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).
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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