Effect of feeding increasing levels of whole cottonseed on milk and milk components, milk fatty acid profile, and total-tract digestibility in lactating dairy cows.

Dietary fat is fed to increase energy intake and provide fatty acids (FA) to support milk fat production. Oilseeds contain unsaturated FA that increase the risk for biohydrogenation-induced milk fat depression, but FA in whole cottonseed (WCS) are expected to be slowly released in the rumen and thus have a lower risk for biohydrogenation-induced milk fat depression. Our hypothesis was that increasing dietary WCS would increase milk fat yield by providing additional dietary FA without induction of milk fat depression. Four primiparous and 8 multiparous lactating Holstein cows, 136 ± 35 and 127 ± 4 DIM, respectively, were arranged in a replicated 4 × 4 Latin square design with 21-d periods. Treatments were WCS provided at 0%, 3.4%, 6.8%, and 9.9% of dietary dry matter, and WCS was substituted for cottonseed hulls and soybean meal to maintain dietary fiber and protein. Treatment did not change milk yield. There was a treatment-by-parity interaction for milk fat percent and yield with a quadratic decreased in primiparous cows but no effect of WCS in multiparous cows. Cottonseed linearly increased milk fat trans-10 18:1 in primiparous cows but not in multiparous cows. Increasing WCS increased milk preformed (18C) FA yield and partially overcame the trans-10 18:1 inhibition of de novo FA synthesis in the primiparous cows. Apparent transfer of 18C FA from feed to milk decreased in all cows as WCS increased, but the magnitude of the change was greater in primiparous cows. Increasing WCS decreased total-tract apparent dry matter, organic matter, and neutral detergent fiber digestibility. There was no change in total FA digestibility. However, 18C FA digestibility tended to be decreased in both parities and 16C FA digestibility was quadratically increased in multiparous cows but not changed in primiparous cows. Total fecal flow of intact WCS increased as WCS level increased, but fecal flow of intact seeds as a percentage consumed was similar across treatments. Fecal flow of intact seeds was greater in multiparous cows (4.3% vs. 1.1% of consumed). Plasma concentrations of glucose, nonesterified FA, triglycerides, and insulin were not changed. However, plasma urea-N increased with increasing WCS. Plasma gossypol increased with WCS (0.08-1.15 µg/mL) but was well below expected toxic levels. In conclusion, WCS maintained milk and milk component yield when fed at up to 9.9% of the diet to multiparous cows without concerns of gossypol toxicity, but primiparous cows were more susceptible to biohydrogenation-induced milk fat depression in the current trial. This highlights the interactions of parity with diet composition when feeding rumen-available unsaturated fat to dairy cows.

A review of recent studies on the enrichment of eggs and poultry meat with omega-3 polyunsaturated fatty acids: novel findings and unanswered questions.

Studies from our laboratory over the past decade have yielded new information with regard to the dietary enrichment of eggs and poultry meat with omega-3 (n-3) polyunsaturated fatty acids (PUFA) but have also generated a number of unanswered questions. In this review, we summarize the novel findings from this work, identify knowledge gaps, and offer possible explanations for some perplexing observations. Specifically discussed are: 1) Why feeding laying hens and broilers an oil rich in stearidonic acid (SDA; 18:4 n-3), which theoretically bypasses the putative rate-limiting step in the hepatic n-3 PUFA biosynthetic pathway, does not enrich egg yolks and tissues with very long-chain (VLC; ≥20 C) n-3 PUFA to the same degree as obtained by feeding birds oils rich in preformed VLC n-3 PUFA; 2) Why in hens fed an SDA-rich oil, SDA fails to accumulate in egg yolk but is readily incorporated into adipose tissue; 3) How oils rich in oleic acid (OA; 18:1 n-9), when co-fed with various sources of n-3 PUFA, attenuates egg and tissue n-3 PUFA contents or rescues egg production when co-fed with a level of docosahexaenoic acid (DHA; 22:6 n-3) that causes severe hypotriglyceridemia; and 4) Why the efficiency of VLC n-3 PUFA deposition into eggs and poultry meat is inversely related to the dietary content of α-linolenic acid (ALA; 18:3 n-3), SDA, or DHA.

Direct Comparison of 18 Carbon n-3 and n-6 Fatty Acids at Equal Levels in an Oil Blend on Tissue Enrichment of Long-Chain Polyunsaturated Fatty Acid in Broiler Chickens.

BACKGROUND: Omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) are of interest because of their health effects. However, most experiments use natural oils and are confounded by PUFA concentrations and other fatty acids (FAs) that impact biosynthesis of the very long-chain derivatives (VLC). OBJECTIVES: To directly compare the effect of 18 C n-3 or n-6 FA fed at similar rates on their elongation and desaturation to VLC PUFA and their incorporation into tissues. METHODS: Oil blends that substituted ∼23% points of stearidonic acid (SDA) with alpha-linolenic acid (ALA), gamma-linolenic acid (GLA), or linoleic acid (LA) while minimizing differences in other FA were prepared. COBB500 broilers were fed the oil blends at 1.25% of the diet from day 14-35 age. RESULTS: There was greater enrichment of VLC PUFA in breast, thigh, liver, and plasma when diets were supplemented with high-SDA and high-GLA oil blends than high-ALA and high-LA oil blends. The efficiency of VLCn-3 PUFA synthesis from SDA and ALA was lower than the efficiency of VLCn-6 PUFA synthesis from GLA and LA, suggesting that the elongation and desaturation enzymes more efficiently utilized n-6 substrates. The efficiency of biotransformation of SDA to VLCn-3 PUFA was greater than that of high-ALA, and synthesis of VLCn-6 PUFA from GLA was higher than that of high-LA in breast, thigh, liver, and plasma. There were minimal effects on tissue-saturated and monounsaturated FA. CONCLUSIONS: The high-SDA and high-GLA oil blends efficiently enriched tissues with their VLC-PUFA more than high-ALA and high-LA treatments.

Kinetics of omega-3 fatty acid transfer to milk differs between fatty acids and stage of lactation in dairy cows.

Fatty acids (FA) differ in their transfer efficiencies and metabolic partitioning and lactating cows provide a robust model to investigate kinetics of FA transport. The objective was to compare kinetics of n-3 polyunsaturated FA (PUFA) trafficking through plasma and into milk. In the first experiment, ten ruminally cannulated multiparous Holstein cows were used in a crossover design with 7 d periods. Cows were milked at 6 h intervals and abomasal treatments provided a single dose of 80.1 g of α-linolenic acid as free FA (ALA-FFA) or 45.5 g EPA and 32.9 g DHA (LCn3-FFA). Transfer of n-3 PUFA to milk was nearly 50% higher for ALA-FFA than LCn3-FFA (48.2 and 32.7% of the bolus) and fit a bi-exponential model. Rapid transport of n-3 PUFA, assumed to be directly through chylomicrons, was nearly twice as high in ALA-FFA than LCn3-FFA and the subsequent slow transport, assumed to be indirect transfer through tissue recycling, was over 2.5-fold higher in LCn3-FFA than in ALA-FFA. Plasma analysis revealed LCn3-FFA enriched phospholipids and cholesterol esters, which had a slow clearance. In the second experiment, 4 cows received a bolus of a mixture of ALA, EPA, and DHA prepartum while not lactating and around d 10, 55, and 225 of lactation. Transfer of ALA to milk did not differ between stages of lactation, but DHA was lower in early compared to mid and late lactation. In conclusion, dietary ALA is rapidly and efficiently transferred to milk in cows while EPA and DHA are rapidly incorporated into plasma or tissue fractions not available to the mammary gland. This demonstrates clear differences in trafficking and partitioning of n-3 PUFA that ultimately impact tissue and organelle enrichment with implications for effective doses.

Comparison of Ahiflower oil containing stearidonic acid to a high-alpha-linolenic acid flaxseed oil at two dietary levels on omega-3 enrichment of egg yolk and tissues in laying hens.

Enrichment of egg yolks with very long chain omega-3 fatty acids (VLCn-3 FA) is of interest because of their beneficial effects on human health. The ability of Ahiflower® oil (AHI; Buglossoides arvensis), which is naturally rich in stearidonic acid (SDA), and a high-alpha-linolenic acid (ALA) flaxseed (FLAX) oil to enrich eggs and tissues of laying hens with VLCn-3 FA was investigated. Forty 54-week-old Hy-Line W-36 White Leghorn hens were fed a diet that contained soybean oil (control; CON) or AHI or FLAX oils at 7.5 or 22.5 g/kg of the diet in substitution for the soybean oil for 28 days. Dietary treatments had no effects on egg number or components or follicle development. Total VLCn-3 FA contents of egg yolk, liver, breast, thigh, and adipose tissue were greater in the n-3 treatments compared to CON, with the greatest increase observed at the higher oil level, especially for AHI oil which had the greater VLCn-3 enrichment than FLAX in yolk (p < 0.001). Efficiency of VLCn-3 enrichment of egg yolks was decreased with n-3 oils and by increasing oil level with lowest efficiency at 22.5 g/kg FLAX. In conclusion, both SDA-rich (AHI) and ALA-rich (FLAX) oils increased VLCn-3 FA deposition into egg yolks and hens' tissues, but dietary AHI oil promoted a greater enrichment than comparative amounts of FLAX oil, especially in liver and egg yolks.

Feeding laying hens docosa hexaenoic acid-rich microalgae oil at 40 g/kg diet causes hypotriglyceridemia, depresses egg production, and attenuates expression of key genes affecting hepatic triglyceride synthesis and secretion, but is rescued by dietary co-supplementation of high-oleic sunflower oil.

The primary goal of this study was to investigate the effect of feeding White Leghorn hens graded levels of a docosahexaenoic acid (DHA)-rich microalgae oil (MAO) on productive performance and enrichment of eggs with very long-chain (VLC) omega-3 (n-3) polyunsaturated fatty acids (PUFA). Forty-nine-week-old hens (8 per diet) were fed the following diets for 28 d: 1) A corn-soybean meal-based diet with no supplemental oil (CON); 2) CON + 10 g/kg MAO; 3) CON + 20 g/kg MAO; 4) CON + 30 g/kg MAO; 5) CON + 40 g/kg MAO; 6) CON + 40 g/kg MAO + 20 g/kg high-oleic sunflower oil (HOSO); and 7) CON + 40 g/kg MAO + 40 g/kg HOSO. Diets 6 and 7 were included because we previously reported that co-feeding high-oleic acid oils with n-3 PUFA-containing oils attenuated egg yolk n-3 PUFA contents vs. feeding hens the n-3 oils alone. All data were collected on an individual hen basis. Egg VLC n-3 PUFA enrichment plateaued, in terms of statistical significance, at the 30 g/kg MAO level (266 mg/yolk). Hens fed 40 g/kg MAO had greatly attenuated measures of hen performance, marked liver enlargement, an altered ovarian follicle hierarchy, greatly lowered circulating triglyceride levels, and depressed hepatic expression of key genes involved in triglyceride synthesis and secretion. As compared to hens fed 40 g/kg MAO alone, feeding hens 40 g/kg MAO co-supplemented with HOSO (Diets 6 and 7) restored egg production, ovarian morphology, and all other measures of hen productive performance to CON levels, elevated plasma triglyceride levels, prevented liver enlargement, and increased the hepatic expression of key genes involved in triglyceride synthesis and secretion. In conclusion, MAO can greatly enrich hens' eggs with VLC n-3 PUFA, but its recommended dietary inclusion should not exceed 20 g/kg. This would allow for near-maximal yolk VLC n-3 PUFA enrichment without impairing hen productive performance, altering the ovarian follicle hierarchy or, based on the work of others, presumably imparting off-flavors in the egg.

Comparison of Ahiflower oil containing stearidonic acid to a high-alpha-linolenic acid flaxseed oil at two levels on tissue omega-3 enrichment in broilers.

Enrichment of broiler meat with very long-chain omega-3 fatty acids (VLCn-3 FA) is of interest because of their beneficial effects on human health. The ability of Ahiflower® (AHI) oil (Buglossoides arvensis), which naturally contains stearidonic acid (SDA), and a high-alpha-linolenic acid (ALA) flaxseed (FLAX) oil to enrich VLCn-3 FA contents in broilers tissues was investigated. Fifty-five Cobb 500 chicks were fed from days 12 to 35 of life either a control (CON) diet that contained 27.9 g/kg soybean oil or AHI or FLAX oils, each individually at 7.5 or 22.5 g/kg of the diet in substitution for soybean oil (all on an as fed basis). Total VLCn-3 FA contents were greater in breast, thigh, liver, adipose tissue, and plasma of all n-3 treatments compared to CON, with the greatest increase observed at the highest level of AHI and FLAX oils (p < 0.001). AHI oil at 7.5 g/kg promoted the most efficient synthesis and deposition of VLCn-3 in broiler tissues measured as deposition of VLCn-3 FA in tissues relative to intake of n3 FA. In conclusion, both ALA and SDA oils increased VLCn-3 FA deposition in tissues, but there were diminishing returns when increasing dietary levels of the oils.

Supplemental dietary oils rich in oleic acid or linoleic acid attenuate egg yolk and tissue n-3 polyunsaturated fatty acid contents in laying hens co-fed oils enriched in either stearidonic acid or α-linolenic acid.

We previously reported that when laying hens were fed diets supplemented with oils enriched in α-linolenic acid (ALA) and oleic acid (OA), the deposition of n-3 PUFA in egg yolk was attenuated as compared to feeding hens a diet supplemented with the ALA-rich oil alone. The present work extends those findings to another n-3 PUFA-rich oil (stearidonic acid [SDA]-enriched soybean oil) and two other high-OA oils, suggesting that the effect is not plant oil-specific. Feeding hens a supplemental linoleic acid (LA)-rich oil plus an oil rich in either SDA or ALA also attenuated egg yolk ALA and SDA contents (Experiment 1), or egg yolk and liver ALA contents (Experiment 2), respectively, as compared to feeding the SDA- or ALA-rich oils alone. Future work should focus on the lack of neutrality of OA and LA in relation to n-3 PUFA nutrition.

Physical characterization of fatty acid supplements with varying enrichments of palmitic and stearic acid by differential scanning calorimetry.

Saturated fatty acid supplements commonly fed to dairy cows differ in their fatty acid (FA) profile. Some supplements with very high enrichments of palmitic acid (PA) or stearic acid (SA) have been reported to have low total-tract digestibility. Saturated FA have the potential to form crystalline structures at high purity that may affect digestibility. Differential scanning calorimetry (DSC) is a thermal technique commonly used in materials science to measure the change in heat flow as energy is absorbed or released from a sample during heating, and it was used to characterize a series of experimental and commercial fat supplements. Our hypothesis was that products with very high enrichment of either PA or SA would differ in thermal characteristics compared with those that include moderate levels of a second FA because of the formation of secondary crystalline structures, which may contribute to decreased digestibility. First, replicated runs demonstrated low variation in melting temperature (MT) and enthalpy (coefficient of variation <4%). The effect of physical form was evaluated by comparing an initial thermal cycle to a second, successive thermal cycle after samples had resolidified in the test pan. Melting temperature was slightly increased by 1.3°C by the second cycle compared with the first, but there was no change in enthalpy. Next, supplements with 98% SA, 98% PA, and an SA/PA (44%/55%) blend with undetectable levels of unsaturated FA were compared. Melting temperature of the SA/PA mixture was 61.2°C and similar to the expected MT of PA (62.9°C). However, the MT of the high-purity SA and PA were increased to 73.7°C and 67.8°C, respectively, and enthalpy increased by 12.5% compared with the SA/PA blend. An FA stock highly enriched in SA (>98%) had the highest MT, and one moderately enriched in PA (∼85%) that contained 10.1% unsaturated FA had the lowest enthalpy value of all FA supplements and experimental stocks that were characterized. Differential scanning calorimetry may be useful to screen and design supplements with improved physical properties that may be associated with digestibility.

Dietary Fat Does Not Overcome trans-10, cis-12 Conjugated Linoleic Acid Inhibition of Milk Fat Synthesis in Lactating mice.

Trans-10, cis-12 conjugated linoleic acid (CLA) is a potent inhibitor of milk fat synthesis in the cow and similarly reduces milk fat in rodents. The objective of this study was to determine whether dietary fat can overcome CLA inhibition of milk fat concentration in lactating mice. Wild type C57Bl/6J mice (n = 31) were fed semipurified diets containing either low fat (LF; 4% fat) or high fat (HF; 23.6% fat) starting 4-6 days postpartum. Dietary fat was increased by inclusion of high oleic sunflower oil. After 2 days on the experimental diets, lactating dams were orally dosed with either water (control) or trans-10, cis-12 CLA (20 mg/day) for 5 days. CLA treatment decreased pup growth similarly in both HF and LF diets. Milk fat percent was increased over 16% by the HF diet and decreased over 12% by CLA, but there was no interaction of dietary fat and CLA. Both CLA and the HF diet reduced the proportion of short- and medium-chain fatty acids that originate from de novo synthesis, and there was no interaction of diet and CLA. CLA had no effect on the percent of preformed fatty acids, but the HF diet increased their abundance. Dietary fat and CLA both modified mammary expression of lipogenic enzymes and regulators, but no interactions were observed. In conclusion, CLA reduced milk fat concentration and litter growth, but these effects were not overcome by increased dietary fat from high oleic sunflower oil. CLA inhibition of milk fat in the mammary gland is not substrate dependent, and the mechanism is independent from dietary supply of oleic acid.

Dietary High-Oleic Acid Soybean Oil Dose Dependently Attenuates Egg Yolk Content of n-3 Polyunsaturated Fatty Acids in Laying Hens Fed Supplemental Flaxseed Oil.

Chickens can hepatically synthesize eicosapentaenoic acid (20:5 n-3) and docosahexaenoic acid (22:6 n-3) from α-linolenic acid (ALA; 18:3 n-3); however, the process is inefficient and competitively inhibited by dietary linoleic acid (LNA; 18:2 n-6). In the present study, the influence of dietary high-oleic acid (OLA; 18:1 n-9) soybean oil (HOSO) on egg and tissue deposition of ALA and n-3 polyunsaturated fatty acids (PUFA) synthesized from dietary ALA was investigated in laying hens fed a reduced-LNA base diet supplemented with high-ALA flaxseed oil (FLAX). We hypothesized that reducing the dietary level of LNA would promote greater hepatic conversion of ALA to very long-chain (VLC; >20C) n-3 PUFA, while supplemental dietary HOSO would simultaneously further enrich eggs with OLA without influencing egg n-3 PUFA contents. Nine 51-week-old hens each were fed 0, 10, 20, or 40 g HOSO/kg diet for 12 weeks. Within each group, supplemental dietary FLAX was increased every 3 weeks from 0 to 10 to 20 to 40 g/kg diet. Compared to controls, dietary FLAX maximally enriched the total n-3 and VLC n-3 PUFA contents in egg yolk by 9.4-fold and 2.2-fold, respectively, while feeding hens 40 g HOSO/kg diet maximally attenuated the yolk deposition of ALA, VLC n-3 PUFA, and total n-3 PUFA by 37, 15, and 32%, respectively. These results suggest that dietary OLA is not neutral with regard to the overall process by which dietary ALA is absorbed, metabolized, and deposited into egg yolk, either intact or in the form of longer-chain/more unsaturated n-3 PUFA derivatives.

Feeding laying hens stearidonic acid-enriched soybean oil, as compared to flaxseed oil, more efficiently enriches eggs with very long-chain n-3 polyunsaturated fatty acids.

The desaturation of α-linolenic acid (ALA) to stearidonic acid (SDA) is considered to be rate-limiting for the hepatic conversion of ALA to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in humans, rodents, and chickens. Thus, we hypothesized that feeding laying hens SDA, as a component of the oil derived from the genetic modification of the soybean, would bypass this inefficient metabolic step and result in the enrichment of eggs with EPA and DHA at amounts comparable to that achieved by direct supplementation of hens' diet with these very long-chain (VLC) n-3 polyunsaturated fatty acids (PUFAs). In a 28-d study, laying hens incorporated 0.132 mg, 0.041 mg, or 0.075 mg of VLC n-3 PUFAs into egg yolk for each milligram of ingested dietary ALA derived primarily from conventional soybean oil (CON), dietary ALA derived primarily from flaxseed oil (FLAX), or dietary SDA derived from SDA-enriched soybean oil, respectively. Moreover, the amounts of total yolk VLC n-3 PUFAs in eggs from hens fed the CON (51 mg), FLAX (91 mg), or SDA (125 mg) oils were markedly less than the 305 mg found in eggs from fish oil-fed hens. Unexpectedly, SDA appeared to be more readily incorporated into adipose tissue than into egg yolk. Since egg yolk FAs typically reflect the hens' dietary pattern, these tissue-specific differences suggest the existence of an alternate pathway for the hepatic secretion and transport of SDA in the laying hen.

Lipid feeding and milk fat depression.

Diets fed to cattle contain mostly unsaturated fatty acids supplied in grains and forages, by-products, and fat supplements. Lipid intake by dairy cattle must be restricted to prevent alterations of microbial populations in the rumen that can negatively affect milk yield. Unsaturated fatty acids consumed by cattle are extensively metabolized through biohydrogenation, intermediates of which include conjugated linoleic acid (CLA) and trans-monoenoic acid isomers. Three specific CLA intermediates of biohydrogenation have been shown to cause milk fat depression in dairy cattle through coordinated suppression of mammary lipogenic genes by a transcription factor that is a central regulator of lipid synthesis.

Supplementation with fish oil as a source of n-3 fatty acids does not downregulate mammary lipogenesis in lactating mice.

The very long chain n-3 (ω-3) polyunsaturated fatty acids (VLCn3PUFAs) are potent regulators of hepatic lipid synthesis, but their effect on lipid synthesis in the lactating mammary gland is less well investigated. The objective of the present study was to examine effects of fish oil (FO) supplementation on mammary lipogenesis and the expression of lipogenic genes in mammary and hepatic tissues of lactating mice. Beginning on day 6 of lactation and continuing for 7 d, female C57BL/6J mice (n = 8/diet) were fed 1 of 3 dietary treatments: a 5%-fat diet containing mainly saturated fatty acids (FAs) (low-fat control) or 2 10%-fat diets, 1 enriched with FO as a source of VLCn3PUFAs and the other enriched with a safflower/palm oil mixture (high-fat control) as a source of oleic acid. Mammary lipogenic capacity, measured by (14)C-glucose incorporation into FAs by mammary explants, was similar among treatments, and there were no treatment effects on the proportion of de novo synthesized FAs in milk fat or on litter weight gain, a proxy for milk energy secretion. Also, there were no treatment effects on mammary mRNA abundance for key lipogenic enzymes and proteins involved in the regulation of milk lipid synthesis. In contrast, there was a treatment effect on hepatic lipogenesis, with FO resulting in a decrease of ~50% in hepatic lipid content and a similar downregulation of lipogenic gene expression compared with the 2 control diets. Overall, there were tissue-specific differences in dietary VLCn3PUFA effects on lipid synthesis with no observed effects for mammary lipogenic variables but marked reductions occurring in hepatic lipogenesis.

Regulation of fat synthesis by conjugated linoleic acid: lactation and the ruminant model.

Conjugated linoleic acid (CLA) isomers effect an impressive range of biological processes including the ability to inhibit milk fatty acid synthesis. Although this has been demonstrated in several mammals, research has been most extensive with dairy cows. The first isomer shown to affect milk fat synthesis during lactation was trans-10, cis-12 CLA, and its effects have been well characterized including dose-response relationships. Recent studies have tentatively identified 2 additional CLA isomers that regulate milk fat synthesis. Regulation by CLA occurs naturally in dairy cows when specific CLA isomers produced as intermediates in rumen biohydrogenation act to inhibit milk fat synthesis; this physiological example of nutritional genomics is referred to as diet-induced milk fat depression. Molecular mechanisms for the reduction in mammary lipid synthesis involve a coordinated down-regulation of mRNA expression for key lipogenic enzymes associated with the complementary pathways of milk fat synthesis. Results provide strong evidence of a role for sterol response element-binding protein 1 and Spot 14 in this translational regulation. Effects of CLA on body fat accretion have also been investigated in nonlactating animals, but CLA effects on mammary fatty acid synthesis occur at an order-of-magnitude lower dose and appear to involve very different mechanisms than those proposed for the antiobesity effects of CLA. Overall, results demonstrate the unique value of cows as a model to investigate the role of CLA in the regulation of milk fat synthesis during lactation.

Trans-10 octadecenoic acid does not reduce milk fat synthesis in dairy cows.

Diet-induced milk fat depression (MFD) involves the interrelation between rumen fermentation and mammary synthesis of milk fat, and the reduction in milk fat coincides with a marked increase in the trans-10 18:1 content of milk fat. Our objective was to directly examine the effect of trans-10 18:1 on milk fat synthesis in dairy cows. Three mid-lactation cows were used in a 3 x 3 Latin square design; treatments were abomasal infusion of: 1) ethanol (control); 2) trans-10 18:1 (t10); and 3) trans-10, cis-12 conjugated linoleic acid (CLA; positive control). The t10 and CLA supplements (>90% purity) were infused for 4 d and provided 42.6 and 4.3 g/d of trans-10 18:1 and trans-10, cis-12 CLA, respectively. Milk yield, feed intake, milk protein, and milk lactose were unaffected by treatment. Compared with the control, the t10 treatment had no effect on milk fat synthesis, whereas the CLA treatment resulted in a 27 and 24% reduction in milk fat content and yield, respectively. The transfer efficiency of the abomasally infused trans-10 18:1 and trans-10, cis-12 CLA into milk fat was 15 +/- 1 and 23 +/- 5% (means +/- SD), respectively. Overall, trans-10 18:1 had no effect on milk fat synthesis when abomasally infused at approximately 43 g/d, although it was taken up by the mammary glands and incorporated into milk fat. Therefore, our results offer no support for the concept that changes in rumen production of trans-10 18:1 within the physiological range play a role in the regulation of fatty acid synthesis during diet-induced MFD.

Fat supplements affect fractional rates of ruminal fatty acid biohydrogenation and passage in dairy cows.

Rates of fatty acid biohydrogenation and passage were determined for fat supplements varying in saturation using lactating dairy cows. First-order fractional passage rates were determined by dividing the duodenal flux of fatty acids by their respective ruminal pool sizes. The determination of rates of biohydrogenation required the development of a model to account for the transfer of fatty acids among pools. Ruminally and duodenally cannulated multiparous Holstein cows (n = 8) were used in a replicated 4 x 4 Latin square design with 21-d periods. Treatments were control and a linear substitution of 25 g/kg supplemented fatty acids varying in saturation as follows: saturated (prilled hydrogenated free fatty acids), intermediate mix of saturated and unsaturated (calcium soaps of long-chain fatty acids), and partially unsaturated fatty acids. Passage rates of 16:0, 18:0, and total 18-carbon fatty acids were linearly decreased with increasing unsaturated fatty acids and the trans-18:1 fractional passage rate was quadratically affected with a maximum for the intermediate treatment. Increasing unsaturated fatty acids increased the extent of 18:2 and 18:3 biohydrogenation and decreased the extent of 18:1 and trans-18:1 biohydrogenation. Calcium salts did not protect PUFA from ruminal biohydrogenation despite a mean ruminal pH of 6.0, and unsaturated fatty acids decreased ruminal biohydrogenation of trans-18:1, resulting in increased duodenal flow of these fatty acids. The model allows a mechanistic description of ruminal biohydrogenation and determination of the extent of 18:1 biohydrogenation.