Pregnancy, decreased feed intake during late gestation, lactogenesis, and parturition have dramatic effects on metabolism in dairy cows during the transition period from 3 wk before calving to 3 wk after calving. Increases in plasma NEFA occur during the 10 d before calving and may precede the decrease in feed intake. Plasma NEFA concentrations are highest at calving and decrease rapidly after calving. Plasma glucose concentration decreases during the transition period except for a transient increase associated with calving. Hepatic glycogen is reduced and lipid is increased during the transition period. Feed intake is usually decreased 30 to 35% during the final 3 wk prepartum, but negative energy and protein balances are not as severe as during the week following parturition. Prepartum feed intake is positively correlated to postpartum feed intake; therefore, efforts to maximize feed intake should begin before calving. Overconditioned cows may be more susceptible to a prepartum decrease in feed intake. Increasing nutrient density of the diet during the transition period may enhance feed intake. Feeding more fermentable carbohydrate during the prepartum transition period may acclimate the microbial population to lactation diets, promote development of ruminal papillae, increase absorptive capacity of the rumen epithelium, and reduce lipolysis by delivering more glucogenic precursor to the liver and enhancing blood insulin. Supplementing fat to transition diets does not seem to alleviate health problems associated with negative energy balance. Enhancing amino acid absorption by the prepartum cow may improve lactation performance and health, although mechanisms of action have not been identified.

Plasma NEFA concentrations increase prior to and at parturition, resulting in increased fatty acid uptake by the liver, fatty acid esterification, and triglyceride storage. Liver triglyceride concentration increases four- to fivefold between d 17 prior to calving and d 1 following calving. Increases in liver triglyceride following calving do not appear to be dramatic. Severity of fatty liver 1 d postpartum is correlated negatively with feed intake 1 d prepartum. Export of newly synthesized triglyceride as very low density lipoprotein occurs slowly in ruminants and is a major factor in the development of fatty liver. Nutritional strategies to minimize the elevation in plasma NEFA prior to calving results in lower liver triglyceride at calving. Fatty liver probably precedes clinical spontaneous ketosis. Liver triglyceride to glycogen ratio may be used to predict susceptibility of cows to ketosis. Consequently, strategies to reduce liver triglyceride at calving may decrease incidence of ketosis. Research to determine methods to reduce fatty acid delivery to the liver or to enhance hepatic export of very low density lipoprotein near calving is warranted. Identification of the cause for the slow rate of assembly and secretion of hepatic very low density lipoprotein in ruminants will be required to assess the feasibility of increasing export of very low density lipoprotein.

Sixty-five Holstein cows were used to evaluate management schemes involving altered dry period (DP) lengths on subsequent milk production, energy balance (EB), and metabolic variables. Cows were assigned to one of 3 treatments: traditional 56-d DP (fed a low-energy diet from -56 to -29 d and a moderate energy diet from -28 d to parturition; T), 28-d DP (continuously fed a high energy diet; S), and no planned DP (continuously fed a high energy diet; N). Prepartum DM intake (DMI), measured from 56 d prepartum through parturition, was lower for cows on the T treatment than for cows on the S treatment and was higher for cows on the N treatment than for cows on the S treatment. There were no differences in prepartum plasma glucose, and beta-hydroxybutryric acid; there was a treatment by time interaction for prepartum plasma nonesterified fatty acid (NEFA). There was no difference in prepartum liver triglyceride (TG); postpartum liver TG was decreased for cows on the N treatment compared with cows on the S treatment, but was similar for cows on the T and S treatments. Postpartum NEFA was similar between cows on the T and S treatments, but was greater for cows on the S treatment than for cows on the N treatment. Postpartum glucose was greater for cows on the N treatment compared with cows on the S treatment and tended to be greater for cows on the S treatment than for cows on the T treatment. There was no difference in postpartum solids-corrected milk (SCM) production or DMI by cows on the T vs. S treatment. However, there was a tendency toward lower postpartum SCM production by cows on the N vs. S treatment and a tendency for greater postpartum DMI by cows on the N vs. S treatment. Postpartum EB was greater for cows on the S vs. T treatment and the N vs. S treatment. In general, T and S management schemes had similar effects on DMI, SCM, and metabolic variables in the first 70 d of the subsequent lactation. Eliminating the DP improved energy and metabolic status.

Researchers attending the Wisconsin Milk Board 1988 Milk Fat Roundtable indicated that the ideal nutritional milk fat would contain 10% polyunsaturated fatty acids, 8% saturated fatty acids, and 82% monounsaturated fatty acids. This cannot be accomplished by modifying diets of lactating cows. Monounsaturated fatty acid (C18:1) content can be increased by 50 to 80% and may approach 50% of milk fatty acids by feeding lipids rich in 18-carbon fatty acids. Because of ruminal hydrogenation and intestinal and mammary desaturase activity, degree of unsaturation of dietary 18-carbon fatty acids is not critical in influencing milk fat C18:1. Feeding low roughage diets increases the proportion of C18:1 in milk fat, and effects of feeding low roughage diets and lipid may be additive. Palmitic acid (C16:0) content of milk fat can be reduced by 20 to 40% unless the supplemented lipid is rich in C16:0. Milk fat alteration is dependent on the level of lipid supplementation. Limited evidence indicates frequency of lipid feeding and physical form of oil (free oil vs. oilseed), and heat treatment of oilseeds has relatively little influence on modification of milk fat. Significant changes in milk fat composition can be achieved on farm via nutritional modifications.

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