Fish oil is used as a ration additive to provide n-3 fatty acids to dairy cows. Fish do not synthesize n-3 fatty acids; they must consume microscopic algae or other algae-consuming fish. New technology allows for the production of algal biomass for use as a ration supplement for dairy cattle. Lipid encapsulation of the algal biomass protects n-3 fatty acids from biohydrogenation in the rumen and allows them to be available for absorption and utilization in the small intestine. Our objective was to examine the use of algal products as a source for n-3 fatty acids in milk. Four mid-lactation Holsteins were assigned to a 4×4 Latin square design. Their rations were supplemented with 1× or 0.5× rumen-protected (RP) algal biomass supplement, 1× RP algal oil supplement, or no supplement for 7 d. Supplements were lipid encapsulated (Balchem Corp., New Hampton, NY). The 1× supplements provided 29 g/d of docosahexaenoic acid (DHA), and 0.5× provided half of this amount. Treatments were analyzed by orthogonal contrasts. Supplementing dairy rations with rumen-protected algal products did not affect feed intake, milk yield, or milk component yield. Short- and medium-chain fatty acid yields in milk were not influenced by supplements. Both 0.5× and 1× RP algae supplements increased daily milk fat yield of DHA (0.5 and 0.6±0.10 g/d, respectively) compared with 1× RP oil (0.3±0.10 g/d), but all supplements resulted in milk fat yields greater than that of the control (0.1±0.10g/d). Yield of trans-18:1 fatty acids in milk fat was also increased by supplementation. Trans-11 18:1 yield (13, 20, 27, and 15±3.0 g/d for control, 0.5× RP algae, 1× RP algae, and 1× RP oil, respectively) was greater for supplements than for control. Concentration of DHA in the plasma lipid fraction on d 7 showed that the DHA concentration was greatest in plasma phospholipid. Rumen-protected algal biomass provided better DHA yield than algal oil. Feeding lipid-encapsulated algae supplements may increase n-3 content in milk fat without adversely affecting milk fat yield; however, preferential esterification of DHA into plasma phospholipid may limit its incorporation into milk fat.

Background Obesity and hyperinsulinemia increase the risk of laminitis in horses and ponies. In mares, obesity also has been associated with increased circulating concentrations of the proinflammatory cytokine, tumor necrosis factor (TNF)‐α. The association of other proinflammatory cytokines with body condition score (BCS) and insulin requires further determination. Hypothesis Plasma concentrations of TNF, interleukin (IL)‐1β, IL‐6, and serum amyloid A (SAA) will positively correlate with BCS or insulin or both in horses. Furthermore, inflammatory protein concentrations will correlate with age and variables associated with BCS, including plasma insulin, triglycerides, nonesterified fatty acids, and leptin concentrations. Animals One hundred and ten mixed light‐breed horses, including mares, geldings, and stallions, aged 4–20 years. Methods Samples were selected from a larger population of plasma samples previously collected during June–July of 2006. Samples were analyzed for TNF, IL‐1β, IL‐6, and SAA using commercially available ELISAs and simple correlations were used to determine relationships with BCS, insulin, age, and sex. Results Plasma TNF (P = .047) and IL‐6 (P = .021) concentrations were higher in females than males, whereas IL‐6 concentrations correlated (P = .001) with age. Plasma SAA concentrations correlated with both insulin (P < .001) and BCS (P = .007). Conclusions and Clinical Importance This study provides evidence for factors, including age and sex, that may be associated with plasma concentrations of inflammatory proteins. Concentrations of SAA correlated with BCS and insulin, independent of age or sex. Because BCS and insulin correlate with increased SAA, it is possible that SAA is a component of laminitis pathophysiology.

Milk fatty acid composition is determined by several factors including diet. The milk fatty acid profile of dairy cows is low in polyunsaturated fatty acids, especially those of the n-3 series. Efforts to change and influence fatty acid profile with longer chain polyunsaturated fatty acids have proven challenging. Several barriers prevent easy transfer of dietary polyunsaturated fatty acids to milk fat including rumen biohydrogenation and fatty acid esterification. The potential for cellular uptake and differences in fatty acid incorporation into milk fat might also have an effect, though this has received less research effort. Given physiological impediments to enriching milk fat with polyunsaturated fatty acids, manipulating the genome of the cow might provide a greater increase than diet alone, but this too may be challenged by the physiology of the cow.

Liver X receptor (LXR) is a nuclear receptor and a known regulator of lipid synthesis in rodents; however, the role of LXR in the regulation of fatty acid synthesis in bovine mammary epithelial cells has not yet been defined. The objective of the study was to evaluate the effect of LXR activation on the de novo synthesis of fatty acids in bovine mammary epithelial cells (BME-UV). Bovine mammary epithelial cells were treated with T0901317 (T09), an LXR agonist. Treatment of BME-UV with T09 increased the transcription of ATP-binding cassette transporter-G1, an LXR target gene, without modifying LXRα mRNA abundance. Acute and chronic treatment of BME-UV with T09 dramatically increased de novo fatty acid synthesis. Activation of LXR resulted in the upregulation of transcription, translation, and proteolytic cleavage of sterol regulatory element-binding protein-1 (SREBP1), a lipogenic transcription factor expressed in the bovine mammary gland. Additionally, the mRNA abundance of fatty acid synthase, an LXR and SREBP1 target gene, increased in response to LXR activation. Our data indicate that SREBP1 is regulated by LXR activation in BME-UV. Controlling LXR activation may prove useful in regulating milk fat production in lactating dairy cows.

Our objectives were to isolate bovine stromal-vascular cells using explants and to determine media components that promote differentiation into mature adipocytes for studies of lipogenic enzyme regulation. Stromal-vascular cells were grown from explants and treated with differentiation media for 8 d after reaching confluence. Differentiation was assessed by measuring radiolabeled acetate incorporation into lipids, glycerol-3-phosphate dehydrogenase activity, and the mRNA expression of fatty acid binding protein-4, PPAR-γ, and acetyl-CoA carboxylase-α (ACCα). After 8 d of differentiation, medium containing 10 μg/mL of insulin, 0.25 μM dexamethasone, 0.5 mM isobutylmethylxanthine, 1 mM octanoate, and 2% Intralipid (Fisher Scientific, Suwanee, GA) produced greater acetate incorporation (P < 0.001) and glycerol-3-phosphate dehydrogenase activity (P < 0.001) compared with other media tested. This differentiation medium also increased mRNA expression of fatty acid binding protein-4, PPARγ, and ACCα by 180-, 7-, and 3-fold, respectively, compared with undifferentiated control cells (P < 0.05). To further improve the differentiation protocol, the effects of Intralipid, rosiglitazone, and troglitazone were examined. Removal of 2% Intralipid did not improve any differentiation measures. Addition of rosiglitazone (1 μM), a PPAR-γ agonist, increased acetate incorporation and ACCα mRNA (P < 0.01). Addition of troglitazone (5 μM), another PPAR-γ agonist, increased acetate incorporation to a similar extent as rosiglitazone and produced the greatest expression of ACCα mRNA (P < 0.01), but was not superior to medium that included rosiglitazone for any other differentiation measures. Cell-seeding density influences the cell divisions required to reach confluence, and increased plating density (2 × 10⁴ cells/cm² vs. 6.7 × 10³ cells/cm²) increased acetate incorporation by 100% (P < 0.001). Differentiating stromal-vascular cells in the presence of trans-10, cis-12 CLA inhibited differentiation of stromal-vascular cells into mature adipocytes, reducing radiolabeled acetate incorporation into lipids (P < 0.001), stearoyl-CoA desaturase-1 mRNA (P < 0.05) and protein abundance (P < 0.05), and ACCα protein abundance (P < 0.05). We have developed a method to differentiate primary bovine adipocytes, which will allow us to study the regulation of lipogenic enzymes by nutrient and endocrine factors.