Milk fatty acids profile and arterial blood milk fat precursors concentration of dairy goats fed increasing doses of soybean oil

The provision of fatty acid sources in ruminant diets allows the manipulation of fatty acid profiles in milk and meat, permitting to increase the fatty acids of interest, such as conjugated linoleic acid. The objectives of this experiment were to evaluate the inclusion of increasing doses of soybean oil (30, 60 or 90 g/d) on intake, total tract digestibility of nutrients, milk production and composition, arterial and milk fatty acid profiles, and arterial concentrations of glucose, acetate, and β-hydroxybutyrate in dairy goats. Four multiparous Saanen goats with mean initial DIM 32 ± 6 and mean initial BW 63 ± 7 kg were assigned in a 4 × 4 Latin square. Does were housed in tie stalls and fed a 40% of corn silage and 60% concentrate diet. Experimental treatments consisted of: (1) basal diet without soybean oil infusion (control); (2) basal diet plus an oral infusion of 30 mL soybean oil; (3) basal diet plus an oral infusion of 60 mL soybean oil; and (4) basal diet plus an oral infusion of 90 mL soybean oil. The DM and OM intakes decreased linearly (P < 0.05) with increasing soybean oil supply. Dry matter digestibility was negatively influenced by oil (P < 0.01); however, the OM digestibility was not affected by soybean oil doses. Milk production tended to decrease (P = 0.07) by soybean oil supply, although when this was corrected to 3.5% fat, it decreased linearly (P < 0.01) as a result of the decreasing (P < 0.05) milk fat content. Vaccenic acid concentration in arterial blood increased (P < 0.01) 127% with 90 g/d of soybean oil addition. Appearance of C18:2 t10, c12 in milk caused a reduction (P < 0.01) in milk fat and reached a 31% reduction when 90 g/d of soybean oil was offered compared to the control diet, while the opposite occurred with C18:2 c9, t11, which decreased (P < 0.05) with increasing doses of soybean oil. Increasing soybean oil had no effect on arterial blood concentrations of glucose, acetate and β-hydroxybutyrate. Therefore, the decrease in milk fat concentration was due to the inhibition of mammary synthesis of fatty acids, but not by a limitation of its precursors for fatty acid synthesis.