29 research outputs found

    Managing Dairy Heifer Growth Investment

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    Accelerated prepubertal growth rates can lower heifer raising costs but may put heifers at risk for impaired mammary development and have been found to be detrimental decreased to milk production in the first lactation. The tradeoff between heifer raising costs and milk production loss is examined in a capital budgeting model. Monthly annuity net present value of a heifer investment through the first lactation is assessed for heifers calving at 20, 22, 24, 26 and 28 months of age. A 24 mo AFC base case strategy with 9009.5 kg subsequent first lactation milk yields 7.34inreturnspermonth.Acceleratedgrowthresultedinhigherreturns(7.34 in returns per month. Accelerated growth resulted in higher returns (12.77/mo for 20 mo AFC; 9.86/mofor22moAFC)whenmilkproductionisnotaffectedastotalraisingcostsdeclinerelativetothebasecase.Slowergrowthresultedinlowerreturns(9.86/mo for 22 mo AFC) when milk production is not affected as total raising costs decline relative to the base case. Slower growth resulted in lower returns (5.12/mo for 26 mo AFC; $3.15/mo for 28 mo AFC). When milk production declines, revenues decline as do feed and marketing costs which are a function of milk produced. Adjusting for factors, breakeven milk production losses were 10.6 % for 20 mo AFC and 5.3 % for 22 mo AFC relative to the 24 mo AFC base. These results were not sensitive to the assumed discount rate, heifer feed costs or discount rate. Other operation-specific heifer management factors including calving season, reproduction, herd size/expansion considerations and, in the longer-term, heifer facilities investments may be more significant economically than the differences found in this analysis.Heifer growth, Economics, Investment, Livestock Production/Industries,

    Managing Dairy Heifer Growth Investment

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    Accelerated prepubertal growth rates can lower heifer raising costs but may put heifers at risk for impaired mammary development and have been found to be detrimental decreased to milk production in the first lactation. The tradeoff between heifer raising costs and milk production loss is examined in a capital budgeting model. Monthly annuity net present value of a heifer investment through the first lactation is assessed for heifers calving at 20, 22, 24, 26 and 28 months of age. A 24 mo AFC base case strategy with 9009.5 kg subsequent first lactation milk yields 7.34inreturnspermonth.Acceleratedgrowthresultedinhigherreturns(7.34 in returns per month. Accelerated growth resulted in higher returns (12.77/mo for 20 mo AFC; 9.86/mofor22moAFC)whenmilkproductionisnotaffectedastotalraisingcostsdeclinerelativetothebasecase.Slowergrowthresultedinlowerreturns(9.86/mo for 22 mo AFC) when milk production is not affected as total raising costs decline relative to the base case. Slower growth resulted in lower returns (5.12/mo for 26 mo AFC; $3.15/mo for 28 mo AFC). When milk production declines, revenues decline as do feed and marketing costs which are a function of milk produced. Adjusting for factors, breakeven milk production losses were 10.6 % for 20 mo AFC and 5.3 % for 22 mo AFC relative to the 24 mo AFC base. These results were not sensitive to the assumed discount rate, heifer feed costs or discount rate. Other operation-specific heifer management factors including calving season, reproduction, herd size/expansion considerations and, in the longer-term, heifer facilities investments may be more significant economically than the differences found in this analysis

    Intramammary infusion of leptin decreases proliferation of mammary epithelial cells in prepubertal heifers

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    High energy intake and excessive body fatness impair mammogenesis in prepubertal ruminants. High energy intake and excessive fatness also increase serum leptin. Our objective was to determine if an infusion of leptin decreases proliferation of mammary epithelial cells of prepubertal heifers in vivo. Ovine leptin at 100 μg/ quarter per d with or without 10 μg of insulin-like growth factor (IGF)-I was infused via the teat canal into mammary glands of prepubertal dairy heifers; contralateral quarters were used as controls. After 7 d of treatment, bromodeoxyuridine was infused intravenously and heifers were slaughtered sim;2 h later. Tissue from 3 regions of the mammary parenchyma was collected and immunostained for bromodeoxyuridine (BrdU), proliferating cell nuclear antigen (Ki-67), and caspase-3. Leptin decreased the number of mammary epithelial cells in the S-phase of the cell cycle by 48% in IGF-I-treated quarters and by 19% in saline-treated quarters. Leptin did not alter the number of mammary epithelial cells within the cell cycle, as indicated by Ki-67 labeling. Caspase-3 immunostaining within the mammary parenchyma was very low in these heifers, but leptin significantly increased labeling in saline-treated quarters. Leptin enhanced SOCS-3 expression in IGF-I-treated quarters but did not alter SOCS-1 or SOCS-5 expression. We conclude that a high concentration of leptin in the bovine mammary gland reduces proliferation of mammary epithelial cells. The reduced proliferation is accompanied by an increase in SOCS-3 expression, suggesting a possible mechanism for leptin inhibition of IGF-I action. Whether leptin might be a physiological regulator of mammogenesis remains to be determined

    Harnessing the genetics of the modern dairy cow to continue improvements in feed efficiency

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    Feed efficiency, as defined by the fraction of feed energy or dry matter captured in products, has more than doubled for the US dairy industry in the past 100 yr. This increased feed efficiency was the result of increased milk production per cow achieved through genetic selection, nutrition, and management with the desired goal being greater profitability. With increased milk production per cow, more feed is consumed per cow, but a greater portion of the feed is partitioned toward milk instead of maintenance and body growth. This dilution of maintenance has been the overwhelming driver of enhanced feed efficiency in the past, but its effect diminishes with each successive increment in production relative to body size and therefore will be less important in the future. Instead, we must also focus on new ways to enhance digestive and metabolic efficiency. One way to examine variation in efficiency among animals is residual feed intake (RFI), a measure of efficiency that is independent of the dilution of maintenance. Cows that convert feed gross energy to net energy more efficiently or have lower maintenance requirements than expected based on body weight use less feed than expected and thus have negative RFI. Cows with low RFI likely digest and metabolize nutrients more efficiently and should have overall greater efficiency and profitability if they are also healthy, fertile, and produce at a high multiple of maintenance. Genomic technologies will help to identify these animals for selection programs. Nutrition and management also will continue to play a major role in farm-level feed efficiency. Management practices such as grouping and total mixed ration feeding have improved rumen function and therefore efficiency, but they have also decreased our attention on individual cow needs. Nutritional grouping is key to helping each cow reach its genetic potential. Perhaps new computer-driven technologies, combined with genomics, will enable us to optimize management for each individual cow within a herd, or to optimize animal selection to match management environments. In the future, availability of feed resources may shift as competition for land increases. New approaches combining genetic, nutrition, and other management practices will help optimize feed efficiency, profitability, and environmental sustainability

    Guidelines to measure individual feed intake of dairy cows for genomic and genetic evaluations

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    The widespread use of genomic information in dairy cattle breeding programs haspresented the opportunity to select for feed intake and feed efficiency. This is becauseanimals from research herds can be used as a reference population to calibrate a genomicprediction equation, which is then used to predict the breeding value for selectioncandidates based on their own genotype. To implement genomic prediction and performgenetic analysis for feed intake, several partners have brought together their expertiseand existing feed intake records. Based on this experience we aim to provide someguidelines on the recording and handling of feed intake records. The consortium used amixture of standardised experimental data coming from larger genetic experiments orseveral smaller nutritional studies. The latter has provided some statistical challenges.Also, data was combined across countries, experimental herds and feeding systems. Despitethe perceived roughness of such data, it has proven to be very successful for genomicprediction, with proper statistical modelling. Ideally the whole lifetime of all cows shouldbe measured, but this is unrealistic. Often, animals are recorded for part of one (or more)lactation(s) only. Guidelines on the proper statistical modelling and usefulness of existingdata are needed. Selection index theory can help to establish the optimal recording periodacross and within lactation. It is also critical to identify how many records are requiredand what are the most informative animals for measuring feed intake. Geneticrelationships with the selection candidates are an important criterion. Finally, since(residual) feed intake is only part of the breeding goal, it is important to consider recordingof other traits as well, and the genetic parameters are needed to define the breeding goalsproperly

    Effects of short- and long-chain fatty acids on the expression of stearoyl-CoA desaturase and other lipogenic genes in bovine mammary epithelial cells

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    Stearoyl-CoA desaturase (SCD) in the bovine mammary gland introduces a cis-double bond at the ¿9 position in a wide range of fatty acids (FA). Several long-chain polyunsaturated fatty acids (PUFA) inhibit expression of SCD, but information on the effect of short-chain fatty acids on mammary SCD expression is scarce. We used a bovine mammary cell line (MAC-T) to assess the effect of acetic acid (Ac) and ß-hydroxybutyric acid (BHBA) in comparison with the effect of various long-chain fatty acids on the mRNA expression of the lipogenic enzymes SCD, acetyl-CoA carboxylase (ACACA), fatty acid synthase (FASN) and their associated gene regulatory proteins sterol regulatory element binding transcription factor 1 (SREBF1), insulin-induced gene 1 protein (INSIG1) and peroxisome proliferator-activated receptor alpha (PPARA)and peroxisome proliferator-activated receptor delta (PPARD) by quantitative real-time PCR. MAC-T cells were treated for 12 h without FA additions (CON) or with either 5 mM Ac, 5 mM BHBA, a combination of 5 mM Ac + 5 mM BHBA, 100 µM C16:0, 100 µM C18:0, 100 µM C18:1 cis-9, 100 µM C18:1 trans-11, 100 µM C18:2 cis-9,12 or 100 µM C18:3 cis-9,12,15. Compared with control, mRNA expression of SCD1 was increased by Ac (+61%) and reduced by C18:1 cis-9 (-61%), C18:2 cis-9,12 (-84%) and C18:3 cis-9,12,15 (-88%). In contrast to native bovine mammary gland tissue, MAC-T cells did not express SCD5. Expression of ACACA was increased by Ac (+44%) and reduced by C18:2 cis-9,12 (-48%) and C18:3 cis-9,12,15 (-49%). Compared with control, FASN expression was not significantly affected by the treatments. The mRNA level of SREBF1 was not affected by Ac or BHBA, but was reduced by C18:1 cis-9 (-44%), C18:1 trans-11 (-42%), C18:2 cis-9,12 (-62%) and C18:3 cis-9,12,15 (-68%) compared with control. Expression of INSIG1 was downregulated by C18:0 (-37%), C18:1 cis-9 (-63%), C18:1 trans-11 (-53%), C18:2 cis-9,12 (-81%) and C18:3 cis-9,12,15 (-91%). Both PPARA and PPARD expression were not significantly affected by the treatments. Our results show that Ac upregulated mRNA expression of SCD1 and ACACA in MAC-T cells. The opposite effect of the PUFA C18:2 cis-9,12 and C18:3 cis-9,12,15 on the these genes and the failure of Ac to mimic the PUFA-inhibited SREBF1 and INSIG1 mRNA expression, suggest that Ac can stimulate mammary lipogenesis via a transcriptional regulatory mechanism different from PUFA
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