Abstract

Five steers (mean BW 526 kg) fitted with ruminal, duodenal, and ileal cannulas were used in a 5 x 6 Youden square design with 14-d periods. Diets contained chopped alfalfa hay, corn silage, and concentrate (25:35:40, DM basis). Treatments were 1) control (no added fat); 2) tallow (T), iodine value (IV) = 51.5; 3) partially hydrogenated tallow (PHT), IV = 30.7; 4) hydrogenated tallow (HT), IV = 6.9; 5) blend (1: 1) of HT and hydrogenated free fatty acids (HTHFA), IV = 9.0; and 6) hydrogenated free fatty acids (HFA), IV = 11.2. Fats replaced cornstarch in the control diet to supply 5% added fatty acids. Intake was restricted to 90% of ad libitum; DMI was similar among diets (mean 9 kg/d). Total fatty acid intake averaged 170, 500, 506, 525, 489, and 491 g/d for treatments 1 to 6, respectively. Flows of total C16, total C18, and total fatty acids to the duodenum were increased by supplemental fat; flows of total C18 and total fatty acids were greater than their intake for all treatments. Flow of total fatty acids associated with ruminal bacteria accounted for 50 and 17% of the total duodenal fatty acid flow for the control and fat-supplemented diets, respectively. Digestibility of total fatty acids entering the small intestine (74, 71, 62, 39, 53, and 63% for treatments 1 to 6, respectively) was greater for the control diet than for fat-supplemented diets and decreased as either saturation (T < PHT < HT) or esterification (HFA < HTHFA < HT) increased. Digestibilities of fatty acids in the total tract followed similar patterns. Ruminal lipolysis of dietary triglycerides decreased linearly as the degree of saturation of fat sources increased. Small intestinal disappearance of triglycerides (89, 75, 51, 44, 64, and 73% of duodenal flow for treatments 1 to 6, respectively) decreased linearly as either saturation or esterification increased. Flows and digestion of gross energy followed patterns similar to those for fatty acids and triglycerides. Resistance to ruminal and small intestinal lipolysis is a major factor contributing to the poor digestibility of highly saturated triglycerides.

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