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      Biology of Dairy Cows During the Transition Period: the Final Frontier?

      Journal of Dairy Science
      American Dairy Science Association

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          Physiological changes at parturition and their relationship to metabolic disorders.

          Most of the metabolic diseases of dairy cows-milk fever, ketosis, retained placenta, and displacement of the abomasum-occur within the first 2 wk of lactation. The etiology of many of those metabolic diseases that are not clinically apparent during the first 2 wk of lactation, such as laminitis, can be traced back to insults that occurred during early lactation. In addition to metabolic disease, the overwhelming majority of infectious disease, in particular mastitis, becomes clinically apparent during the first 2 wk of lactation. Three basic physiological functions must be maintained during the periparturient period if disease is to be avoided: adaptation of the rumen to lactation diets that are high in energy density, maintenance of normocalcemia, and maintenance of a strong immune system. The incidence of both metabolic and infectious diseases is greatly increased whenever one or more of these physiological functions are impaired. This paper discusses the etiological role of each of these factors in the development of common diseases encountered during the periparturient period.
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            Etiology of lipid-related metabolic disorders in periparturient dairy cows.

            R Grümmer (1993)
            Plasma NEFA concentrations increase prior to and at parturition, resulting in increased fatty acid uptake by the liver, fatty acid esterification, and triglyceride storage. Liver triglyceride concentration increases four- to fivefold between d 17 prior to calving and d 1 following calving. Increases in liver triglyceride following calving do not appear to be dramatic. Severity of fatty liver 1 d postpartum is correlated negatively with feed intake 1 d prepartum. Export of newly synthesized triglyceride as very low density lipoprotein occurs slowly in ruminants and is a major factor in the development of fatty liver. Nutritional strategies to minimize the elevation in plasma NEFA prior to calving results in lower liver triglyceride at calving. Fatty liver probably precedes clinical spontaneous ketosis. Liver triglyceride to glycogen ratio may be used to predict susceptibility of cows to ketosis. Consequently, strategies to reduce liver triglyceride at calving may decrease incidence of ketosis. Research to determine methods to reduce fatty acid delivery to the liver or to enhance hepatic export of very low density lipoprotein near calving is warranted. Identification of the cause for the slow rate of assembly and secretion of hepatic very low density lipoprotein in ruminants will be required to assess the feasibility of increasing export of very low density lipoprotein.
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              Regulation of mammalian acetyl-coenzyme A carboxylase.

              H. Kim (1996)
              Long-chain fatty acids are involved in all aspects of cellular structure and function. For controlling amounts of fatty acids, cells are endowed with two acetyl-coenzyme A carboxylase (ACC) systems. ACC-alpha is the rate-limiting enzyme in the biogenesis of long-chain fatty acids, and ACC-beta is believed to control mitochondrial fatty acid oxidation. These two isoforms of ACC control the amount of fatty acids in the cells. Phosphorylation and dephosphorylation of ACC-alpha cause enzyme inactivation and activation, respectively, and serve as the enzyme's short-term regulatory mechanism. Covalently modified enzymes become more sensitive toward cellular metabolites. In addition, many hormones and nutrients affect gene expression. The gene products formed are heterogeneous and tissue specific. The ACC-beta gene is located on human chromosome 12; the cDNA for this gene has just been cloned. The gene for the alpha-isoform is located on human chromosome 17. The catalytic core of the beta-isoform is homologous to that of the alpha-isoform, except for an additional peptide of about 150 amino acids at the N terminus. This extra peptide sequence makes the beta-form about 10,000 daltons larger, and it is thought to be involved in the unique role that has been assigned to this enzyme. The detailed control mechanisms for the beta-isoform are not known.
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                Author and article information

                Journal
                Journal of Dairy Science
                Journal of Dairy Science
                American Dairy Science Association
                00220302
                November 1999
                November 1999
                : 82
                : 11
                : 2259-2273
                Article
                10.3168/jds.S0022-0302(99)75474-3
                10575597
                bc60a388-d44e-4d14-9c66-6d478caba3b1
                © 1999
                History

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