of both protein and lipid synthesis and packaging. Alterations in these metabolic functions can cause negative effects on the health of human subjects or animals. The objectives of this paper were to review the latest developments in the biological mechanisms of these processes and the role of nutritional and hormonal factors. The present study addresses the following issues: i) the main steps in the hepatic metabolism of lipids (long-chain fatty acids, triacylglycerols, phospholipids) and proteins (apolipoprotein B, microsomal transfer protein) primarily involved in the synthesis and secretion of VLDL particles; ii) the metabolic deviations of hepatic VLDL (hypo-and overproduction) in man, rodents and farm animals (poultry, dairy cows).

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Dairy fat contains high amounts of saturated fatty acids (FA), which are associated with cardiovascular disease (CVD) risk. Manipulation of dairy cows nutrition allows to decrease the saturated FA content of milk fat, and is associated with increases either in conjugated linoleic acid (CLA) and trans-11-C18:1 contents, or in trans-10-C18:1 content. CLA putatively exhibits beneficial properties on CVD risk, whereas trans FA are suspected to be detrimental. The present study compared the effects of a trans-10-C18:1-rich butter (T10 butter), a trans-11-C18:1 þ CLA-rich butter (T11-CLA butter) and a standard butter (S butter) on lipid parameters linked to the CVD risk and fatty streaks. Thirty-six White New Zealand rabbits were fed one of the three butters (12% of the diet, plus 0.2% cholesterol) for 6 (experiment 1) or 12 (experiment 2) weeks. Liver lipids, plasma lipids and lipoprotein concentrations (experiments 1 and 2) and aortic lipid deposition (experiment 2) were determined. The T10 butter increased VLDL-cholesterol compared with the two others, and total and LDL-cholesterol compared with the T11-CLA butter ( P , 0.05). The T10 butter also increased non-HDL/HDL ratio and aortic lipid deposition compared with the T11-CLA butter ( P , 0.05). The T11-CLA butter non-significantly reduced aortic lipid deposition compared with the S butter, and decreased HDLcholesterol and increased liver triacyglycerols compared with the two other butters ( P , 0.05). These results suggest that, compared with the S butter, the T10 butter had detrimental effects on plasma lipid and lipoprotein metabolism in rabbits, whereas the T11-CLA butter was neutral or tended to reduce the aortic lipid deposition.

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Plant oils in the diet are known to alter milk fat composition owing to changes in the supply of fatty acid precursors and/or activity of lipogenic enzymes in the mammary gland. Thirteen mid-lactating Alpine goats were used in a 3 x 3 Latin square design with 28-d periods to evaluate possible mechanisms regulating milk fat synthesis and fatty acid composition on grass hay-based diets containing none (H) or 55 g/kg diet dry matter of sunflower-seed oil (HSO) or linseed oil (HLO). Inclusion of oils in the diet had no effect on milk yield but enhanced (P<0.05) milk fat secretion. Compared with the control, HLO and HSO decreased (P<0.05) C10-C16 secretion and increased (P<0.05) C18 output in milk, responses that were accompanied by reductions in milk fat cis-9 14:1/14:0, cis-9 18:1/18:0 and cis-9, trans-11 18:2/cis-9 18:1 concentration ratios. Plant oil supplements decreased (P<0.05) mammary stearoyl-CoA desaturase (SCD) activity but had no effect on SCD mRNA. Treatments had no effect on glucose-6-phosphate dehydrogenase, malic enzyme and glycerol-3-phosphate dehydrogenase activity, or mRNA abundance and/or activity of lipoprotein lipase, acetyl-CoA carboxylase and fatty acid synthase in mammary, hepatic or adipose tissue. The results provided little support for milk fatty acid secretion responses to HLO and HSO being mediated via changes in mammary, hepatic or adipose mRNA abundance or in the activity of key lipogenic enzymes. In conclusion, plant oils in the diet enhance milk fat synthesis, alter milk fatty acid composition and specifically inhibit mammary SCD activity in the goat. Furthermore, the results suggest that the regulation of mammary lipogenesis in response to plant oils appears related to factors other than altered mammary gene expression or potential lipogenic enzyme activity.

Diets rich in n-3 polyunsaturated fatty acids (PUFA) improve the nutritional value of ruminant products but also increase the risk of lipoperoxidation in plasma and tissues. The relative effectiveness of dietary antioxidants such as vitamin E (vit E) given alone or with plant extracts rich in polyphenols (PERP) containing rosemary, grape, citrus, and marigold was investigated in the plasma of mid-lactation dairy cows given diets enriched in 18:3 n-3. For a 30-d period, the animals were given a maize silage-based diet (control group C, n = 6) or the same basal diet supplemented with extruded linseed rich in 18:3 n-3 [50 g of oil/kg of diet dry matter (DM); group L, n = 6], extruded linseed + vit E (375 international units/kg of diet DM; 7,500 IU/cow per day; group LE, n = 6), or extruded linseed + vit E + PERP (10 g/kg of diet DM; group LEP, n = 5). Plasma susceptibility to lipoperoxidation was evaluated using in vitro parameters of conjugated diene formation (lag phase and maximum oxidation rate). Plasma indicators of lipoperoxidation and antioxidant status were analyzed in the 4 experimental groups as well as the fatty acid (FA) composition of total plasma lipids. At d 30, group L significantly increased plasma cholesterol esters (+57%) and phospholipids (+35%) compared with group C. It also increased plasma n-3 PUFA (4.7-fold increase) to the detriment of n-6 PUFA (-30%), leading to a higher peroxidizability index (+20%). Plasma in vitro lipoperoxidation was higher in group L (rich in 18:3 n-3) than in group C. Vitamin E alone had no effect on lipoperoxidation, whereas vit E in association with PERP lowered lipoperoxidation by increasing the resistance time against peroxidation (+47%) and by decreasing the oxidation rate (-48%) compared with group L at d 30. Surprisingly, in vivo plasma lipoperoxidation estimated by the plasma level of the major lipoperoxidation product (malondialdehyde) was not significantly increased in group L. This study shows, for the first time, that PERP supplied in association with vit E were able to reduce lipoperoxidation in lactating cows given a diet rich in 18:3 n-3, thereby helping to protect cows against the deleterious consequences of lipoperoxidation and potentially ensuring antioxidant potential for 18:3 n-3-enriched dairy products.

We examined the effects of weight loss induced by restricting energy and fluid intake on antioxidant status and oxidative stress of judo athletes. Twenty male judoka were randomly assigned to one of two groups (Group A: called diet, n = 10; height 174.8 +/- 1.9 cm, body weight 75.9 +/- 3.1 kg; they were asked to lose approximately 5 % of their body weight through self-determined means during the week before the competition; Group B: called control, n = 10; height 176.4 +/- 1.1 cm, body weight 73.3 +/- 6.3 kg maintained their body weight during the week before the competition). A battery of tests was performed during a baseline period (T1) on the morning of a simulated competition (T2) and 10 minutes after the end of the competition (T3). These tests included assessment for body composition, determination of lag phase (Lp) before free radical induced oxidation, maximum rate of oxidation (Rmax) during the propagating chain reaction and maximum amount of conjugated dienes (CDmax) accumulated after the propagation phase, and lipidic profile. Uric acid concentrations were also evaluated in plasma. Dietary data were collected using a 7-day diet record. We noted that the athletes followed a low carbohydrate diet whatever the period of the investigation. Concerning antioxidant nutrients, we can notice that mean nutritional intakes are in the normal range values for vitamin A, C and E at T1 and T2. Rapid weight loss induced a significant increase in Lp values (p < 0.05) and uric acid concentrations without alterations in oxidative stress. Our data also showed that the competition induced the same changes of oxidative-antioxidant status whatever the dietary intake during the seven days before the competition. Moreover, the effect of the competition on the antioxidant and oxidant parameters was more pronounced than the diet. Theses results could be linked to the food containing a large proportion of PUFA and a relative low proportion of carbohydrates.