Enzymes and Factors Controlling Vitamin D Metabolism and Action in Normal and Milk Fever Cows

• Published in: Journal of dairy science 1991-11, Vol.74 (11), p.4022-4032
• Main Authors: Goff, Jesse P., Reinhardt, Timothy A., Horst, Ronald L.
• Format: Article
• Language: English
• Subjects: Absorption; AGE; Aging - metabolism; Animals; Biological and medical sciences; Bone and Bones - metabolism; CALCIO; Calcitriol - secretion; CALCIUM; Calcium - metabolism; Cattle; Cattle Diseases - etiology; Cattle Diseases - metabolism; DIETA; ECHANGE D'ION; EDAD; Female; FIEVRE VITULAIRE; Fundamental and applied biological sciences. Psychology; General aspects; HORMONAS; HORMONE; Hypocalcemia - complications; Hypocalcemia - veterinary; INTERCAMBIO IONICO; INTESTIN; INTESTINOS; LACTACION; LACTATION; Lactation - metabolism; milk fever; PARALISIS PUERPERAL; Parathyroid Hormone - secretion; parturient paresis; Parturient Paresis - etiology; Parturient Paresis - metabolism; PEPTIDE; PEPTIDOS; PLASMA SANGUIN; PLASMA SANGUINEO; Pregnancy; RECEPTEUR D'HORMONE; RECEPTORES DE HORMONAS; receptors; REGIME ALIMENTAIRE; VACAS LECHERAS; VACHE LAITIERE; Vertebrates: anatomy and physiology, studies on body, several organs or systems; vitamin D; Vitamin D - metabolism; VITAMINA D; VITAMINE D
• ISSN: 0022-0302; 1525-3198
• DOI: 10.3168/jds.s0022-0302(91)78597-4

In milk fever (parturient paresis), calcium homeostatic mechanisms, regulated by parathyroid hormone and 1,25-dihydroxyvitamin D, fail to maintain normal blood calcium concentrations, resulting in severe hypocalcemia. The precise nature of the endocrine defect is unknown. Secretion of parathyroid hormone and production of 1,25-dihydroxyvitamin D is similar in most cows with milk fever or without. However, there are some cows that fail to produce adequate 1,25-dihydroxyvitamin D at the onset of lactation. These tend to be cows that will suffer prolonged hypocalcemia and relapse after treatment. Assuming that most cows produce adequate amounts of both hormones, the next logical cause of milk fever might be a failure of tissues to respond to calcium-regulating hormones. Older cows are more likely to develop milk fever than younger ones. We have found that tissue 1,25-dihydroxyvitamin D receptor concentrations decline with age, leaving the tissues less able to respond to 1,25-dihydroxyvitamin D. We also have found that tissue 1,25-dihydroxyvitamin D receptor concentrations increase during pregnancy and lactation in the cow. Intestinal 1.25-dihydroxyvitamin D receptor concentration does not appear to be different in cows with or without milk fever in cows of similar ages. However, intestinal 1,25-dihydroxyvitamin D receptor numbers decrease precipitously at parturition, which may in part be responsible for the development of hypocalcemia in dairy cattle.