Effect of yeast culture (Saccharomyces cerevisiae) on adaptation of cows to postpartum diets and on lactational performance.
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Multiparous (n = 26) and primiparous (n = 18) Holstein cows were fed prepartum and postpartum total mixed diets that were, or were not, supplemented with a yeast culture (YC) for approximately 23 d prepartum and 56 d postpartum. Multiparous cows supplemented with YC selected a prepartum diet higher in CP than did unsupplemented cows, although prepartum performance of cows of both parities, as assessed by DMI and measures of body status, was not influenced by YC. The extent of the prepartum DMI depression was not influenced by YC supplementation in cows of either parity. An intake behavior study with six multiparous cows suggested that cows supplemented with YC exhibited repeated diurnal feed intake patterns until approximately 7 d prepartum, vs 10 d prepartum for unsupplemented cows. Cows of both parities supplemented with YC had numerically higher DMI and production of milk and milk components, although only DMI for multiparous cows and milk production for primiparous cows approached statistical significance. Intake behavior results suggested that cows supplemented with YC achieved repeated diurnal feed intake patterns by approximately 14 d postpartum, vs 20 d postpartum for unsupplemented cows. Concentrations of ruminal metabolites and pH did not differ between treatments, although ruminal fluid collection occurred while diurnal feed intake patterns were repeated (regular). Overall, our results can be interpreted to support a trend toward a modest postpartum improvement in performance of primiparous and multiparous cows supplemented with this YC for 23 d prepartum and 56 d postpartum. However, primiparous cows seemed to achieve this modest overall improvement primarily through enhanced postpartum DMI, whereas in multiparous cows it was due almost equally to enhanced postpartum DMI and higher energy density of the diet. (+info)
Metabolic adaptation of endothelial cells to substrate deprivation.
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Endothelial cells are known to be metabolically rather robust. To study the mechanisms involved, porcine aortic endothelial cells (PAEC), cultured on microcarrier beads, were perfused with glucose (10 mM) or with substrate-free medium. Substrate-free perfusion for 2 h induced an almost complete loss of nucleoside triphosphates (31P-NMR) and decreased heat flux, a measure of total energy turnover, by >90% in parallel microcalorimetric measurements. Heat flux and nucleoside triphosphates recovered after addition of glucose. Because protein synthesis is a major energy consumer in PAEC, the rate of protein synthesis was measured ([14C]leucine incorporation). Reduction or blockade of energy supply resulted in a pronounced reduction in the rate of protein synthesis (up to 80% reduction). Intracellular triglyceride stores were decreased by approximately 60% after 2 h of substrate-free perfusion. Under basal perfusion conditions, PAEC released approximately 30 pmol purine. mg protein-1. min-1, i.e., 16% of the cellular ATP per hour, while ATP remained constant. Substrate deprivation increased the release of various purines and pyrimidines about threefold and also induced a twofold rise in purine de novo synthesis ([14C]formate). These results demonstrate that PAEC are capable of recovering from extended periods of substrate deprivation. They can do so by a massive downregulation of their energy expenditure, particularly protein synthesis, while at the same time using endogenous triglycerides as substrates and upregulating purine de novo synthesis to compensate for the loss of purines. (+info)
Metabolic adjustments during daily torpor in the Djungarian hamster.
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Djungarian hamsters (Phodopus sungorus) acclimated to a short photoperiod (8:16-h light-dark cycle) display spontaneous daily torpor with ad libitum food availability. The time course of body temperature (Tb), metabolic rate, respiratory quotient (RQ), and substrate and enzyme changes was measured during entrance into torpor and in deep torpor. RQ, blood glucose, and serum lipids are high during the first hours of torpor but then gradually decline, suggesting that glucose is the primary fuel during the first hours of torpor, with a gradual change to lipid utilization. No major changes in enzyme activities were observed during torpor except for inactivation of the pyruvate dehydrogenase (PDH) complex in liver, brown adipose tissue, and heart muscle. PDH inactivation closely correlates with the reduction of total metabolic rate, whereas in brain, kidney, diaphragm, and skeletal muscle, PDH activity was maintained at the initial level. These findings suggest inhibition of carbohydrate oxidation in heart, brown adipose tissue, and liver during entrance into daily torpor. (+info)
Pancreatic function in CCK-deficient mice: adaptation to dietary protein does not require CCK.
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A CCK-deficient mouse mutant generated by gene targeting in embryonic stem cells was analyzed to determine the importance of CCK for growth and function of the exocrine pancreas and for pancreatic adaptation to dietary changes. RIAs confirmed the absence of CCK in mutant mice and demonstrated that tissue concentrations of the related peptide gastrin were normal. CCK-deficient mice are viable and fertile and exhibit normal body weight. Pancreas weight and cellular morphology appeared normal, although pancreatic amylase content was elevated in CCK-deficient mice. We found that a high-protein diet increased pancreatic weight, protein, DNA, and chymotrypsinogen content similarly in CCK-deficient and wild-type mice. This result demonstrates that CCK is not required for protein-induced pancreatic hypertrophy and increased proteolytic enzyme content. This is a novel finding, since CCK has been considered the primary mediator of dietary protein-induced changes in the pancreas. Altered somatostatin concentrations in brain and duodenum of CCK-deficient mice suggest that other regulatory pathways are modified to compensate for the CCK deficiency. (+info)
Homeobox genes, fossils, and the origin of species.
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Ever since Darwin there has been a history of debate on the tempo and mode of evolution. Is speciation a gradual process involving the accumulation of minute variations extant within a species, or is it rapid, the result of major organismal reorganization? Does one define a species on the basis of genes, morphology, or geographic or reproductive isolation? In this communication I present a model of evolutionary change that is based on the Mendelian inheritance of mutations in regulatory genes and the fact that most nonlethal mutations arise in the recessive state. Since the new recessive allele will spread through many generations without expression until there is a critical mass of heterozygotes capable of producing homozygotes for the mutation, the novel feature thus produced will appear abruptly in the population and in more than one individual. This picture of punctuation is consistent with the fossil record, which typically fails to provide evidence of smoothly transitional states of morphological change. Given that the first of their kind in the fossil record are organisms in which their novel characteristics are often more fully expressed or complex than in their descendants, it would seem that, after the mutation involving a regulatory gene is introduced, the general tendency is for its effects to become diminished. Among the implications for speciation is that this process does not depend on either reproductive isolation or genetic incompatibility. Rather, barring effects on reproductive organs or behavior, homozygotes for a novelty should be able to breed with heterozygotes and homozygotes for the wild state of the original population. This, in turn, suggests that the species barrier between individuals is probably a matter of mate recognition. (+info)
Adaptation in the vertebral column: a comparative study of patterns of metameric variation in seven species of small mammals.
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The pattern of variation of certain vertebral measurements along the vertebral column is known to differ in man and mouse. This paper investigates changes in this pattern in 7 species of small mammals and attempts to correlate them with locomotor adaptations and limb dimensions. (+info)
CD4(+) T cells and the proinflammatory cytokines gamma interferon and interleukin-6 contribute to alveolar bone loss in mice.
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In this study, we used a mouse model to examine the role of the adaptive immune response in alveolar bone loss induced by oral infection with the human gram-negative anaerobic bacterium Porphyromonas gingivalis. Severe combined immunodeficient mice, which lack B and T lymphocytes, exhibited considerably less bone loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute to this process. Bone loss after oral infection was decreased in mice deficient in major histocompatibility complex (MHC) class II-responsive CD4(+) T cells, but no change in bone loss was observed in mice deficient in MHC class I-responsive CD8(+) T cells or NK1(+) T cells. Mice lacking the cytokine gamma interferon or interleukin-6 also demonstrated decreased bone loss. These results suggest that the adaptive immune response, and in particular CD4(+) T cells and the proinflammatory cytokines that they secrete, are important effectors of bone loss consequent to P. gingivalis oral infection. The studies also reinforce the utility of the mouse oral infection model in dissecting the pathobiology of periodontal disease. (+info)
Evolutionary genetics: The economics of mutation.
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The presence of mutator genotypes in populations of bacteria may be favoured by selection because they produce rare beneficial mutations and thereby increase the rate of adaptive evolution. Recent work, however, shows that the relationship between mutation rates and adaptive evolution is more complicated. (+info)