Effect of source and amount of rumen-protected choline on hepatic metabolism during induction of fatty liver in dairy cows

Objectives were to determine the effect of supple-menting increased amounts of rumen-protected choline (RPC) from sources with low (L, 28.8%) or high (H, 60.0%) concentration of choline chloride on hepatic metabolism when cows were subjected to feed restric-tion to develop fatty liver. It was hypothesized that increased supplementation of RPC reduces hepatic triacylglycerol and enhances glycogen concentrations. Pregnant, nonlactating multiparous Holstein cows (n = 110) at mean (+/- standard deviation) 232 +/- 3.9 d of gestation were blocked by body condition (4.01 +/- 0.52) and assigned to receive 0 (CON), 12.9 (L12.9 or H12.9), or 25.8 (L25.8 or H25.8) g/d of choline ion. Cows were fed for ad libitum intake on d 1 to 5 and restricted to 50% of the NEL required for maintenance and pregnancy from d 6 to 13. Intake of metaboliz-able methionine was maintained at 19 g/d during the feed restriction period by supplying rumen-protected methionine. Hepatic tissue was sampled on d 6 and 13 and analyzed for triacylglycerol, glycogen, and mRNA expression of genes involved in choline, glucose, and fatty acids metabolism, cell signaling, inflammation, autophagy, lipid droplet dynamics, lipophagy, and endoplasmic reticulum stress response. Blood was sampled and analyzed for concentrations of fatty acids, beta-hydroxybutyrate (BHB), glucose, triacylglycerol, to-tal cholesterol, and haptoglobin. Orthogonal contrasts evaluated the effect of supplementing RPC [CON vs. (1/4 center dot L12.9 + 1/4 center dot L25.8 + 1/4 center dot H12.9 + 1/4 center dot H25.8)], source of RPC [(1/2 center dot L12.9 + 1/2 center dot L25.8) vs. (1/2 center dot H12.9 + 1/2 center dot H25.8)], amount of RPC [(1/2 center dot L12.9 + 1/2 center dot H12.9) vs. (1/2 center dot L25.8 + 1/2 center dot H25.8)], and interaction between source and amount [(1/2 center dot L12.9 + 1/2 center dot H25.8) vs. (1/2 center dot H12.9 + 1/2 center dot L25.8)]. Least squares means and standard error of the means are presented in sequence as CON, L12.9, L25.8, H12.9, H25.8. Supplementation of RPC reduced hepatic triacylglycerol (9.3 vs. 6.6 vs. 5.1 vs. 6.6 vs. 6.0 +/- 0.6% as-is) and increased glycogen contents (1.8 vs. 2.6 vs. 3.6 vs. 3.1 vs. 4.1 +/- 0.2% as-is) on d 13 of the experiment. Feeding RPC reduced serum haptoglobin (136.6 vs. 85.6 vs. 80.6 vs. 82.8 vs. 81.2 +/- 4.6 mu g/mL) during the feed restriction period; however, blood concentrations of fatty acids, BHB, glucose, tria-cylglycerol, and total cholesterol did not differ among treatments. During feed restriction, supplementation of RPC enhanced the mRNA expression of genes related to choline metabolism (BHMT), uptake of fatty acids (CD36), and autophagy (ATG3), and reduced the ex-pression of a transcript associated with endoplasmic reticulum stress response (ERN1). An increase in the amount of choline ion from 12.9 to 25.8 g/d enhanced the mRNA expression of genes associated with synthe-sis and assembly of lipoproteins (APOB100), and in-flammation (TNFA), whereas it reduced the expression of genes linked to gluconeogenesis (PC), oxidation of fatty acids (ACADM, MMUT), ketogenesis (ACAT1), and synthesis of antioxidants (SOD1) on d 13 of the experiment. Feeding RPC, independent of the product used, promoted lipotropic effects that reduced hepatic lipidosis in dairy cows.