Abstract #T456
Section: Ruminant Nutrition
Session: Ruminant Nutrition: Dairy II
Format: Poster
Day/Time: Tuesday 7:30 AM–9:30 AM
Location: Gatlin Ballroom
Session: Ruminant Nutrition: Dairy II
Format: Poster
Day/Time: Tuesday 7:30 AM–9:30 AM
Location: Gatlin Ballroom
# T456
Effects of exogenous C16:0 and C18 fatty acids (FA) on milk lipid metabolism in bovine mammary epithelial cells.
N. Dan*1, H. Zhang2, C. J. Ao1, Khas-Erdene1, 1College of Animal Science, Inner Mongolia Agricultural University, Hohhot, Inner Mongolia, China, 2College of Animal Science, Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, China.
Key Words: milk fat, lipid metabolism, gene expression
Effects of exogenous C16:0 and C18 fatty acids (FA) on milk lipid metabolism in bovine mammary epithelial cells.
N. Dan*1, H. Zhang2, C. J. Ao1, Khas-Erdene1, 1College of Animal Science, Inner Mongolia Agricultural University, Hohhot, Inner Mongolia, China, 2College of Animal Science, Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, China.
The objective of this study was to examine the regulatory effects of C16:0, C18:0, C18:1c9, C18:2n6, and C18:3n3 on lipid metabolism of bovine mammary epithelial cells. After plating for 48h, bovine mammary epithelial cells cultured from Chinese Holstein cows were bathed in one of the 6 treatments: 100 μM of C16:0 + 5 μM of C18:0 + 100 μM of C18:1c9 + 25 μM of C18:2n6 + 1.2 μM of C18:3n3 as Control; C18:0 + C18:1c9 + C18:2n6 + C18:3n3 as C16:0 absent treatment(A-C16:0); C16:0 + C18:1c9 + C18:2n6 + C18:3n3 as C18:0 absent treatment (A-C18:0); C16:0 + C18:0 + C18:2n6 + C18:3n3 as C18:1 absent treatment (A-C18:1); C16:0 + C18:0 + C18:1c9 + C18:3n3 as C18:2 absent treatment (A-C18:2); C16:0 + C18:0 + C18:1c9 + C18:2n6 as C18:3 absent treatment (A-C18:3). Key lipogenic genes were analyzed using quantitative PCR, and the FA composition in cells was quantified with gas chromatography. Data were analyzed by the ANOVA procedure of SAS. Cellular triglyceride contents in cells treated with A-C18:0, A-C18:2, A-C18:3 (P < 0.01) and A-C18:1 (P < 0.05) were decreased compared with the control. Absence of C16:0 induced greater level of LPL (P < 0.05). The level of ACSL1 in A-C18:3 was higher (P < 0.05) than that of A-C16:0 and A-C18:2. The mRNA abundance of FABP3 was enhanced by A-C18:3 (P < 0.05). The expression of SCD was reduced by A-C18:1 (P < 0.05). The abundance of CD36 showed reduction in A-C16:0, A-C18:1, and A-C18:2 (P < 0.05). Expression of SREBP-1 in A-C18:0, A-C18:1 and A-C18:2 were lower than that of A-C18:3 (P < 0.05). No effects of the treatments on ACACA and FASN were observed (P > 0.05). Furthermore, C18:2n6 and C18:1c9 compositions in cells were increased by A-C16:0 and A-C18:0 (P < 0.05), respectively. Percentage of C16:0 in A-C18:1, and that of C16:0 and C18:0 in A-C18:3 were enhanced (P < 0.05), respectively. Cells in A-C18:3 had greater SFA and lower UFA compared with other treatments (P < 0.05). In general, extracellular C18 FA availability has a strong effect on cellular triglyceride synthesis; different exogenous long-chain FAs showed no difference on inhibition of de novo FA synthesis, but greatly influence expression of lipogenic genes and milk FA composition.
Key Words: milk fat, lipid metabolism, gene expression
