To meet the energy requirements of high-yielding dairy cows, grains and fats have increasingly been incorporated in ruminant diets. Moreover, lipid supplements have been included in ruminant diets under experimental or practical conditions to increase the concentrations of bioactive n-3 fatty acids and conjugated linoleic acids in milk and meat. Nevertheless, those feeding practices have dramatically increased the incidence of milk fat depression in dairy cattle. Although induction of milk fat depression may be a management tool, most often, diet-induced milk fat depression is unintended and associated with a direct economic loss. In this review, we give an update on the role of fatty acids, particularly originating from rumen biohydrogenation, as well as of rumen microbes in diet-induced milk fat depression. Although this syndrome seems to be multi-etiological, the best-known causal factor remains the shift in rumen biohydrogenation pathway from the formation of mainly trans-11 intermediates toward greater accumulation of trans-10 intermediates, referred to as the trans-11 to trans-10 shift. The microbial etiology of this trans-11 to trans-10 shift is not well understood yet and it seems that unraveling the microbial mechanisms of diet-induced milk fat depression is challenging. Potential strategies to avoid diet-induced milk fat depression are supplementation with rumen stabilizers, selection toward more tolerant animals, tailored management of cows at risk, selection toward more efficient fiber-digesting cows, or feeding less concentrates and grains.

Growth in demand for foods with potentially beneficial effects on consumer health has motivated increased interest in developing strategies for improving the nutritional quality of ruminant-derived products. Manipulation of the rumen environment offers the opportunity to modify the lipid composition of milk and meat by changing the availability of fatty acids (FA) for mammary and intramuscular lipid uptake. Dietary supplementation with marine lipids, plant secondary compounds and direct-fed microbials has shown promising results. In this review, we have compiled information about their effects on the concentration of putative desirable FA (e.g. c9t11-CLA and vaccenic, oleic, linoleic and linolenic acids) in ruminal digesta, milk and intramuscular fat. Marine lipids rich in very long-chain n-3 polyunsaturated fatty acids (PUFA) efficiently inhibit the last step of C18 FA biohydrogenation (BH) in the bovine, ovine and caprine, increasing the outflow of t11-18:1 from the rumen and improving the concentration of c9t11-CLA in the final products, but increments in t10-18:1 are also often found due to shifts toward alternative BH pathways. Direct-fed microbials appear to favourably modify rumen lipid metabolism but information is still very limited, whereas a wide variety of plant secondary compounds, including tannins, polyphenol oxidase, essential oils, oxygenated FA and saponins, has been examined with varying success. For example, the effectiveness of tannins and essential oils is as yet controversial, with some studies showing no effects and others a positive impact on inhibiting the first step of BH of PUFA or, less commonly, the final step. Further investigation is required to unravel the causes of inconsistent results, which may be due to the diversity in active components, ruminant species, dosage, basal diet composition and time on treatments. Likewise, research must continue to address ways to mitigate negative side-effects of some supplements on animal performance (particularly, milk fat depression) and product quality (e.g. altered oxidative stability and shelf-life).

Several technologies have been tested to reduce enteric methanogenesis, but very few have been successfully used in practical conditions for livestock. Furthermore, the consequences of reduced rumen methane production on animal performance and milk quality are poorly understood. The aim of this work was to investigate the effect of feeding bromochloromethane (BCM), a halogenated aliphatic hydrocarbon with potential antimethanogenic activity, to dairy goats on rumen methane production, fermentation pattern, the abundance of major microbial groups, and on animal performance and milk composition. Eighteen goats were allocated to 2 experimental groups of 9 animals each: treated (BCM+) or not (BCM-) with 0.30 g of BCM/100 kg of body weight per day. The BCM was administered per os in 2 equal doses per day from parturition to 2 wk postweaning (10 wk). After weaning, methane emissions were recorded over 2 consecutive days (d 57 and 58 on treatment) in polycarbonate chambers. On d 59, individual rumen fluid samples were collected for volatile fatty acid (VFA) analysis and quantification of bacterial, protozoal, and archaeal numbers by real-time PCR. On d 69 and 70, daily milk production was recorded and samples were collected for determination of fat, protein, lactose, casein, and total solids concentration by infrared spectrophotometry, and fatty acid composition by gas chromatography. Treatment with BCM reduced methane production by 33% (21.6 vs. 14.4 L/kg of DMI) compared with nontreated animals, although it did not affect the abundance of rumen bacteria, protozoa, and total methanogenic archaea. The observed improvement in the efficiency of digestive processes was accompanied by a 36% increase in milk yield, probably due to the more propionic type of rumen fermentation and an increase in VFA production. The increase in milk yield was not accompanied by any changes in the concentrations or yields of fat, protein, or lactose. Despite the substantial decrease in methane production, only minor changes in milk fatty acid profile were observed, suggesting that ruminal biohydrogenation pathways were not affected. Compounds that influence terminal biochemical pathways for methane production deserve further development for future application in the dairy goat sector.

A study with 2 ruminant species (goats and cows) with inherent differences in lipid metabolism was performed to test the hypothesis that milk fat depression (MFD) due to marine lipid supplements or diets containing high amounts of starch and plant oil is caused by different mechanisms and that each ruminant species responds differently. Cows and goats were allocated to 1 of 3 groups (4 cows and 5 goats per group) and fed diets containing no additional oil (control) or supplemented with fish oil (FO) or sunflower oil and wheat starch (SOS) according to a 3 × 3 Latin square design with 26-d experimental periods. In cows, milk fat content was lowered by FO and SOS (-31%), whereas only FO decreased milk fat content in goats (-21%) compared with the control. Furthermore, FO and SOS decreased milk fat yield in cows, but not in goats. In both species, FO and SOS decreased the secretion of C16 FA output. However, SOS increased milk secretion of >C16 FA in goats. Compared with the control, SOS resulted in similar increases in milk trans-10,cis-12 conjugated linoleic acid (CLA) in both species, but caused a 2-fold larger increase in trans-10 18:1 concentration in cows than for goats. Relative to the control, responses to FO in both species were characterized by a marked decrease in milk concentration of 18:0 (-74%) and cis-9 18:1 (-62%), together with a ~5-fold increase in total trans 18:1, but the proportionate changes in trans-10 18:1 were lower for goats. Direct comparison of animal performance and milk FA responses to FO and SOS treatments demonstrated interspecies differences in mammary lipogenesis, suggesting a lower sensitivity to the inhibitory effects of trans-10,cis-12 CLA in goats and that ruminal biohydrogenation pathways are more stable and less prone to diet-induced shifts toward the formation of trans-10-containing intermediates in goats compared with cows. Even though a direct cause and effect could not be established, results suggest that regulation of milk fat synthesis during FO-induced MFD may be related to a shortage of 18:0 for endogenous mammary cis-9 18:1 synthesis, increase in the incorporation of trans FA in milk triacylglycerols, and limitations in the synthesis of FA de novo to maintain milk fat melting point. However, the possible contribution of biohydrogenation intermediates with putative antilipogenic effects in the mammary gland, including trans-9,cis-11 CLA, trans-10 18:1, or cis-11 18:1 to FO-induced MFD cannot be excluded.

In an attempt to develop strategies for enhancing the nutritional value of sheep milk fat, dairy ewe diet was supplemented with 3 incremental levels of marine algae (MA), in combination with sunflower oil, to evaluate the effects of these marine lipids on milk fatty acid (FA) profile and animal performance. Fifty Assaf ewes in mid lactation were distributed in 10 lots of 5 animals each and allocated to 5 treatments (2 lots per treatment): no lipid supplementation (control) or supplementation with 25 g of sunflower oil/kg of DM plus 0 (SO), 8 (SOMA(1)), 16 (SOMA(2)), or 24 (SOMA(3)) g of MA (56.7% ether extract)/kg of DM. Milk production and composition, including FA profile, were analyzed on d 0, 3, 7, 14, 21, and 28 of treatment. Neither intake nor milk yield were significantly affected by lipid addition, but all MA supplements decreased milk fat content from d 14 onward, reaching a 30% reduction after 28 d on SOMA(3). This milk fat depression might be related not only to the joint action of some putative fat synthesis inhibitors, such as trans-9,cis-11 C18:2 and probably trans-10 C18:1, but also to the limited ability of the mammary gland to maintain a desirable milk fat fluidity, that would have been caused by the noticeable increase in trans-C18:1 together with the lowered availability of stearic acid for oleic acid synthesis through Delta(9)-desaturase. Furthermore, all lipid supplements, and mainly MA, reduced the secretion of de novo FA (C6:0-C14:0) without increasing the yield of preformed FA (>C16). Supplementation with sunflower oil plus MA resulted in larger increases in cis-9,trans-11 C18:2 than those observed with sunflower oil alone, achieving a mean content as high as 3.22% of total FA and representing a more than 7-fold increase compared with the control. Vaccenic acid (trans-11 C18:1) was also significantly enhanced (on average +794% in SOMA treatments), as was C22:6 n-3 (DHA) content, although the transfer efficiency of the latter, from the diets to the milk, was very low (5%). However, the highest levels of MA inclusion (SOMA(2) and SOMA(3)) reduced the milk n-6:n-3 ratio, but MA supplements caused an important increase in trans-10 C18:1, which would rule out the possibility that this milk has a healthier fat profile before determining the specific role of each individual FA and ensuring that this trans-FA is at least innocuous in relation to cardiovascular disease risk.

Ruminant diet supplementation with sunflower oil (SO) and fish oil (FO) has been reported as a good strategy for enhancing some milk fat compounds such as conjugated linoleic acid (CLA) and n-3 polyunsaturated fatty acids in dairy cows, but no information is available regarding dairy sheep. In this work, ewe diet was supplemented with FO, alone or in combination with SO, with the aim of improving milk nutritional value and evaluating its effect on animal performance. Sixty-four Assaf ewes in mid lactation, fed a high-concentrate diet, were distributed in 8 lots of 8 animals each and assigned to 4 treatments (2 lots/treatment): no lipid supplementation (control) or supplementation with 20 g of SO/kg (SO), 10 g of FO/kg (FO), or 20 g of SO plus 10 g of FO/kg (SOFO). Milk production and composition, including a complete fatty acid profile, were analyzed on d 0, 3, 7, 14, 21, and 28 of treatments. Supplementation with FO tended to reduce dry matter intake compared with the control treatment (-15%), and its use in combination with SO (SOFO) resulted in a significant decrease in milk yield as well (-13%). All lipid supplements reduced milk protein content, and FO also reduced milk fat content by up to 21% alone (FO) and 27% in combination with SO (SOFO). Although the mechanisms involved in FO-induced milk fat depression are not yet well established, the observed increase in some milk trans-FA that are putative inhibitors of milk fat synthesis, such as trans-9,cis-11 CLA, and the 63% decrease in C18:0 (consistent with the theory of reduced milk fat fluidity) may be involved. When compared with the control, lipid supplementation remarkably improved the milk content of rumenic acid (cis-9,trans-11 CLA; up to 4-fold increases with SO and SOFO diets), whereas FO-containing diets also increased milk n-3 polyunsaturated fatty acids, mainly docosahexaenoic acid (with mean contents of 0.29 and 0.38% of total fatty acids for SOFO and FO, respectively), and reduced the n-6:n-3 FA ratio to approximately half the control value. All lipid supplements resulted in high levels of some trans-FA, mainly trans-11 C18:1 (vaccenic acid) but also trans-10 C18:1.