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  • Title: Fatty acid metabolism in liver of dairy cows fed supplemental fat and nicotinic acid during an entire lactation.
    Author: Grum DE, Drackley JK, Clark JH.
    Journal: J Dairy Sci; 2002 Nov; 85(11):3026-34. PubMed ID: 12487468.
    Abstract:
    Liver biopsies from 38 multiparous Holstein cows were used to determine rates of peroxisomal beta-oxidation and total beta-oxidation of palmitate in liver homogenates and contents of total lipid, triglyceride, and glycogen during the lactation cycle. Cows were assigned to one of four diets from wk 4 through wk 42 of lactation: control, control plus nicotinic acid (12 g/d), supplemental fat, or supplemental fat plus nicotinic acid. Liver biopsies were obtained at wk 3 (covariate), 6, 12, 24, and 42 of lactation. Neither supplemental fat nor nicotinic acid affected palmitate oxidation in liver homogenates or liver composition. Peroxisomal beta-oxidation capacity and the ratio of peroxisomal to total beta-oxidation decreased from wk 3 to 12 and then increased at wk 42. Contents of total lipid and triglyceride decreased, and content of glycogen increased, from wk 3 to 12. Total oxidation capacity in liver homogenates was correlated negatively with total lipid and triglyceride in liver, yields of milk and solids-corrected milk (SCM), and plasma nonesterified fatty acids (NEFA), and was correlated positively with liver glycogen, dry matter intake (DMI), energy balance, and plasma glucose. Peroxisomal beta-oxidation was correlated negatively with yields of milk and SCM. The ratio of peroxisomal to total beta-oxidation was correlated positively with liver total lipid, liver TG, and plasma NEFA and negatively with DMI and energy balance. When only data from wk 3 postpartum were considered, both total and peroxisomal beta-oxidation were correlated negatively with hepatic concentrations of total lipid and TG. Peroxisomal beta-oxidation in liver of dairy cows is not affected by feeding supplemental fat or nicotinic acid during wk 4 to 42 of lactation but may be a part of the hepatic adaptations to negative energy balance.
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