~ 228 ~ The Pharma Innovation Journal 2019; 8(5): 228-230 ISSN (E): 2277- 7695 ISSN (P): 2349-8242 NAAS Rating: 5.03 TPI 2019; 8(5): 228-230 © 2019 TPI www.thepharmajournal.com Received: 12-03-2019 Accepted: 13-04-2019 K Sethy Assistant Professor, Department of Animal Nutrition, CV. Sc & AH, OUAT, Bhubaneswar, Odisha, India V Dhaigude MVSc. Scholar, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India RD Mukherjee MVSc. Scholar, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India P Dwibedy MVSc. Scholar, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India M Nayak MVSc Scholar, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India P Priyadarshinee MVSc Scholar, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India Correspondence K Sethy Assistant Professor, Department of Animal Nutrition, CVSc. & AH, OUAT, Bhubaneswar, Odisha, India Calcium homeostasis in transition cows K Sethy, V Dhaigude, RD Mukherjee, P Dwibedy, M Nayak, and P Priyadarshinee Abstract Milk fever is a metabolic disease of cows occurring around the time of parturition, generally within 48 hr after calving, but also occurs several weeks before or after calving. A decreased level of blood calcium is responsible for milk fever in transition cows. This is due to imbalance between calcium output in the colostrums and intake of calcium through feed. A cow producing 10 kg of colostrums will loose around 23g of calcium in single milking. This is about nine times as much as calcium present in the entire plasma calcium pool of the cow. The feedstuffs high in calcium and potassium can increase the occurrence of milk fever by reducing the mobilisation of calcium from the bones. Feeding anionic salt or manipulating the dietary cation and anion difference of the diet has become a common approach for maintaining calcium homeostasis in transition cows. Keywords: Cow, calcium, homeostasis, milk fever Introduction Milk fever, a complex metabolic disease, affects high producing dairy animals usually within one or two days after calving, resulting in a huge reduction in milk production and thus becomes economically most important. Although treatment with intravenous infusion of calcium salt solutions cure most clinical cases of hypocalcaemia, such cows are later more susceptible to other metabolic and infectious diseases (Curtis et al., 1985) [1] . Clinical symptoms of this disease include inappetence, tetany, inhibition of urination and defecation, lateral recumbency, and eventual coma and death if left untreated. It is also known as parturient paresis. It is estimated that this disease affects 3 to 8% of cows with some herds having prevalence as high as 25 to 30%. Symptoms appear when blood calcium levels are low; hence the synonym of milk fever is hypocalcaemia. Incidence of milk fever is increased with cow age. Economic losses due to medicines, veterinary services and reduced production increased significantly in a commercial farm with occurrence of milk fever (Mandali, 2004) [2] . Losses are also associated with increased incidence of secondary diseases, such as ketosis, mastitis, retained placenta, displacement of abomasum, uterine prolapse, limb injuries, and pneumonia can further inflate losses. Milk fever occurs in dairy cattle after calving because of low blood calcium levels as a result of calcium moving into milk (Chamberlain and Wilkinson, 1996) [3] . There are about 23 grams of calcium in 10 liters of colostrums, and when this is added to the normal amount of calcium needed for maintenance, the needs of the cow can be more than 10 times the supply of calcium in her bloodstream. When the demand for calcium is greater than the supply in the blood, it causes the problem of milk fever, unless the cow can rapidly mobilize stored calcium in her body (e.g. in bones) to offset the situation (Westerhuis, 1975) [4] . Calcium regulation mechanism Cattle can absorb Ca from gut according to their needs. They are able to alter the absorption efficiency to meet changes in Ca requirement. When cattle consume more Ca than needed, the proportion of Ca absorbed is decreased (Horst, 1986) [5] . Ca is regulated by parathyroid hormone (PTH) and calcitonin, which are secreted from parathyroid gland and thyroid gland respectively. The decrease in Ca intake stimulates the secretion of parathyroid hormone (PTH) from the parathyroid gland. PTH enhances renal reabsorption of Ca (Capen and Rosol, 1989) [6] and promotes the synthesis of 1,25- dihydroxycholecalciferol from 25- hydroxycholecalciferol in the kidney (Allen and Sansom, 1985) [7] . As result of stimulated 1,25-dihydroxycholecalciferol, bone Ca resorption and intestinal Ca absorption increase (Horst et al., 1997) [8] .