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During the transition period, dairy cows undergo large metabolic adaptations in glucose, fatty acid, and mineral metabolism to support lactation and avoid metabolic dysfunction. The practical goal of nutritional management during this timeframe is to support these metabolic adaptations. The National Research Council addressed nutritional management of transition cows for the first time in 2001; however, a substantial amount of research has been reported since this publication was released. Results support 2-group nutritional strategies for dry cows to minimize overfeeding of nutrients during the early dry period but increase nutrient supply to facilitate metabolic adaptation to lactation during the late dry period. Increasing the amount of energy supplied through dietary carbohydrate during the prepartum period results in generally positive effects on metabolism and performance of transition cows. Recent research, however, suggests that the form of that carbohydrate (i.e., starch vs. highly digestible neutral detergent fiber) may be of lesser importance. Attempts to increase energy supply by feeding dietary fat sources or decrease energy expenditure by supplying specific fatty acids such as trans-10, cis-12 conjugated linoleic acid to decrease milk fat output during early lactation do not decrease the release of nonesterified fatty acids (NEFA) from adipose tissue. Although the view that nutritional means have limited ability to enhance hepatic export of NEFA as triglycerides in lipoproteins in ruminants has become dogma, recent evidence suggests that nutrients such as choline or specific fatty acids may enhance this process in transition cows. Adaptation of calcium metabolism to lactation is facilitated by nutritional strategies to decrease the cation-anion difference (DCAD) of the diet fed prepartum, although the degree to which the DCAD must be decreased to sufficiently prevent hypocalcemia remains controversial. Recent research also has provided possible physiological links between the associations of primary infectious disease with the occurrence of secondary metabolic disorders, thereby enabling investigation of factors affecting variation in response to nutritional management programs for transition cows on dairy farms.

Four multiparous lactating cows (175 to 220 d in milk [DIM]) were used in a 4 x 4 Latin square design to assess the effects of four doses (0.0, 0.5, 1.0, and 1.5 microgram/kg of body weight) of lipopolysaccharide (LPS; Escherichia coli 0111:B4) on performance and plasma metabolite and hormone concentrations. In addition, effects of immune activation on in vitro hepatic metabolic capacity were evaluated in 12 multiparous lactating cows (150 to 220 DIM) infused with 0 (n = 6), 1.0 (n = 4) or 2.0 (n = 2) microgram of LPS/kg. Milk production and DMI decreased linearly with LPS dose for 24 h after LPS infusion. Overall mean plasma tumor necrosis factor-alpha, insulin, glucagon, and cortisol concentrations increased linearly with LPS dose, and plasma beta-hydroxybutyrate decreased linearly by dose after LPS infusion. Infusion of LPS decreased the insulin:glucagon molar ratio, but did not affect plasma concentrations of growth hormone, insulin-like growth factor-1, leptin, or L-(+)-lactate. Plasma concentrations of glucose tended to increase initially and subsequently decrease, and there was a quadratic tendency for increased plasma nonesterified fatty acid concentrations after LPS administration. In vitro hepatic capacity for conversion of [1-14C]L-(+)-lactate and [1-14C]palmitate, but not [1-14C]propionate or [1-14C]L-alanine, to CO2 increased after LPS administration. Hepatic capacity to convert [1-14C]propionate to glucose tended to increase, but neither esterification nor the conversion of palmitate to acid soluble products was altered by LPS. The LPS infusion resulted in significant changes of endocrine mediators responsible for regulation of energy metabolism of lactating cows and tended to alter subsequent in vitro hepatic metabolic capacity.

Data from multiparous Holstein cows (n=43) were used to determine whether supplementation of anions to low-potassium (K) prepartum diets would improve periparturient energy and macromineral status and affect performance during the postpartum period. Beginning 21 d before expected parturition, cows were fed a control diet (1.29% K; +10mEq/100g; n=21) or a low dietary cation-anion difference (DCAD) diet (1.29% K; −15mEq/100g; n=22) with anions provided through a combination of sulfate from calcium sulfate dihydrate (0.40% S total ration) and chloride (1.17% Cl total ration) from SoyChlor 16–7 (West Central, Ralston, IA). All cows were fed the same postpartum diet from parturition through 63 d postpartum. Feeding anions decreased overall urine pH (8.17 vs. 6.70) during the prepartum period. Overall, peripartum concentrations of plasma Ca, P, and Mg were similar between treatments; however, concentrations of plasma Ca tended to be increased during the first 24h postcalving in cows fed the low DCAD diet. Overall, concentrations of plasma P tended to be increased by feeding the anionic diet prepartum; this effect was more pronounced during the immediate peripartal period. Anionic supplementation did not affect incidence of clinical (<5mg/dL) and subclinical (5 to 8mg/dL) hypocalcemia, clinical hypophosphatemia (<2mg/dL), or clinical (<1.1mg/dL) and subclinical (1.1 to 1.8mg/dL) hypomagnesemia. Nevertheless, subclinical hypophosphatemia (2 to 4mg/dL) tended to be decreased at 16h postcalving and was decreased at d 2 postpartum for cows fed the anionic diet prepartum. Anion supplementation decreased prepartum dry matter intake (15.6 vs. 14.4kg/d), but did not affect postpartum dry matter intake (22.4 vs. 23.0kg/d), milk yield (46.5 vs. 46.1kg/d), or content and yield of milk fat and true protein. Plasma concentrations of energy-related metabolites (glucose, nonesterified fatty acids, β-hydroxybutyrate) were similar for both groups during the prepartum and postpartum periods. Glucose rate of appearance was determined by continuous infusion of 6,6-dideuterated glucose in a subset of cows between 6 and 10 d prepartum (control, n=12; low DCAD, n=9) and 7 and 10 d postpartum (control, n=9; low DCAD, n=8) periods. Glucose rate of appearance was not affected by treatment during the prepartum or postpartum periods. Overall, anion supplementation of low K diets improved P status during the early postpartum period, but did not affect aspects of energy metabolism or periparturient performance.

Four multiparous lactating cows (175 to 220 d in milk) were used in a 4 x 4 Latin square design to assess the effects of four doses (0.0, 0.5, 1.0, 1.5 microgram/kg of body weight) of lipopolysaccharide (LPS; Escherichia coli 0111:B4) on circulating concentrations of macrominerals and vitamin D metabolites. Treatments were dissolved in 100 ml of sterile saline and infused intravenously over a period of 100 min. Blood was sampled immediately before infusion (0 h), at 60-min intervals for 8 h, and at 24 and 48 h postinfusion. Vitamin D metabolites were analyzed in samples collected at 0, 2, 6, 24, and 48 h only. Serum Ca and P concentrations decreased after LPS infusion, but there was no effect on serum magnesium concentration. Plasma 25-OH vitamin D3 and 1,25-(OH)2 vitamin D3 were not affected by LPS infusion; however, when analyzed as 0 vs. all other doses of LPS combined, there was a tendency for plasma 1,25-(OH)2 vitamin D3 concentration to decrease when cows were infused with LPS. The inflammatory response elicited by LPS altered plasma macromineral concentrations, a result that may have important implications for calcium homeostasis and metabolic health of lactating dairy cows.

Holstein cows (n = 72) entering second or later lactation were used to determine whether metabolic indices and hepatic capacities for oxidation and gluconeogenesis from propionate are affected by source of carbohydrate in the prepartum diet and chromium-L-methionine (Cr-Met) supplementation throughout the periparturient period. Cows were fed prepartum diets as total mixed rations with the concentrate portion based either on starch-based cereals [high nonfiber carbohydrate (NFC); 1.59 Mcal/kg of net energy for lactation (NEL), 14.4% crude protein (CP), 40.3% NFC] or nonforage fiber sources (low NFC; 1.54 Mcal/kg of NEL, 14.5% CP, 33.6% NFC) from 21 d before expected parturition until parturition. After parturition all cows were fed a common lactation total mixed ration (1.74 Mcal/kg of NEL, 16.5% CP, 40.0% NFC). The Cr-Met was supplemented once daily via gelatin capsule at dosages of 0, 0.03, or 0.06 mg of Cr/kg of BW⁰.⁷⁵. Thus, treatments were in a 2 (carbohydrate source) x 3 (Cr-Met) factorial arrangement. There was no effect of prepartum carbohydrate source on pre- and postpartum plasma concentrations of glucose, nonesterified fatty acids (NEFA), β-hydroxybutyrate (BHBA), insulin, glucagon, or insulin to glucagon ratio. However, cows fed the low NFC diet during the prepartum period tended to have greater plasma NEFA and lower BHBA concentrations postpartum. Liver glycogen concentrations tended to be greater on d 1 postpartum for cows fed low NFC prepartum. Supplementing 0.03 mg/kg of BW⁰.⁷⁵ of Cr as Cr-Met increased prepartum plasma glucose and glucagon concentrations and tended to decrease prepartum plasma NEFA concentrations compared with either 0 or 0.06 mg of Cr/kg of BW⁰.⁷⁵. Postpartum plasma glucose concentrations decreased linearly and glucagon concentrations were increased quadratically by administering increasing amounts of Cr-Met. Supplementing Cr-Met did not affect prepartum plasma concentrations of insulin or BHBA, postpartum NEFA or BHBA, or liver composition. There was an interaction of prepartum carbohydrate source and Cr-Met supplementation such that in vitro hepatic conversion of [1-¹⁴C]propionate to both CO₂ and glucose was similar or increased when Cr-Met was supplemented to cows fed the low NFC diet but decreased when Cr-Met was supplemented to cows fed the high NFC diet. Insulin addition in vitro did not affect hepatic metabolism of propionate on d 1 postpartum. Overall, both the NFC content of the prepartum diet and Cr-Met had only modest effects on metabolic indices in this experiment.

Thiazolidinediones (TZD) are potent, synthetic ligands for peroxisome proliferator activated receptor-gamma (PPAR-γ) that reduce plasma nonesterified fatty acids (NEFA) and potentiate the action of insulin in peripheral tissues of several species. Holstein cows (n=9) entering their second or greater lactation were used to determine whether late prepartum administration of TZD would affect periparturient metabolism and milk production. Cows were limit-fed a total mixed ration (TMR) during the prepartum period to provide no more than 130% of predicted energy requirements. During the postpartum period cows were fed a common TMR for ad libitum intake. Cows were administered either 2,4-TZD (4.0 mg/kg of body weight) or saline (control) by intrajugular infusion once daily from 25 d before expected parturition until parturition. Plasma samples were collected daily from 26 d before expected parturition through 7 d postpartum. Plasma NEFA concentrations decreased during the prepartum period (d −21 to −1; 70 vs. 83±4μEq/L) and tended to be decreased during the peripartum period (d −7 to d +7; 113 vs. 205±32μEq/L) due to prepartum TZD administration. Plasma concentrations of glucose were not affected by treatment; however, plasma β-hydroxybutyrate concentrations decreased in TZD-treated cows (8.6 vs. 10.7±1.7 mg/dL) as parturition approached, and plasma insulin concentrations increased during the peripartum period (0.65 vs. 0.38±0.07 ng/mL). Postpartum liver triglyceride and glycogen content was not affected by treatment. Prepartum TZD administration tended to increase dry matter intake during the peripartum and postpartum periods (16.6 vs. 14.6±0.8 kg/d and 20.0 vs. 17.2±1.2 kg/d, respectively). Milk yield for the first 30 d postpartum and milk composition measured on d 8 postpartum were not affected by treatment. There was no effect of prepartum TZD administration on insulin-dependent glucose utilization assessed using insulin challenge during either the prepartum or postpartum periods. These results suggest that administration of TZD during the late prepartum period has the potential to improve metabolic health and DMI of periparturient dairy cows and warrants further investigation.

Holstein cows (n=72) entering second or later lactation were used to determine whether productive performance and dry matter intake (DMI) are affected by carbohydrate source in the prepartum diet and chromium-l-methionine (Cr-Met) supplementation throughout the periparturient period. Cows were fed either a TMR with the concentrate portion based on starch-based cereals [high nonfiber carbohydrate (NFC); 1.59 Mcal/kg of net energy for lactation (NEL), 14.4% crude protein (CP), 40.3% NFC] or a TMR with the concentrate portion based on nonforage fiber sources (low NFC; 1.54 Mcal/kg NEL, 14.5% CP, 33.6% NFC) from 21 d before expected parturition until parturition. After parturition all cows were fed a lactation TMR (1.74 Mcal/kg NEL, 16.5% CP, 40.0% NFC). The Cr-Met was supplemented once daily via gelatin capsule at dosages of 0, 0.03, or 0.06mg of Cr/kg of metabolic body weight. Thus, treatments were in a 2 (carbohydrate source)×3 (Cr-Met) factorial arrangement. Neither prepartum nor postpartum DMI was affected by prepartum dietary carbohydrate source. Administering increasing amounts of Cr-Met linearly increased milk yield and, subsequently, postpartum DMI. Prepartum carbohydrate source did not affect postpartum milk yield; however, cows fed the low NFC diet tended to yield milk with a lower content of total solids. These data indicate that prepartum carbohydrate source has little influence on performance during the immediate peripartal period, and that increases in milk yield for cows supplemented with Cr-Met are independent of prepartum dietary carbohydrate source.

Forty-eight Holstein cows, entering second or later lactation, were utilized to determine the effects of 2-hydroxy-4-(methylthio)-butanoic acid (HMB) on milk production, hepatic lipid metabolism, and gluconeogenesis during the periparturient period. Cows were fed one of 3 diets as TMR starting 21 d before expected calving. These diets contained 0 (the basal diet), 0.09 (+HMB), or 0.18 (++HMB)% HMB. From parturition to 84 DIM, cows were fed diets that contained 0, 0.13, or 0.20% HMB. Prepartum and postpartum dry matter intakes were similar among cows fed the basal diet, +HMB and ++HMB. There was a quadratic effect on milk yield such that cows fed +HMB had the greatest milk yield; yields of milk by cows fed the basal diet and ++HMB were similar. This led to trends for increased yields of 3.5% fat-corrected milk and total solids when cows were fed +HMB. Percentages of fat, protein, and total solids in milk were not affected by treatment. Despite differences in milk yield, calculated energy balance was not affected by treatment. Plasma concentrations of NEFA, β-hydroxybutyrate, and glucose were not different among treatments. Liver triglyceride content was similar among treatments on d 1 postpartum and was increased for cows consuming +HMB on d 21 postpartum compared with the other dietary treatments. Capacities for metabolism of [1-14C]palmitate by liver slices in vitro were not affected by treatment; however, conversion of [1-14C]propionate to CO2 and glucose decreased as the amount of HMB consumed by cows increased on d 21 postpartum. Cows consuming +HMB had greater days to first ovulation compared with cows consuming the basal diet and ++HMB as measured by plasma progesterone concentrations. These data suggest that adding HMB to low Met diets to achieve a predicted Met supply of approximately 2.3% of metabolizable protein supply is beneficial for increasing milk production but does not appear to benefit hepatic energy metabolism during early lactation.

Twenty Holstein cows in early lactation (7 d in milk) were administered 100 [micro]g of Escherichia coli lipopolysaccharide (LPS) dissolved in 10 mL of sterile 0.9% NaCl saline (treatment; TRT) or 10 mL of sterile saline (control) into both right mammary quarters to test the hypothesis that acute experimental mastitis would have negative impacts on aspects of energy metabolism that might lead to the development of metabolic disorders. A primed continuous intravenous infusion (14-[micro]mol/kg of BW priming dose; 11.5-[micro]mol/kg of BW per h continuous infusion) of 6,6-dideuterated glucose was used to determine pre- and posttreatment glucose kinetics using steady-state tracer methodologies. The LPS-treated cows displayed productive, clinical, and physiological signs of moderate to severe inflammation; control cows displayed no signs of immune activation. Pretreatment glucose rates of appearance (Ra) into plasma were similar (715 and 662 ± 33 mmol/h for TRT and control, respectively) between treatment groups. Intramammary LPS infusion into TRT cows resulted in increased glucose Ra relative to control cows (mean glucose Ra from 150 through 270 min after intramammary infusion were 815 and 674 ± 21 mmol/h for TRT and control cows, respectively). Furthermore, plasma concentrations of glucose increased, whereas plasma nonesterified fatty acids, glycerol, and {szligbeta}-hydroxybutyrate concentrations decreased, in TRT relative to control cows. Interestingly, plasma insulin concentration increased dramatically in TRT cows and occurred prior to the small increase in plasma glucose concentration. Although these results only represent the early stages of inflammation, they are not consistent with a causal relationship between mastitis and energy-related metabolic disorders and instead suggest a coordinated protective effect by the immune system on metabolism during the early stages of mammary insult.

Twenty Holstein cows in early lactation (7 d in milk) were administered 100μg of Escherichia coli lipopolysaccharide (LPS) dissolved in 10mL of sterile 0.9% NaCl saline (treatment; TRT) or 10mL of sterile saline (control) into both right mammary quarters to test the hypothesis that acute experimental mastitis would have negative impacts on aspects of energy metabolism that might lead to the development of metabolic disorders. A primed continuous intravenous infusion (14-μmol/kg of BW priming dose; 11.5-μmol/kg of BW per h continuous infusion) of 6,6-dideuterated glucose was used to determine pre- and posttreatment glucose kinetics using steady-state tracer methodologies. The LPS-treated cows displayed productive, clinical, and physiological signs of moderate to severe inflammation; control cows displayed no signs of immune activation. Pretreatment glucose rates of appearance (Ra) into plasma were similar (715 and 662±33 mmol/h for TRT and control, respectively) between treatment groups. Intramammary LPS infusion into TRT cows resulted in increased glucose Ra relative to control cows (mean glucose Ra from 150 through 270min after intramammary infusion were 815 and 674±21 mmol/h for TRT and control cows, respectively). Furthermore, plasma concentrations of glucose increased, whereas plasma nonesterified fatty acids, glycerol, and β-hydroxybutyrate concentrations decreased, in TRT relative to control cows. Interestingly, plasma insulin concentration increased dramatically in TRT cows and occurred prior to the small increase in plasma glucose concentration. Although these results only represent the early stages of inflammation, they are not consistent with a causal relationship between mastitis and energy-related metabolic disorders and instead suggest a coordinated protective effect by the immune system on metabolism during the early stages of mammary insult.