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Transition Period

BIOLOGY OF TRANSITION & ADAPTIVE MECHANISMS José Eduardo P. Santos Veterinary Medicine Teaching and Research Center School of Veterinary Medicine University of California - Davis. Transition Period. 3 wk before to 3 wk after parturition

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Transition Period

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  1. BIOLOGY OF TRANSITION & ADAPTIVE MECHANISMSJosé Eduardo P. SantosVeterinary Medicine Teaching and Research Center School of Veterinary MedicineUniversity of California - Davis

  2. Transition Period • 3 wk before to 3 wk after parturition • Biggest metabolic and endocrine challenge during the lactation cycle • Dramatic increase in nutrient requirements • Dramatic decrease in DMI • Period when the cow is most susceptible to metabolic and infectious problems

  3. Four Major Tasks Must be Achieved During the Transition Period: • Adapt the rumen to a high energy diet • Rumen papillae and microflora • Minimize the degree of negative EB • Maintain normocalcemia • Reduce the degree of immunosuppression around parturition

  4. Mechanisms of Adaptation by the Cow to Dietary Changes and the Onset of Lactation

  5. Rumen Papillae Measurements in Transition Dairy Cows

  6. Dietary Energy Concentration, Papillae Surface Area and Rate of VFA Absorption(Dirksen et al., 1985)

  7. VFA Absorption from the Forestomachs • Passive diffusion or transcellular transport • Damage to the epithelium of rumen papillae: Parakeratosis • Reduces VFA absorption from the forestomachs (keratinized epithelium works as a barrier) • Turnover time of rumen epithelium (Goodlad, 1985) • Sheep • high concentrate diet: 10.9 d

  8. Impaired VFA Absorption • VFA accumulation in the forestomachs • Propionate reduces smooth muscle motility • Increases osmolarity and decreases pH of the rumen fluid • Decreases DMI • Reduces energy absorption

  9. Impaired VFA Absorption • Predisposes the cow to digestive disorders: • Indigestion • Displacement of abomasum • Ruminal acidosis-laminitis

  10. Metabolic and Endocrine Adaptations • Dramatic increase in nutrient requirements (colostrum synthesis) • Cow has two mechanisms to compensate: • Increase DMI • Redistribute nutrients away from nonmammary tissues • However, DMI decreases!!

  11. Endocrine changes: • ­ bST levels • ­ ß-adrenergic receptors on adipose tissue • ­ insulin resistance in the adipose tissue  insulin concentration in plasma  glucagon concentration in plasma Altered ratio insulin:glucagon ­ activity of HS Lipase  IGF-1 concentration in blood

  12. Parturition: • ­ cortisol • ­ estrogens  progesterone Such changes increase hepatic gluconeogenesis and increase lipid mobilization from the adipose tissue Adaptation to supply precursors for lactose, fat and protein synthesis in milk

  13. Changes in the ratio lipolysis:lipogenesis • Increased liver output of glucose • Decrease in the ratio glycogen:TG in the liver • Increased protein synthetic activity of the liver • Higher plasma levels of: • NEFA • BHBA • Glucose

  14. Decreased plasma Ca and P • Decreased plasma retinol (38%), a-tocopherol (47%), and ß-carotene (30%) • Impaired leukocyte function: • Neutrophils exhibit impaired ability to ingest and kill bacteria • Lymphocytes exhibit depressed blastogenic activity • Results in lower antibody production

  15. Supply and Demands of Glucose for Transition Cows Fed for Ad Libitum Intake Adapted from Overton (1998)

  16. Decrease in Whole Body Glucose Oxidation in Cows During the Transition Period(Bennink et al., 1972)

  17. Conversion of Propionate and Alanine to Glucose During the Transition Period(Overton et al., 1998)

  18. Lipid Accumulation in the Liver Adipose tissue LIVER - Oxidized - Ketogenesis - Reesterified to TAG NEFA VLDL Other tissues

  19. Disposal of FA by the Bovine Liver • Oxidation of TAG by hepatic cells: • Limited by the lack of high hepatic lipase activity in ruminants • Limited by the lack of precursors for oxidation of Acetyl CoA • Limited by the lack of Carnithine to transport FA from the cytosol to the mitochondria of the cell

  20. Disposal of FA by the Bovine Liver • TAG secretion • Limited by the low secretion of VLDL • Limited TAG hydrolysis • Transfer of FFA from the cytosol of the cell to the SER • Activity of Microssomal Transfer Protein (TAG to the site of VLDL packaging) • Apo B synthesis and incorporation into VLDL • Ketogenesis

  21. Why Transition Cows are More Susceptible to Metabolic Disorders and Become Sick? Adaptation Failures • Digestive problems happen because the rumen epithelium and its microflora are not adapted to the new diet • Indigestion, rumen acidosis, displacement of abomasum, laminitis

  22. Problems related to mineral metabolism happen because the endocrine system is capable of setting homeorrhetic controls to overcome the high demand for minerals • Hypocalcemia • Immunosuppression: Decrease in plasma concentration of vitamins and minerals with antioxidant properties, energy and protein deficiency, endocrine challenges, and hypocalcemia • Retained placenta, mastitis, and secondary problems such as ketosis, LDA, and laminitis

  23. Immunosuppression • Progesterone drop (not a factor) • Estrogen rise (may play a role) • Cortisol rise (contributes, but too late) • Milk Production?? • Mastectomy study from Iowa

  24. Nutritional Strategies to Prevent Metabolic Disorders During Transition • Energy is the most important factor • Formulate diets with high fermentable energy content • This supplies energy as VFA and amino acids in the form of microbial protein • Adapts the rumen epithelium and its microflora to periods of high intakes of high energy diets • Avoid drastic changes in diet energy content ( 10%)

  25. Manage BCS at the End of Lactation • Difficult in one-group TMR herds • Reproductive efficiency is a key factor to avoid a large number of obese cows in the herd • Avoid any loss of BCS during the dry period • Weight loss will predispose cows to ketosis and subsequent problems

  26. Effect of BCS at Calving on LDA Incidence 1401 cows in 95 Michigan dairy herds (Dyk et al., 1995) Prepartum DMI, % BW * BCS < 3 1.76 > 3 to 4 1.76 > 4 1.65

  27. Adjust fiber level and forage source for the target group • Corn silage: high in fermentable energy, low in Na and K • Add some high quality long hay to the TMR to provide adequate physically effective NDF (23%) • Increases rumen fill, stimulates rumination and helps prevent digestive problems • Adjust CP for primiparous cows • Multiparous cows: more prone to TAG infiltration in the liver  Reduces ureagenesis • No evidence that feeding prepartum a high protein diet to mature cows is beneficial to lactation performance • Caution with high prepartum protein diets to Multiparous

  28. Use acidogenic salts whenever necessary for multiparous cows, but avoid it in prepartum heifer diets • Potential for reducing DMI • Data from laboratory animals suggest that a slight metabolic acidosis may: • compromise hepatic gluconeogenesis • reduce amino acid uptake by the liver for gluconeogenesis • Data from dairy cows: reduced insulin secretion and impaired hepatic uptake of NEFA

  29. Boost trace mineral and vitamin content of prepartum diets • Zn, CU, Se, Vit. E and Vit. A • This might partially minimize the degree of immunosuppression • Reduces incidence of new IMI • Use gluconeogenic precursors when necessary • Insulin response: inhibits HSL, which decreases the flux of NEFA from the adipose tissue and reduces ketogenesis

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