This study aimed to estimate individual and herd-level energy balance (EB) using blood and milk traits in 90 multiparous high-yielding Holstein cows, held on a research farm, from wk 1 to 10 postpartum (p.p.) and to investigate the precision of prediction with successively decreased data sets simulating smaller herd sizes and with pooled samples. Dry matter intake, milk yield, and BW were measured daily from parturition through wk 10 p.p. Milk composition was determined 4 times per week, and milk acetone was measured weekly. Blood samples for the determination of metabolites, hormones, electrolytes, and enzyme activities were taken weekly from wk 1 to 10 p.p. between 0730 and 0900. Body condition scores and ultrasonic measurements of backfat thickness and fat depth in the pelvic area were evaluated in wk 1, 4, and 8 p.p. Concentrations of glucose, cholesterol, urea, insulin, insulin-like growth factor-1, triiodothyronine, and thyroxine (T4) in blood plasma and of lactose and urea in milk were positively correlated with EB, whereas concentrations of nonesterified fatty acids (NEFA), creatinine, albumin, beta-hydroxybutyrate, and growth hormone and enzyme activities in blood, and concentrations of fat, protein, fat:lactose ratio, and acetone in milk were negatively correlated with EB. Leptin concentration was not correlated to EB over the first 10 wk p.p. To estimate EB linear mixed-effects, models were developed by backward selection procedures. The most informative traits for estimation of EB were the fat:lactose ratio in milk and NEFA and T4 concentrations in blood. The precision of estimation of EB in individual cows was low. Using blood in addition to milk traits did not result in higher precision of estimation of herd-level EB, and decreasing sample sizes considerably lowered the precision of EB prediction. Estimation of overall mean herd-level EB over the first 10 wk p.p. using pooled samples was precise even with small sample sizes, but does not consider the level of EB in particular weeks. In conclusion, estimation of herd-level EB at individual weeks using milk traits only has practical implication with herd sizes of > or = 100 cows if calving is highly seasonal and of or = 400 cows if calving is uniformly distributed. Using blood in addition to milk traits does not improve precision of estimation of herd-level EB, regardless of sample size.

We studied the effects of amounts of colostrum consumed on intestinal morphology and proliferation and digestive enzyme activities in neonatal calves. Group GrCmax calves were fed colostrum from the first milking undiluted on d 1-3 and diluted with 25, 50, 75 and 75 parts of a milk replacer on d 4-7. Group GrC1-3 calves were fed colostrum from milkings 1-6 up to d 3 and then a milk replacer up to d 7. Group GrF1-3 calves were fed a milk-based formula (containing only traces of growth factors and hormones) up to d 3 and then a milk replacer up to d 7. Calves were killed on d 8. Differences in feeding affected villus sizes and villus height/crypt depth ratios in the duodenum (GrCmax > GrC1-3), villus areas and villus height/crypt depth ratios in the jejunum (GrC1-3 > GrF1-3) and crypt depths in the colon (GrF1-3 > GrC1-3). Furthermore, different feeding protocols affected the proliferation rates of epithelial cells in the duodenum (GrC1-3 > GrCmax; GrC1-3 > GrF1-3) and the jejunum (GrF1-3 > GrC1-3; based on Ki-67 labeling). Lipase activities in the pancreas were influenced by colostrum feeding (GrC(max) > GrC(1-3)). Colostrum intake differentially affected intestinal epithelial surface and proliferation and enzyme activities. Feeding high amounts of first colostrum seemed to enhance the survival of mature mucosal epithelial cells in selected parts of the small intestine, whereas the lack of colostrum seemed to decrease epithelial growth.

Plasma glucose concentrations in neonates are influenced by colostrum feeding and by glucocorticoids. We have tested whether a high-glucocorticoid status after birth, as well as colostrum feeding, influences glucose metabolism in association with changes of hepatic expression and activities of gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) and pyruvate carboxylase (PC; EC 6.4.1.1) in neonatal calves. Calves (n = 14 per group) were fed either colostrum or a milk-based formula with nutrient and energy contents similar to colostrum. Half the calves in each feeding group were treated with dexamethasone (DEXA; 30 microg/[kg BW x d]). Pre- and postprandial blood samples were taken on d 1, 2, 4, and 5 and liver samples were collected on d 5 of life. Dexamethasone treatment increased (P < or = 0.05) plasma concentrations of glucose, insulin, and glucagon more in colostrum-fed than in formula-fed calves but increased (P < or = 0.05) urea concentrations and decreased (P < or = 0.05) concentrations of NEFA, ACTH, and cortisol independent of colostrum vs. formula feeding. Colostrum feeding increased (P < 0.05) plasma glucose, but decreased (P < 0.05) plasma urea concentrations. Glucagon-to-insulin ratios in DEXA-treated and colostrum-fed calves were decreased (P < 0.05). Dexamethasone treatment decreased hepatic mRNA levels and activities of PC (P < 0.001 and P < 0.10) and activities of PEPCK (P < 0.001) but increased (P < 0.001) the glycogen content. Colostrum feeding increased (P < 0.05) mitochondrial PEPCK mRNA levels and PEPCK activities in calves not treated with DEXA but decreased (P < 0.1) amounts of PC mRNA. In conclusion, increased plasma glucose concentrations after DEXA treatment were not associated with a stimulation of hepatic gluconeogenic enzyme activities; however, colostrum feeding probably raised plasma glucose concentrations because of increased hepatic gluconeogenic activities.

No abstract

The neonatal development of the gastrointestinal tract around parturition in precocious mammals is greatly affected by endocrine factors like glucocorticoids as well as by nutritional factors. We have studied the effects of glucocorticoids and colostrum supply on intestinal morphology, cell proliferation, digestive enzyme activities, and xylose absorption in neonatal calves to test the hypothesis that the intestinal development in neonatal calves is influenced by glucocorticoids, dependent on colostrum feeding. Calves designated GrFD^– and GrFD⁺ were fed a milk-based formula, whereas those designated GrCD^– and GrCD⁺ received colostrum. Dexamethasone (DEXA; 30 µg/kg/day) was injected at feeding times to calves of GrFD⁺ and GrCD⁺. On day 3, the D-xylose absorption was measured. The calves were euthanized on day 5 of life. Colostrum feeding increased villus sizes in jejunum and ileum, enhanced xylose absorption capacity, and increased peptidase activities in the ileum. DEXA treatment diminished sizes and cell proliferation rates of Peyer’s patches in the ileum, yet increased proliferation of crypt cells in the ileum of formula-fed calves. DEXA reduced aminopeptidase N activities in the jejunum of formula-fed calves, but increased the peptidase activities mainly of colostrum-fed calves in the ileum. Thus, DEXA effects depended on intestinal segment and on different feeding, resulting in stimulation of crypt cell proliferation in the less mature ileum (of formula-fed calves) and in stimulation of peptidase activities in the more mature ileum (of colostrum-fed calves). We conclude that the effects of DEXA were related to the developmental stage of the neonatal intestine and promoted the intestinal development, depending on the developmental stage.