ABSTRACT
Primary cultures of hepatocytes were used to study the effects of extracellular oleate concentration and hormones on fatty acid metabolism and gluconeogenesis. Rates of oleate uptake and oxidation to acid-soluble products varied linearly as oleate concentrations increased (0.1 to 2 mM), but rates of triglyceride accumulation varied quadratically. Insulin increased the proportion of oleate that was esterified by 22% without affecting the formation of acid-soluble products. Cells incubated with 2 mM [1-(14)C]oleate for 24 h eliminated 9.6% of the labeled intracellular lipid as acid-soluble products in the following 24 h when no oleate was present during depletion and eliminated 7.7% when 2 mM oleate was present. Insulin reduced labeled triglyceride depletion by 49%. Gluconeogenesis from [2-(14)C] propionate was depressed by 24%, and formation of acid-soluble products was increased by 46% in cells infiltrated with lipid because of previous exposure to 2 mM oleate for 45 h. Rates of gluconeogenesis from propionate were reduced 23% when 2 mM oleate was present during the 3-h period that gluconeogenesis was measured, and the effect was not modified by lipid infiltration. Lipid infiltration influenced hepatic function, and insulin regulated hepatic triglyceride concentration.
Subject(s)
Cattle/metabolism , Estrogens/pharmacology , Fatty Acids/metabolism , Fatty Acids/pharmacology , Glucagon/pharmacology , Gluconeogenesis/drug effects , Insulin/pharmacology , Liver/metabolism , Animals , Cattle/physiology , Cells, Cultured , Fatty Acids/pharmacokinetics , Fatty Acids, Nonesterified/blood , Gluconeogenesis/physiology , Glucose/metabolism , Keto Acids/metabolism , Lipid Metabolism , Lipids/pharmacokinetics , Liver/chemistry , Liver/cytology , Male , Oleic Acid/metabolism , Oleic Acid/pharmacokinetics , Triglycerides/analysis , Triglycerides/metabolismABSTRACT
Depression in feed intake during the final week before calving was hypothesized to be a major factor in the etiology of fatty liver development near parturition. Eleven cows were allowed to eat for ad libitum intake prior to calving (control), and 11 cows were maintained at the same level of DMI recorded during d 21 to 17 prior to calving by force feeding the feed refusals via rumen cannulas. Feed intake by control cows decreased 28% during the final 17 d prior to calving. Lipid triglyceride increased 227 and 75% for control and force-fed cows between d 17 prior to parturition and d 1 following calving. Dry matter intake prior to calving was correlated negatively with liver triglyceride immediately after calving (r = -.80). Plasma glucose concentrations for control and force-fed cows were 63 and 76 mg/dl 2 d prior to calving and also were related closely to liver triglyceride immediately after calving (r = -.50). By d 28 after calving, there were no differences in liver triglyceride between treatments. Cows that were force-fed prior to calving tended to yield milk with greater fat percentage (4.22 vs. 3.88%) and to yield more 3.5% FCM (46.1 vs. 41.7 kg/d) during the first 28 d postpartum.
