Effects of Polyunsaturated w-3 Fatty Acids on Short Term Regulation of Hepatic Fat Metabolism in Liver Tissue from Dairy Cows

Introduction

Hepatic lipidosis is a common disorder in dairy cows in the peri-parturient period, and the negative aspects have been well documented [1]. The accumulation of fat in the liver is caused by an increased influx of nonesterified fatty acids (NEFA) to the liver in situations of high mobilization. This indicates that an increased amount of long chain fatty acids (LCFA) is directed towards triglyceride (TG) synthesis rather than towards oxidation. In rat liver tissue it has been found that w-3 polyunsaturated fatty acids (ω-3 PUFA) like eicosapentaenoic acid (EPA; (20:5, ω-3)) and a-linolenic acid (LIN; 18:3, ω-3) are capable of depressing the rate of TG synthesis and stimulating rate of LCFA oxidation [2, 3]. The aim of the present study was to investigate if w-3 PUFA in the bovine liver could act to prevent hepatic TG accumulation within a few hours of acutely increased mobilization. The aim was addressed by examining the short-term effect of EPA and LIN on the capacity for in vitro oxidation, ketogenesis, and TG formation from palmitate in liver tissue from lactating dairy cows.

Material and methods

The liver tissue was obtained from 3 mid-lactating dairy cows fed a standard TMR. Fresh tissue was prepared by slicing cored liver on a motorized tissue slicer. The slices were incubated for 3 h in basal media containing 1.0 mM palmitate and one of either EPA, LIN or palmitate (control) in a final concentration of 1.2 mM. The capacity for oxidation (¹⁴CO2), ketogenesis (¹⁴C acid-soluble product (ASP)), and TG synthesis (¹⁴C TG) of [1-¹⁴C] palmitate in the tissue incubation system was measured.

Results and discussion

The capacity for TG synthesis was not affected by the 2 ω-3 PUFA's. Compared to incubation with palmitate alone, the complete oxidation of palmitate to CO₂ was decreased by 17% in the presence of ω-3 PUFA, but this was only significant for LIN (P = 0.006). The ASP formation was depressed by 30% in the presence of LIN (P = 0.01), but was unaffected by EPA. In conclusion, we were not able to demonstrate any positive short-term effects of ω-3 PUFA on hepatic LCFA metabolism in dairy cows with respect to prevention of hepatic lipidosis. There is need for further experiments to examine any potential longer time effects of ω-3 PUFA on hepatic fat metabolism in dairy cows, mediated by increased or decreased enzyme abundance.