Feeding rations with low dietary cation-anion difference (DCAD) to dairy cows during late gestation is a common strategy to prevent periparturient hypocalcemia. Although the efficacy of low-DCAD rations in reducing the incidence of clinical hypocalcemia is well documented, potentially deleterious effects have not been explored in detail. The objective of the study presented here was to determine the effect of fully compensated metabolic acidosis on calcium and phosphorus homeostasis, insulin responsiveness, and insulin sensitivity as well as on protein metabolism. Twenty multiparous Holstein-Friesian dairy cows were assigned to 1 of 2 treatment groups and fed a low-DCAD ration (DCAD = -9 mEq/100g, group L) or a control ration (DCAD = +11 mEq/100g, group C) for the last 3 wk before the expected calving date. Blood and urine samples were obtained periodically between 14 d before to 14 d after calving. Intravenous glucose tolerance tests and 24-h volumetric urine collection were conducted before calving as well as 7 and 14 d postpartum. Cows fed the low-DCAD ration had lower urine pH and higher net acid excretion, but unchanged blood pH and bicarbonate concentration before calving. Protein-corrected plasma Ca concentration 1 d postpartum was higher in cows on the low-DCAD diet when compared with control animals. Urinary Ca and P excretion was positively associated with urine net acid excretion and negatively associated with urine pH. Whereas metabolic acidosis resulted in a 6-fold increase in urinary Ca excretion, the effect on renal P excretion was negligible. A more pronounced decline of plasma protein and globulin concentration in the periparturient period was observed in cows on the low-DCAD diets resulting in significantly lower total protein and globulin concentrations after calving in cows on low-DCAD diets. Intravenous glucose tolerance tests conducted before and after calving did not reveal group differences in insulin response or insulin sensitivity. Our results indicate that fully compensated metabolic acidosis increased the Ca flux resulting in increased urinary calcium excretion before calving and increased plasma Ca concentration on the day after calving, whereas the effect on P homeostasis was unlikely to be clinically relevant. The clinical relevance of the effect of metabolic acidosis on the plasma protein and globulin concentration is unclear but warrants further investigation.

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The effect of adding an oral rehydration therapy (ORT) solution containing bicarbonate, citrate, and acetate to cow's milk on milk clotting, abomasal luminal pH, and abomasal emptying rate was determined in suckling calves. Six male Holstein-Friesian calves with abomasal cannulae, 5 to 13 d of age, were used in a crossover design. Calves were fed 2 L of cow's milk alone, milk with an ORT solution containing a low bicarbonate concentration (25 mmol/L), acetate (12 mmol/L), citrate (12 mmol/L), and glycine (7 mmol/L; group BACG), or milk with an ORT solution containing formate (58 mmol/L) and acetate (15 mmol/L) in randomized order. Clotting of milk was assessed in vivo and in vitro. Abomasal luminal pH was monitored continuously. Abomasal emptying rates were determined by using the change in abomasal luminal pH, acetaminophen absorption, and glucose absorption. The addition of a BACG-ORT solution to cow's milk increased in vitro clotting time by approximately 6 min. All 3 test solutions clotted in vivo by 15 min after the beginning of suckling. The addition of a BACG-ORT solution to cow's milk increased the pH of cow's milk and abomasal fluid by approximately 0.3 pH units. The addition of a BACG-ORT or a formate and acetate-ORT solution to cow's milk increased solution osmolality and slowed the rate of abomasal emptying. We concluded that the addition of BACG-ORT solution to cow's milk did not affect milk clotting in vivo. Recommendations based on the results of in vitro studies that bicarbonate- or citrate-containing ORT solutions should not be fed concurrently with cow's milk do not appear to be relevant to in vivo conditions when 2 L of a low-bicarbonate (25 mmol/L), low-citrate (12 mmol/L) ORT solution is fed.

Results suggested hypokalemia was associated with hypochloremia, alkalemia, low feed intake with high amount of milk produced, hypovolemia, and hyperglycemia in lactating dairy cows. Treatment of hypokalemia should include surgical correction of abomasal displacement, increased dietary potassium intake via dietary dry matter intake or oral administration of KCl, and correction of hypochloremia, alkalemia, metabolic alkalosis, and dehydration.

Over the last decades, several genetic disorders have been discovered in cattle. However, the genetic background of disorders in calves is less reported. Recently, German cattle farmers reported on calves from specific matings with chronic diarrhea and retarded growth of unknown etiology. Affected calves did not respond to any medical treatment and died within the first months of life. These calves were underdeveloped in weight and showed progressive and severe emaciation despite of normal feed intake. Hallmark findings of the blood biochemical analysis were pronounced hypocholesterolemia and deficiency of fat-soluble vitamins. Results of the clinical and blood biochemical examination had striking similarities with findings reported in human hypobetalipoproteinemia. Postmortem examination revealed near-complete atrophy of the body fat reserves including the spinal canal and bone marrow. To identify the causal region, we performed a genome-wide association study with 9 affected and 21,077 control animals genotyped with the Illumina BovineSNP50 BeadChip (Illumina Inc., San Diego, CA), revealing a strong association signal on BTA 11. Subsequent autozygosity mapping identified a disease-associated haplotype encompassing 1.01 Mb. The segment of extended homozygosity contains 6 transcripts, among them the gene APOB, which is causal for cholesterol disorders in humans. However, results from multi-sample variant calling of 1 affected and 47 unaffected animals did not detect any putative causal mutation. The disease-associated haplotype has an important adverse effect on calf mortality in the homozygous state when comparing survival rates of risk matings vs. non-risk matings. Blood cholesterol values of animals are significantly associated with the carrier status indicating a codominant inheritance. The frequency of the haplotype in the current Holstein population was estimated to be 4.2%. This study describes the identification and phenotypic manifestation of a new Holstein haplotype characterized by pronounced hypocholesterolemia, chronic emaciation, growth retardation, and increased mortality in young cattle, denominated as cholesterol deficiency haplotype. Our genomic investigations and phenotypic examinations provide additional evidence for a mutation within the APOB gene causing cholesterol deficiency in Holstein cattle.