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Ketosis 2011 samiei
Ketosis 2011 samiei
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Ketosis 2011 samiei

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Ketosis in Dairy Herds

Ketosis in Dairy Herds

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  • Reducing the severity and duration of negative energy balance is crucial in the prevention of fatty liver and ketosis.
  • Superficial wall of greater omentum
    Deep wall of greater omentum
    Descending duodenum
  • Reduced ketogenesis and transient hyperglycemia results in improved appetite, which increases the intake of energy precursors, proprionate, helps drive turn-around of destructive cycles
    Slow IV infusion over several hours (20L 2.5% still doesn’t meet requirements - may want to do this at 60g/hr in cows with severe hepatic lipidosis)
  • Reduced ketogenesis and transient hyperglycemia results in improved appetite, which increases the intake of energy precursors, proprionate, helps drive turn-around of destructive cycles
    Slow IV infusion over several hours (20L 2.5% still doesn’t meet requirements - may want to do this at 60g/hr in cows with severe hepatic lipidosis)
  • Reduced ketogenesis and transient hyperglycemia results in improved appetite, which increases the intake of energy precursors, proprionate, helps drive turn-around of destructive cycles
    Slow IV infusion over several hours (20L 2.5% still doesn’t meet requirements - may want to do this at 60g/hr in cows with severe hepatic lipidosis)
  • Add predef to their notes
    When we talk about the gluconeogenic effect of glucocorticoids we really mean their ability to increase blood glucose. In ruminants it appears that total amount of glucose in the body does not change much, just shifts, also there is low induction of gluconeogenic enzymes in the liver
  • They need to add in the predef stuff and the hyperkalemia stuff
  • Transcript

    • 1. Dr A. Samiei Dairy Cow Nutrition (Ph.D(
    • 2. Milk production Milk production STRESS COW HEALTH and PRODUCTIVITY HomeostasisHomeostasis CalvingCalving
    • 3. Metabolic stress Metabolic stress Digestive stress Digestive stress Abusive cow handling Abusive cow handling Poor sanitation Poor sanitation CalvingCalving Milk production Milk production STRESS COW HEALTH and PRODUCTIVITY
    • 4. Abusive cow handlingAbusive cow handling Digestive stressDigestive stress Poor sanitation Poor sanitation Milk feverMilk fever DADA MastitisMastitis Calving CalvingMilk production Milk production Metabolic stress Metabolic stress STRESS COW HEALTH and PRODUCTIVITY
    • 5. When are cows leaving herds 25% of culls leave before 60 DIM Stewart et al., 2001
    • 6. Study Dohoo Markusfeld Bigras-Poulin Grohn n 2,875 5600 2204 73368 Milk Fever - 1.5 5.6 3.8 Metritis 18.2 - 10.7 2.3 Mastitis 16.8 - 24.2 5.4 Ketosis 17 16.6 3.3 6 RP 8.6 19.4 7.7 4.8 Cystic Ovary 10.4 - 5 6.8
    • 7. Thomas Geishauser
    • 8. The last 3 wk before to 3 wk after parturition (Grummer 1995(  Most infectious and metabolic diseases in dairy cows occur during or soon after this time Pregnant Nonlactating Nonpregnant Lactating Extreme CHALLENGE
    • 9. 0 5 10 15 20 25 30 35 -20 -18 -16 -14 -12 -10 -8 -6 -4 -2 0 2 4 6 day relative to calving lbofdrymatter/day Parturition Bertice 1992
    • 10. Days Relative to Calving Balance NEl, Mcal/day (NEl intake - NEl expanded( Drop in DMI -21 -14 -7 0 7 14 21 Colostrum & milk synthesis -15 -10 -5 0 5 Grummer, 1995
    • 11. The growing fetus might induce space constraints and restrict rumen volume. Growth of the fetus is more gradual during the final trimester of gestation, whereas the drop in DMI does not occur in earnest until the last few days before parturition. Ruminal water-holding capacity did not change as cows transitioned from the dry period to lactation, indicating that physical capacity of the rumen is not the cause of prepartum DMI depression
    • 12. Blood estrogen might be responsible for the depression in feed intake before parturition. Injection of estradiol-17β reduced feed intake in lactating cows.
    • 13. Dry matter intake depression during the final 2 to 3 weeks before parturition: 25%for young (first or second parity) cows or (1.69% BW( 52%for aged (third parity or greater) cows or (1.88% BW(
    • 14. Predisposition to disorders at and immediately following parturition may be indicated by reduced DMI prepartum. Cows fed the high-fiber (NDF) diet with added fat had the lowest DMI.
    • 15. Postpartum feed intake is decreased in cows that are over conditioned at parturition. Total DMI depression during the final 3 weeks was 28%, 29%, and 40% for thin, moderate, and obese cows, respectively. Overcrowding, group changes, diet changes, bunk space, water quality, and so on, may be critical factors affecting prepartum DMI.
    • 16. 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
    • 17. Overall, increases plasma glucose levels.
    • 18. Liver Muscle Adipose tissue
    • 19. X Adipose Tissue Free fatty acids Liver Ketone BodiesInsulin Pancreas Mechanism for prevention of ketosis due to excess ketone body production that can lead to ketoacidosis
    • 20. Liver Adipose tissue
    • 21. Protein Hormone Similar structure to Insulin Stimulates cell growth Inhibits apoptosis
    • 22. Hormonal activation of triacylglycerol (hormone-sensitive( lipase. Hormone signals from epinephrine or glucagon promote mobilization of fatty acids (lipolysis( via production of cyclic AMP. Activated protein kinase A, phosphorylates HSL-b to the active HSL-a form . RECEPTORS ATP protein kinase A cell membrane Epinephrine Glucagon HORMONES cyclic AMP ATP ADP = activation - = inhibition Triacylglycerol Fatty acid + Diacylglycerol OPHSL-a protein phosphatase Pi + Insulin - caffeine Phospho- diesterase AMP + Adenylyl cyclase (inactive form( HSL-b OH inactiveactive + + insulin
    • 23. Adipose Tissue NEFA TG NEFA CPT BETA-OXIDATION TG VLDL Liver CO2 Ketone Bodies Fatty Liver Peroxisomes Mitochondria - Insulin + Stress Hormones Glucagon, Epinephrine, Somatotropine
    • 24. Month Phase 4Phase 4 Phase1Phase1 Phase 6Phase 6 Phase3Phase3 Phase 5Phase 5 Phase2Phase2 Dry Matter IntakeDry Matter Intake Body WeightBody Weight MilkMilk ProductionProduction Peak DMIPeak DMIPeak MilkPeak Milk Tail EndTail End FreshFresh Far Off Far Off Close Up Close Up
    • 25. 65% Propionate and AA 15-20% Lactate (endogenic/diet) Glycerol (lipases FA) Deficit of 500 g/d Glucose Protein (Muscle)
    • 26. 0 2500 2000 1500 1000 500 +21-21 0 Energy needed Energie available Glucoseg/d - 500 g/d
    • 27. Liver utilises 25% of available oxygen representing only 2% of the whole body weight! > During the first part of lactation liver metabolical activity increases (Gluconeogenesis). Liver dimensions doesn’t change much although oxygen demand doubles.
    • 28. Prepartum Postpartum increase Hepatic Blood Flow 1140 l/h 2099 l/h + 84% DMI 9.8 kg/d 14.1 kg/d + 44 % Liver Oxygen Utilization 1619 mmol/h 3159 mmol/h + 95 % Liver Metabolic Activity 4.4 mmol O2/g 8.6 mmol O2/g X 2
    • 29. MITOCHONDRION cell membrane FA = fatty acid LPL = lipoprotein lipase FABP = fatty acid binding protein A C S FABP FABP FA [3] FABP acyl-CoA [4] CYTOPLASM CAPILLARY FAalbumin FA FA FA from fat cell FA [1] acetyl-CoA TCA cycle β-oxidation [6] [7] carnitine transporter acyl-CoA [5] Overview of fatty acid degradation ACS = acyl CoA synthetase L P L Lipoproteins (Chylomicrons or VLDL) [2]
    • 30. GLUCOSE Triose - P Pyruvic acid GLYCEROL Lactic acid MPG Oxaloacetic acid Niacin Niacin Succinic acid Transformation cycle (Krebs) Energy PROPIONATE B12 LIVER RUMEN PROPIONATE BLOOD Acetyl-CoA
    • 31. Ketone body formation (ketogenesis) in liver mitochondria from excess acetyl CoA derived from the β-oxidation of fatty acids MITOCHONDRION (excess acetyl CoA) Hydroxymethylglutaryl CoA HMG-CoA synthase acetyl CoA CoA Acetoacetate HMG-CoA-lyase acetyl CoA β-Hydroxybutyrate β-Hydroxybutyrate dehydrogenase NAD+ NADH Acetone (non-enzymatic) 2 Acetyl CoAFatty acid β-oxidation Citric acid cycle oxidation to CO2 Acetoacetyl CoA CoA Thiolase
    • 32. 1. Availability of the substrate (Long Chain Fatty Acids) : from increased production by lipolysis with increased delivery of FA to the liver. 2. The level of Malonyl Co A in the liver, with its influence to inhibit the Carnitine Palmitoyl Transferase I (CPT I) 3. The Glucagon / Insulin Ratio : a high ratio increases lipolysis and activation of oxidative ketogenesis , a low ratio counteracts ketogenisis
    • 33. MAMMARY GLAND ADIPOSE TISSUE LIVER TG FA NEFA NEFA MILK FAT NEFA Peroxysomes Mitochondria Acetyl-CoA Keton Bodies TG VLDL CO2 Propionate 1 2 3 (Drackley, 1997) CPT-1 Apolipoprotein B, is the main protein in VLDL
    • 34. NEFAconce Days from parturition Underwood 1998
    • 35. LIVER TG NEFA NEFA Peroxysomes Mitochondries Acetyl-CoA Keton Bosies TG CO2 Propionate KETOSIS STEATOSIS !! !!
    • 36. LIVER TG STEATOSIS !! TGTG TG TG TG TG TG TG TG GLUCONEOGENESIS TG TG TG NH3 UREA   TG TG TG Steatosis reduces liver capacity to metabolise ammonia to urea. Hy ammoniac concentration reduces glucose production of hepatocytes (Cadorniga-Valino, 1997; Strang, 1998)
    • 37. BHBA Ac
    • 38. Monitoring Subclinical Ketosis β-Hydroxybutyrate Concentration in Blood Urine Ketone Body Test Milk Ketone Body Test
    • 39. The ‘‘gold standard’’ test for subclinical ketosis (SCK( is blood BHBA. This ketone body is more stable in blood than acetone or acetoacetate (Tyopponen and Kauppinen, 1980(. β-Hydroxybutyrate Concentration in Blood
    • 40. Dr A. Samiei
    • 41. Position )μmol/L) βHBA Normal Less than 1000 Uncertain 1000to 1400 Sub-clinical ketosis ≤1400 Clinical ketosis ≤3200 Dr G. Oetzel, Wisconsin University
    • 42. Position )μmol/L) βHBA Normal Less than 1000 Uncertain 1000to 1200 Sub-clinical ketosis ≤1200 Clinical ketosis ≤2600 Dr T. Duffield, Guelph University
    • 43. Position )μmol/L) βHBA Normal Less than 600
    • 44. Prepartum NEFAs: There is an increased incidence of postcalving diseases (displaced abomasum, metritis/retained placenta and clinical ketosis), decreased milk yield and decreased reproductive performance in the first 30 days in milk in Holstein dairy cows (fed TMR) with NEFA values > 0.30 mEq/L when tested 2-14 days before calving. Postpartum NEFAs: There is an increased incidence of postcalving diseases (displaced abomasum, metritis/retained placenta and clinical ketosis), decreased milk yield and decreased reproductive performance in the first 30 days in milk in Holstein dairy cows (fed TMR) with NEFA values > 0.60-0.70 mEq/L when tested 3-14 days after calving. In the Cornell studies, postcalving NEFAs were actually a better predictor of than postcalving β-hydroxybutyrate concentrations or precalving NEFAs
    • 45. It is more difficult to collect a urine sample than a milk sample. This test has excellent sensitivity but poor specificity (Nielen, 1994). This makes it a useful test for evaluating individual sick cows, but not very useful for herd-based monitoring. The best test for cowside urine ketone evaluation is a semiquantitative dipstick (Ketostix; Bayer Corp. Diagnostics Division, Elkhart, Indiana) that measures acetoacetate. The urine ketone tests are semiquantitative tests based on degree of color change that occurs when sodium nitroprusside reacts with acetoacetate and, to a lesser degree, acetone.
    • 46. ββHBA HBA
    • 47. Cowside milk tests have tremendous advantages over urine cowside tests for ease of collection and for assurance that all eligible cows can be tested. Milk tests are generally not as sensitive as urine tests in detecting SCK. This test has a much higher sensitivity in milk (>70%) and reasonably good specificity (>70%, up to 90%). The best cutoff point for herd monitoring when using the milk BHB strip appears to be ≥200 µmol/L (Oetzel, 2004).
    • 48. Test Sensitivity Specificity Ketocheck powder (AcAc in milk) 41% 99% Ketostik strip (AcAc in milk) 78% 96% Keto Test strip (BHBA in milk) 73% 96% Sample proportion of subclinical ketosis was 7.6% (5 to 33%)
    • 49. Either the Ketostik (AcAc in urine) or Keto Test strips (BHB in milk) would provide acceptable results for screening of individual cows for sub-clinical ketosis in commercial dairy herds. Low False (-) Over the prevalence range, the Keto Check powder (AcAc in milk)test would have limited application as a screening test. High False (-) Incidence (5-30%)
    • 50. range for milk fat : milk protein ratio is 1 - 1.25 A milk fat: protein ratio greater than 1.5 is considered a risk factor for metabolic problems such as ketosis. There are two mechanisms responsible for increase in milk fat: protein ratio. The first mechanism is an increase in milk fat due to mobilization of body reserves by the animal caused by a negative energy balance. The second mechanism is a decrease in milk protein as the result of a lack of energy in the ration and/or decreased voluntary dry matter intake. When
    • 51. Sato et al (2005) reported 34.7% of SCK and 15.3% clinical ketosis in a study of 150 dairy cows in Japan. Zilaitis et al (2007) reported that 57.7% of cows had SCK in Lithuania. In Iran, Sakha et al (2007) using 1,200 µmol BHBA/L blood cutoff point,reported 14.4% of the tested cows (13 out of 90 cows) were subclinically ketotic in the Kerman province More than 90% of SCK cases occur in the first and second months after calving. During this period, approximately 40% of all cows are affected by SCK at least once, although the incidence and prevalence are highest in the first and second weeks after parturition (Duffield, 2000; Geishauser et al., 2001).
    • 52. Oetzel (2010) investigated 1,047 cows in 74 herds in Wisconsin, USA reported an overall ketosis prevalence of 15.7% with only 26% of the herds investigated showing the ketosis prevalence of below 10% (a cutoff point considered as an alarming level for herd-based ketosis testing). Duffield and LeBlanc (2009) reported that 24 out of 136 (17.6%) transitionally raised cows had BHBA concentrations ≥1400 μmol/L of serum in the first week post-calving. Pourjafar and Heidari (2003) determined the prevalence of SCK was 38% in 12 Torbat-Heydarieh (Khorasan province) herds were studied from March 1998 to May 1999.
    • 53. Disorder Mean (%) Range (%) Milk fever 7.2 0to 44.1 Displaced abomasum 3.3 0to 14 Ketosis 3.7 0to 20 Retained fetal membranes 9 0to 22.6 Metritis 12.8 0to 66 Journal of Dairy Science Vol. 82, No. 11, 1999
    • 54. 0 5 10 15 20 25 30 PercentKetosis Dry '1-2 '3-4 '5-8 '7-8 '9-10 Week Post-Calving Duffield, et al., 1997. Can Vet J 38:713
    • 55. 0 1 2 3 4 5 6 7 8 PercentKetosis 1 2 3 >3 Parity Duffield, et al., 1997. Can Vet J 38:713 ab aba b
    • 56. Type I. Low Dry Matter Intake Type II. Over Condition (Fat Cow( Type III. Butyric Acid Silage Ketosis Dr G. Oetzel, 2004, 2005, 2007 and 2010
    • 57. Type I diabetes mellitus. Blood insulin concentration is low hypoglycemia due to a shortage of glucose precursors.
    • 58. Over-crowding and/or lack of bunk space. insufficient energy intake in early lactation cows. over-feeding protein and under-feeding energy in post-fresh groups in TMR-fed herds. Fat supplementation
    • 59. Grummer, 1993 5 10 15 20 25 Dry Matter Intake Kg/day Weeks relative to calving 0-1-2 1 2 3 200 400 600 800 1000 Non-Esterified Fatty Acid um/l 30 -35% intake depression 300% Increased fat mobilization
    • 60. Ketosis Displaced abomasum Retained placenta VandeHaar et al., 1995 452 450 449 574 619 585 Plasma non-esterified fatty acids (NEFA) the week prior to calving, µM, for cows that developed a disorder (positive) and those who did not (negative) Negative PositiveType of metabolic disorder
    • 61. Fat supplementation does not provide the glucose precursors needed to fuel gluconeogenesis, but rather floods the liver with more of the fatty acids it is already struggling to oxidize completely. Fat supplementation also tends to depress dry matter intake, particularly in early lactation.
    • 62. The key to preventing type I ketosis is to maximize energy intake in early lactation. A little less grain might be the correct solution if the cows simultaneously have subacute ruminal acidosis (SARA) causing depressed dry matter intake.
    • 63. type II diabetes mellitus fat cow syndrome. blood insulin concentrations are high and blood glucose concentrations are high begin mobilizing body fat prior to calving (dry matter intake depression around calving). thinner cows are also at risk if pre-fresh nutritional management is poor.
    • 64. Insulin resistance, cell membranes have reduced sensitivity to insulin and High levels of serum insulin, glucose and triglycerides increased adipose sensitivity, which is the tendency to mobilize body fat very rapidly under conditions of stress or negative energy balance. heifers have more difficulty than cows Fatty liver infiltration impairs both gluconeogenic potential and immune function by hepatocytes. Many cows with type II ketosis die from infections (metritis, mastitis, pneumonia) and displaced abomasum.
    • 65. 2,00 2,25 2,50 2,75 3,00 3,25 3,50 3,75 0,05 0,10 0,15 0,20 0,25 0,30 -12 3 18 44 76 104 133 218 B C S F F A / N E F A The average days of lactation. Association between FFA (NEFA) values and BCS FFA (NEFA), mmol/l BCS Gergácz ey al, 2008
    • 66. Over condition Change BCS during close-up Moving cows to a different pen just prior to calving over-crowding cows prior to calving moving cows to different pens frequently after calving over-crowding after calving
    • 67. excellent pre-fresh nutritional management combined with prevention of obesity in dry cows. Preventing negative energy balance prior to calving requires good dry matter intakes as well as proper energy density of the pre-fresh diet
    • 68. The best option is to destroy the feed, i.e., haul it away in a manure spreader to be spread on the fields (it is good fertilizer). this forage could diverted away from the pre- and post- fresh cows fed only to replacement heifers, late lactation cows, and/or far- off dry cows.
    • 69. Cows in the negative energy balance period show an impairment of udder defence mechanisms. The capacity for phagocytosis by polymorphonuclear cells and macrophages may be reduced in negative energy balance. Concentration of BHB showed a strong positive correlation to the severity of mastitis (E. coli mastitis(. Several epidemiological studies have shown that clinical ketosis is associated with an increased risk of clinical mastitis It was found that parity, calving in summer and fall seasons, and being ketonemic at a threshold of >1400 ìmol/L BHB was significantly associated with an increased risk of clinical mastitis. National Mastitis Council Regional Meeting Proceedings (2000)
    • 70. Immune Function in Periparturient Cows as a Percentage of Control Steers Week Around ParturitionWeek Around Parturition ImmuneFunction(%Controls)ImmuneFunction(%Controls) Goff & Horst, JDS, 1997
    • 71. Ketosis has been associated with an increased risk to develop metritis, (Markusfeld, 1984; Markusfeld, 1987; and Reist et al, 2003.( There is an association between subclinical ketosis and metritis (Dohoo and Martin, 1984(. Kaneene et al. (1997( showed that metabolic events related to negative energy balance were related to increased risk of metritis and RFM. Higher energy consumption during the last weeks of the dry period (more grain content of the ration( was related to reduced disease risk at parturition.
    • 72. LIVER TG TGTG TG TG TG TG TG TG TG GLUCONEOGENESIS TG TG TG  TG TG TG Fatty Liver
    • 73. Fatty liver is observed in different metabolic diseases such as ketosis, displaced abomasum, milk fever, retained placenta, infertility, downer syndrome, mastitis, and metritis. Diseases such as mastitis, metritis, and milk fever are not related to NEB. Feeding diets with greater energy content (>1.65 Mcal of NEL/kg DM) during the far-off dry period is associated with a higher incidence of fatty liver. Burim N. Ametaj Advances in Dairy Technology (2005) Volume 17, page 97
    • 74. Reduction in milk yield ranged between 4-10 kg/day for clinical ketosis and 3 kg/day for subclinical ketosis.
    • 75. Heinrichs, J., et al., Milk components: understanding the causes and importance of milk fat and protein variation in your dairy herd, Penn State University, DAS 05-97 Breed Total Fat Total Protein Fat:Protein Ratio Ayrshire 3.86 3.18 1.21 Brown Swiss 4.04 3.38 1.20 Guernsey 4.51 3.37 1.34 Holstein 3.65 3.06 1.19 Jersey 4.60 3.59 1.28
    • 76. Duffield, et al., 1997. Can Vet J 38:713 • Using BHBA measurements Duffield, et al., constructed receiver operator characteristic curves to assess the sensitivity and specificity of fat, protein and protein/fat • A 1% increase in FAT is associated with a 2X increase in subclinical ketosis risk. • A 1% increase in PROTEIN reduces the risk by over 50%.
    • 77. 20 22 24 26 28 30 32 34 36 38 40 Conceptionrate,% < 3.0 3.0 - 4.0 4.0 - 4.5 >4.5 Milk fat, Percent Kristula, et al., 1995. Prev. Vet. Med 23:95
    • 78. Nutritional Management Propylin Glycol Niacin Rumen-Protected Choline Rumen-Protected Methionine and Lysine Monensin
    • 79. Energy density of diets must increase to compensate for: 1-decreasing feed intake to meet the energy requirement of the cows, 2-adapt rumen microflora to higher non fiber carbohydrate diets, condition the rumen papillae, and reduce fat mobilization from adipose tissue.
    • 80. Day Relative to Calving -21 -7 10 22 Length, mm 8.3 7.6 6.4 8.6 Width, mm 2.5 2.1 2.2 2.5 Surface area, mm2 17.8 14.2 14 17 Reynolds (1999(.
    • 81. 0 5 10 15 20 25 30 35 40 45 50 Low High Low Diet Energy Density Surface area (mm2( Absorption rate (mmol/min(
    • 82. 725-kg Cow 570-kg Heifer Function Pre Post Pre Post Maintenance 11.2 10.1 9.3 8.5 Pregnancy 3.3 --- 2.8 --- Growth --- --- 1.9 1.7 Milk production --- 18.7 --- 14.9 Total (Mcal) 14.5 28.8 14.0 25.1 Calculated from NRC (2001(. Assumes milk production of 25 kg/d for cow and 20 kg/d for heifer, each containing 4% fat.
    • 83. 302520151050-5-10-15-20-25 5 10 15 20 25 30 Control Force Fed Day Relative to Calving DMIkg/d Force-feeding prepartum cows via rumen cannula Bertics et al., 1992
    • 84. 0 5 10 15 20 25 30 LiverTriglycerides, %DM -17 1 28 Day Relative to Calving Force Fed Control Bertics et al., 1992 Fat content in liver of force-fed cows
    • 85. Effect of Prepartum DMI on Energy Metabolism of Transition Cows Control Force-Fed D -2 D 1 D 28 D –2 D 1 D 28 Glucose, mg/dl 63.4 60.3 56.7 76.5** 59.0 50.1 BHBA, mg/dl 11.9 17.6 17.1 12.5 18.1 18.2 NEFA, mEq/l 0.876 0.992 0.395 0.641 1.064 0.534 Hepatic (DM basis( Total lipid, % 30.7* 30.6 --- 23.5 35.1 TG, % 23.2** 26.9 --- 12.4 25.3 Glycogen, % 2.5 3.6 --- 4.2 2.7 Bertics et al. (1992)
    • 86. 0 0.5 1 1.5 2 2.5 3 3.5 4 umol/h*gwetweight -21 1 21 65 Propionate Alanine
    • 87. GLUCOSE Triose - P Pyruvic acid Lactic acid MPG Oxaloacetic acid Niacin Niacin Succinic acid Transformation cycle (Krebs) Energy PROPIONATE B12 LIVER RUMEN MPG PROPIONATE BLOOD Acetyl-CoA Transformation of the ingredients in Propylene glycol into glucose… Calcium propionate 50% 50%
    • 88. Grummer et al., (1994) conducted an showed that propylene glycol linearly increased glucose and insulin and decreased BHB and NEFA in blood. Propylene glycol as an oral drench or mixed with concentrate resulted in higher serum insulin and lower plasma NEFA concentrations than did feeding propylene glycol as part of a TMR system (Christensen et al., 1997).
    • 89. Effect of PG Dosage on Blood Metabolites of Feed Restricted Heifers PG dose (d 12( 0 ml/d 296 ml/d 592 ml/d 887 ml/d Contrast Glucose, mg/dl 75.2 80.0 81.1 82.0 *** Insulin, µIU/ml 13.0 17.7 18.2 19.8 ** BHBA, mg/dl 8.5 4.8 3.6 3.9 *** NEFA, mEq/L 0.746 0.425 0.332 0.282 *** Grummer et al. (1994)
    • 90. Effect of PG on Performance and Blood Metabolites of Cows Item Treatment Milk, kg/d Insulin, µIU/ml Glucose, mg/dl BHBA, mg/dl NEFA, mEq/L Reference 0 ml/d 300 ml/d 24.5 27.0 NA NA 65.4 66.0 6.73 4.80 0.415 0.384 Fonseca et al. (1998( 0 ml/d 500 ml/d NA NA 6.5 11.1 53.0 59.2 NA NA 0.386 0.290 Miyoshi et al. (1995( 0 ml/d 1,000 ml/d 33.2 32.6 0.354 0.679*** Low High*** Low High 0.403** 0.234 Studer et al. (1993(
    • 91. 32 34 36 38 40 42 1 2 3 4 5 6 7 8 ‫شیرواری‬ ‫ماههای‬ (kg(‫شیر‬‫تولید‬ Treated Group Control Group Propylene Glycol fed at 100g per day for 3 weeks pre- and 4 weeks post-calving 1600 cow trial; Arizona
    • 92. energy density of glycerol to be 0.90 to 1.03 Mcal/lb NEL Feeding glycerol: 1)increasing ruminal propionate would increase the supply of this gluconeogenic substrate to the liver, 2)increasing ruminal butyrate would support the growth of the ruminal epithelial tissue and perhaps increase nutrient absorption from the rumen as indicated by Dirksen et al. (1985), finally and 3)increasing water intake would supply the mammary gland with the water necessary for milk synthesis.
    • 93. GLUCOSE Triose - P Pyruvic acid GLYCEROL Oxaloacetic acid Niacin Niacin Succinic acid Transformation cycle (Krebs) Energy LIVER RUMEN Butyric Acid BLOOD Acetyl-CoA Transformation of the ingredients in glycerol into glucose… GLYCEROL BLOOD 52% PROPIONATE 48%
    • 94. Ruminal fluid from cows fed the propylene glycol- supplemented concentrate offered ad libitum contained significantly less butyrate than the other treatments and accordingly concentrations of BHBA in blood were decreased. propylene glycol was its tendency to reduce the production of ruminal butyrate, and accordingly the occurrence of ketosis. Feeding glycerol vs. propylene glycol could potentially improve intakes if delivered as a top-dress.
    • 95. Ca-propionate supplementation had no effect on the incidence of ketosis. Amy Elizabeth Beem. Louisiana State University, December, 2003 Sodium propionate has been used as an effective treatment by providing propionate to the cow. However, if inhaled, sodium propionate can cause significant damage to lung tissue (Fox, 1971(. Other salts of propionic acid such as calcium propionate may decrease the risk of adverse health effects. Lipker and Schlatter (1997) and Stokes and Goff (2001) reported decreased incidence of ketosis when Ca-propionate was fed during the entire transition period or as a bolus at calving.
    • 96. Calcium propionate is a compound poorly fermented by the rumen microorganism. At parturition, calcium propionate increases blood glucose 24 hrs after its administration, and reduces BHB and NEFA during the first two days postpartum. Furthermore, calcium propionate increases blood calcium, reduces the incidence of clinical and subclinical hypocalcemia and increases milk yield by 3.8 kg/d during the first 2 weeks after calving (Higgins et al., 1996). In transition cows fed anionic salts prepartum, a calcium propionate (510 g) plus propylene glycol (400 g) drench did not affect postpartum concentrations of Ca, P, Mg, glucose, NEFA, or BHB (Melendez et al., 2002).
    • 97. Components Glyco-Line MPG Glocusa MPG 35.5 14.7 6.78 Glycerol 8 18.2 18.5 Propionate Ca 11.5 5.8 8.2 Propionic acid 9 4.42 6.49 Ca 1.5 1.35 6.61 DM 73 65.7 79.45 Produce Glucose 285 123 98.9
    • 98. Adipose Tissue NEFA TG NEFA CPT BETA-OXIDATION TG VLDL Liver CO2 Ketone Bodies Fatty Liver Peroxisomes Mitochondria - Insulin + Stress Hormones Reducing NEFA mobilization Stimulating peroxisomal β-oxidation Boosting VLDL synthesis Stimulating mitochondrial β- oxidation
    • 99. Adipose Tissue Triacylglycerol HSL Diacylglycerol Monoacylglycerol NEFA Blood Compartment Niacin -
    • 100. Zinnet al., 1987and Santschiet al., 2005, data combined
    • 101. Effect of Niacin on Performance of Dairy Cows Increment over control diet Diets Studies, No. Milk, kg/d Fat, % Protein, % Regular 19 + 0.76 + 0.165 + 0.06 Supplemented with fat 5 - 0.36 - 0.044 + 0.10 Hutjens (1991(
    • 102. Effect of NFC and Niacin on Prepartum DM and Energy Intakes Diet LNFC HNFC LNFC + N HNFC + N Niacin effect DMI, kg/d 10.2 13.0 10.1 12.6 No NEL intake, Mcal/d 13.5 21.2 13.5 20.4 No EB, Mcal/d 0.10 7.39 -0.24 6.76 No Minor et al. (1998)
    • 103. Effect of Prepartum Diet on Plasma and Liver Metabolites of Transition Cows Diet LNFC HNFC LNFC + N HNFC + N Niacin effect Glucose, mg/dl 59.4 62.2 61.0 64.0 No NEFA, µM 378 293 389 225 No BHBA, mg/dl 11.4 8.0 11.0 7.8 No Hepatic Glycogen, % 4.5 6.8 4.5** 8.2 No TG, % 5.0 4.1 7.9* 4.3 No Minor et al. (1998)
    • 104. Choline is used for phosphatidylcholine synthesis, a major phospholipid required for cell maintenance and replication. Phosphatidylcholine is needed for synthesis of very low density lipoprotein (VLDL), the lipoprotein responsible for export of triacylglycerol from hepatocytes. The data from Cooke et al. (2007) implied that rumen- protected choline can prevent and possibly alleviate fatty liver because of an increase rate of triacylglycerol depletion from the liver, at least when induced by feed restriction.
    • 105. apolipoprotein B (apoB ) Phospholipids Cholestrol (FC) Cholesteryl ester Triglyceride (TG) ( PC , SM , lys oPC ) (CE)
    • 106. Methionine and lysine are considered the most limiting amino acids (AA) when high producing dairy cows are fed a variety of corn-based diets in early and mid-lactation (Schwab et al., 1992; Rulquin et al., 1993; NRC, 2001). Bobe et al. (2004) reported that addition to diets of components thought to increase VLDL synthesis and removal from the liver, such as carnitine, choline, inositol, lysine and methionine.
    • 107. Methionine is a precursor of apolipoprotein B 100 (apoB100) in the liver (Grummer, 1993). It is also a donor of methyl groups necessary for the synthesis of phospholipids, essential components of VLDL. Journal of Animal and Feed Sciences, 18, 2009, 28–41
    • 108. Effect of Supplemental Methionine on Hepatic Metabolism Item Treatment Hepatic TG, mg % NEFA, mEq/l Glucose, mg/dl Reference Control 23.0 0.270 61.2 Bertics and Grummer, 1998 13 g Met 20.0 0.346 59.4 Control 12.7 0.820 58.0** Bertics and Grummer, 1997 13 g Met 15.4 1.076** 50.3
    • 109. Effect of Methionine or Methionine + Lysine on Metabolism Item Treatment Hepatic TG, mg % NEFA, mEq/l Glucose, mg/dl 16 % CP wk 1 wk 3 Control 28.6 26.7 0.399 80.8* 10.5 g Met 24.8 24.6 0.374 78.3 10.2 g Met. + 16 g Lys 35.6 27.7 0.461 73.8 18.5 % CP Control 21.5 24.2 0.377 80.1* 10.5 g Met 24.8 24.9 0.447 79.0 10.2 g Met. + 16 g Lys 26.2 25.5 0.431 74.1 Socha (1994(
    • 110. Carnitine transports FA inside the mitochondria where they are burnt to produce energy (β-oxidation(.
    • 111. Figure 2 (top). Activation of palmitate to palmitoyl CoA (step 4, Fig. 1) and conversion to palmitoyl carnitine Intermembrane Space OUTER MITOCHONDRIAL MEMBRANE palmitoyl-carnitine CoA palmitoyl-CoA carnitine Cytoplasm palmitoyl-CoA AMP + PPi ATP + CoA palmitate CPT-I [2] ACS [1] CPT-I defects cause severe muscle weakness because fatty acids are an important muscle fuel during exercise.
    • 112. Figure 2 (bottom). Mitochondrial uptake via of palmitoyl- carnitine via the carnitine-acylcarnitine translocase (CAT) (step 5 in Fig. 1). Matrix INNER MITOCHONDRIAL MEMBRANE Intermembrane Space palmitoyl-carnitinecarnitine CoApalmitoyl-CoA CAT [3] palmitoyl-carnitine CPT-II carnitine CoApalmitoyl-CoA [4] CPT-I
    • 113. CAT Intermembrane Space OUTER MITOCHONDRIAL MEMBRANE palmitoyl-carnitine CoA carnitine Cytoplasm palmitoyl-CoA AMP + PPi ATP + CoA palmitate palmitoyl-CoA Matrix INNER MITOCHONDRIAL MEMBRANE [3] palmitoyl-carnitinecarnitine CoApalmitoyl-CoA [4] CPT-I [2] ACS [1] CPT-II
    • 114. Figure 3. Processing and β-oxidation of palmitoyl CoA matrix side inner mitochondrial membrane 2 ATP 3 ATP respiratory chain recycle 6 times Carnitine translocase Palmitoylcarnitine Palmitoylcarnitine Palmitoyl-CoA + Acetyl CoACH3-(CH)12-C-S-CoA O oxidation FAD FADH2 hydration H2O thiolase CoA oxidation NAD+ NADH Citric acid cycle 2 CO2
    • 115. Monensin is an ionophore antibiotic that alters VFA production in the rumen in favor of propionate (Richardson et al., 1976). Propionate is a major precursor for glucose in the ruminant. A monensin has been shown to decrease the incidence of subclinical ketosis, displaced abomasum (DA) with increased glucose and decreased BHBA postcalving.
    • 116. Effect of Sodium Monensin on Metabolic Parameters of Dairy Cows Item Treatment BHBA, mg/dl Glucose, mg/dl NEFA Reference At calving C M 23.70 11.74** 55.1 58.3* 3.90 3.75 Abe et al. (1994) Prepartum C 150 mg/d 300 mg/d 450 mg/d 14.91 13.91 13.90 14.31 58.6 58.9 61.0** 60.31* 0.46 0.38** 0.40 0.39* Wade et al. (1996) Prepartum C M 15.24 12.46* 65.1* 62.8 0.438 0.581 Stephenson et al. (1994) Postpartum C M 5.15 4.34 63.3 65.5 NA NA Phipps et al. (1997)
    • 117. 500mls 50% dextrose IV (250g( transient (<2hr) ↑ glucose, most lost in urine minimal input to daily glucose requirements -60 0 60 120 180 Insulin ng/ml Glucose mg/dl AA mg/dl 0 2 0 200 0 10
    • 118. ↓ Lipolysis, ↓ gluconeogenesis ↓ supply of NEFA’s to liver ↓ transport of NEFA’s into mitochondria insulin:glucagon ratio Result is ↓ ketogenesis
    • 119. IV over ~ 5 min Not SC tissue necrosis, abscesses Rapid resolution of clinical signs ↑ milk yield May relapse (~2d(
    • 120. Oral Propylene glycol (PG( -8 14oz as a drench SID-BID 3-5 d rumen motility required for absorption most absorbed rapidly from rumen as PG metabolized in liver to glucose peak conversion ~ 4 hrs, preinfusion levels ~12 hrs Toxicity appetite suppression, diarrhea
    • 121. Shift glucose distribution and utilization ↑ blood glucose ↓ milk production Stimulate appetite Use in fatty liver controversial unchanged or ↑ lipolyis and blood NEFA’s good data lacking Not in pregnant cows
    • 122. Dexamethasone (Azium: Schering-Plough( -5 20mg IV or IM q 24 hr Isoflupredone acetate (Predef 2X: Pharmacia- Upjohn( -10 20mg IM q 24 hr May ↑ risk for hypokalemia (mineralocorticoid activity( Administer in conjunction with dextrose Caution in cows with concurrent infectious disease
    • 123. Monitor for relapses, other conditions Nicotinic acid antilipolytic, increases blood glucose mode of action?, efficacy data lacking Insulin antilipolytic, antiketogenic hypoglycemia, so should be administered in conjunction with glucose, glucocorticoids good data lacking
    • 124. Prevalence of healthy cows (milk BHB < 100 mmol/l) after treatment with Catosal P. Sarasola and B. Schmidt
    • 125. A. Samiei Ph.D Thesis Universiti Putra Malaysia
    • 126. Lack of knowledge in Ketosis in Iran Diagnosis of Ketosis in herd Poor nutritional management Drop in milk yield after calving Economical loss
    • 127. The main objective: Prediction and prevention of ketosis in fresh dairy cows in Iran. The specific objective: To investigate the prevalence of ketosis (subclinical and clinical) and it’s relationship with parity, lactation stage and peak milk yield. Using Sanketo-paper as a diagnostic tool for SCK in farms. To investigate determine the best days for diagnosis of SCK. To determine the effects of SCK on milk yield and components during 60d after calving. To investigate the relationship between energy level, BCS and butyric silage with SCK. to investigate the effects of levels of NFC and glucose precursor on incidence of ketosis.
    • 128. PREVALENCE OF KETOSIS AND ITS CORRELATION WITH LACTATION STAGE, PARITY, PEAK MILK YIELD AND REGIONS IN IRANIAN DAIRY COWS
    • 129. Variables Mean Standard Deviation Minimum Maximum Parity (n) 2.64 1.587 1 12 Lactation Stage (d) 20.91 12.236 5 80 Glucose (mg/dl) 52.91 9.948 30 111 BHBA (µmol/L) 763.27 0.788 100 4,900 Peak Milk Yield (kg) 42.57 8.578 14 64
    • 130. BHBA Glucose Lactation stage Parity Peak milk yield (µmol/L) (mg/dl) (day) (n) (kg) Normal 477±8c 54±0.30a 22±0.44a 2.6±0.06a 45±0.26a SCK 1780±37b 48±0.90b 17±0.90b 2.8±0.13a 35±.51b Clinical 3597±92a 35±1.20c 14±1.00b 2.7±0.24a 28±.97c
    • 131. Source of Variation Sum of Squares df F P Region 25.23 12 4.67 >0.0001 Parity 2.03 2 2.26 0.105 Lactation Stage 5.11 1 11.35 0.0008 Blood Glucose 29.03 1 64.44 >0.0001 Peak Milk Yield 80.54 1 178.79 >0.0001 Error 443.27 984
    • 132. Regions BHBA Glucose Lactation stage Parity Peak milk yield (µmol/L) (mmol/L) (day) (n) (kg) Arak 602±118cd 53±1.20ab 24±1.80ab 1.8±0.16b 39±1.00d Qazvin 730±87abcd 54±1.40ab 20±1.20abc 2.6±0.19ab 50±1.00a Gorgan 1056±119ab 52±1.60ab 21±1.30abc 2.4±0.15ab 37±1.00d Isfahan 654±44b 52±0.70ab 20±0.90abc 3±0.12a 47±0.60ab Karaj 688±62bcd 54±0.70ab 26±2.00a 2.6±0.15ab 41±0.70cd Mashhad 671±95bcd 56±2.00a 22±1.60abc 2.7±0.30a 44±1.00bc Rey 851±67abc 55±0.70a 22±0.70abc 2.6±0.13ab 40±0.70d Sari 1145±154a 49±1.10bc 10±0.50d 2.7±0.18ab 45±1.40bc Semnan 890±387abc 46±1.60c 18±2.20bc 2.2±0.40ab 41±1.60cd Shahrekord 926±164abc 49±2.80bc 16±1.60cd 2.6±0.34ab 46±2.00ab Shiraz 377±56d 51±2.20ab 17.5±2.00bc 2.5±0.45ab 40±1.20d Tabriz 571±121cd 56±2.20a 22±2.50abc 3.1±0.47a 47±1.70ab Varamin 743±45abcd 53±0.60ab 21±0.70abc 2.5±0.12ab 40±0.52d
    • 133. Regions Ketosis SCK Clinical ketosis (%) (%) (%) Arak 9.75 7.30 2.45 Qazvin 12.00 8.60 3.40 Gorgan 31.00 23.65 7.35 Isfahan 15.00 12.60 2.40 Karaj 11.11 9.00 2.11 Mashhad 9.50 7.10 2.40 Rey 21.26 16.09 5.17 Sari 28.60 19.04 9.56 Semnan 9.00 0.00 9.00 Shahrekord 30.00 30.00 0.00 Shiraz 0.00 0.00 0.00 Tabriz 9.50 9.50 0.00 Varamin 17.80 15.90 1.90
    • 134. Parity Lactation Stage Glucose BHBA Peak Milk Yield Parity 1 Lactation Stage p -0.046 0.144 1 Glucose p -0.056 0.072 0.145* 0.0001 1 BHBA p -0.003 0.919 -0.154* 0.0001 -0.311* 0.0001 1 Peak Milk Yield p 0.019 0.530 0.013 0.664 0.178* 0.0001 -0.415* 0.0001 1
    • 135. AN EVALUATION OF Β-HYDROXYBUTYRATE IN MILK AND BLOOD FOR PREDICTION OF SUBCLINICAL KETOSIS IN DAIRY COWS
    • 136. Plasma and milk factors Unit Mean Plasma BHBA concentration µmol/L 1234 Milk BHBA concentration µmol/L 145 Plasma NEFA concentration mEq/L 0.284 Milk yield 28d kg 29.5 Milk yield 60d kg 32 Fat percent % 3.9 Protein percent % 2.8
    • 137. Plasma and milk factors Unit Normal SCK Plasma BHBA concentration µmol/L 730 1600 Milk BHBA concentration µmol/L 65 203 Plasma NEFA concentration mEq/L 0.335 0.587 Milk yield 28d kg 30 29 Milk yield 60d kg 34 30 Fat percent % 3.94 3.98 Protein percent % 1.12 1.35
    • 138. 0 10 20 30 40 50 60 70 80 90 100 0 4.76 23.81 66.67 False Positive Rate (1- Specificity) (%) TruePositiveRate(Sensitivity)(%) 500 200 100 50
    • 139. 0 5 10 15 20 25 30 35 40 3 7 10 14 17 21 24 28 32 36 40 44 48 52 56 60 Days in Milk MilkYield(Kg) Non SCK SCK
    • 140. EFFECTS OF ENERGY LEVEL, BUTYRIC SILAGE AND BODY CONDITION SCORE ON INCIDENCE OF SUBCLINICAL KETOSIS IN DAIRY COWS
    • 141. Farm Milk yield1 BCS2 BW3 Pariety 1 10,065 3.40 716 3.8 2 10,522 3.65 790 4 3 11,000 3.90 667 4 4 9,800 3.42 729 4.4 5 10,500 3.05 633 4 6 9,607 3.25 664 4.4 7 10,300 3.35 638 4 8 11,100 3.5 657 3.6 9 10,600 4.25 740 3.6 10 9,950 3.95 704 4.4 1 Average milk yield during 305d 2 Average body condition score at calving 3 Average body weight at calving
    • 142. Farm SCK (BHBA) Normal (BHBA) 1 2138±117ab 853±48ab 2 1842±115b 920±85a 3 1860±170b 770±62abc 4 1923±118ab 873±58a 5 1905±107b 658±59bc 6 2085±100ab 870±86a 7 1800±112b 630±61cd 8 2286±95a 834±77ab 9 1479±57c 453±44d 10 2005±80ab 910±70a
    • 143. Item Dairy farms 1 2 3 4 5 6 7 8 9 10 DM 56.95±5.54b 49.75±2.12bc 54.26±2.9b 52.57±0.75bc 51.98±1.73bc 54.72±0.79b 87.26±1.95a 45.07±1.25c 49.26±1.14bc 55.96±0.91b CP 14.93±0.58a 13.91±0.36ab 11.56±0.58cd 13.86±0.29ab 14.57±0.62ab 12.95±0.49bc 13.16±0.28bc 10.85±0.24d 15.54±0.95a 15.30±0.16a NEL 1.58±0.02ab 1.50±0.04bc 1.47±0.06c 1.53±0.02abc 1.53±0.006abc 1.56±0.01abc 1.50±0.009bc 1.47±0.03c 1.59±0.006a 1.48±0.01c NDF 44.42±1.83a 44.90±2.33a 48.93±2.88a 44.66±2.05a 45.21±0.41a 44.10±0.8a 43.42±2.64a 47.92±0.65a 35.18±0.51b 45.482.03a ADF 29.11±1.71bc 23.32±2.57abc 25.46±3.89a 21.77±1.48abc 21.83±0.39abc 20.38±0.62abc 25.18±2.17a 23.75±0.55ab 25.20±0.69a 18.30±0.3c NFC 30.48±2.31b 30.0±2.387b 32.36±3.66b 31.47±1.95b 30.53±1.09b 35.80±1.08ab 30.76±2.35b 29.65±0.78b 41.15±0.52a 34.75±1.91b EE 2.84±0.52a 2.57±0.31a 1.36±0.29cd 1.11±0.09d 1.51±0.11cd 1.25±0.08d 2.22±0.18abc 2.22±0.35abc 1.61±0.19bcd 2.42±0.09ab Ash 7.31±0.31bc 8.53±0.73ab 5.76±0.61d 8.88±0.26a 8.18±0.53ab 5.88±0.13cd 8.06±0.26ab 7.03±0.21bcd 5.94±0.18cd 7.30±0.34bc Ca 0.72±0.12ab 0.65±0.05bc 0.44±0.08c 0.80±0.08ab 0.82±0.05ab 0.76±0.06ab 0.76±0.03ab 0.73±0.04ab 0.80±0.02ab 0.91±0.03a P 0.45±0.03ab 0.30±0.03cd 0.25±0.03d 0.32±0.03cd 0.35±0.03cd 0.37±0.01bc 0.31±0.038cd 0.31±0.02cd 0.38±0.02abc 0.47±0.01a
    • 144. Item Dairy farms 1 2 3 4 5 6 7 8 9 10 DM 23.17±1.35b 22.55±0.72b 28.86±0.5a 24.12±0.8b 28.12±2.3a 28.03±0.33a 25.62±1.15ab 24.65±0.67ab 25.65±0.67ab 28.63±0.40a CP 7.86±0.2abc 7.56±0.19abc 6.92±0.1c 7.78±0.19abc 7.86±0.36abc 8.25±0.07ab 7.37±0.16bc 7.47±0.16bc 8.53±0.58a 7.86±0.18abc NEL 0.97±0.02ab 0.91±0.01abcd 0.83±0.02cd 0.92±0.03abcd 0.82±0.04d 0.85±0.01bcd 0.96±0.009abc 0.94±0.009abc 1.02±0.08a 0.91±0.20abcd NDF 58.30±0.68ab 51.60±3.02b 54.06±1.1ab 62.05±3.24a 56.45±0.43ab 53.06±0.93ab 54.25±5.30ab 53.25±5.30ab 51.85±1.8b 55.96±0.48ab ADF 32.15±0.75ab 30.25±0.47abcd 27.66±0.9cd 33.95±2.74a 27.25±1.5d 28.06±0.3bcd 31.80±0.3abc 30.80±0.3abc 30.45±1.16abcd 30.06±0.69abcd NFC 24.12±0.59c 26.40±0.55abc 30.58±0.89ab 18.37±3.1c 32.32±2.32ab 31.69±0.9ab 29.15±4.99ab 26.30±0.50abc 33.68±2.89a 27.42±0.09ab EE 1.47±0.22 1.82±0.1 1.43±0.04 1.74±0.21 1.63±0.02 1.45±0.05 1.45±0.15 1.54±0.10 1.58±0.10 1.67±0.07 Ash 8.15±0.44ab 7.02±0.42b 7.00±0.36b 10.05±2.07a 6.32±0.39b 5.53±0.12b 7.77±0.29ab 7.67±0.29ab 5.32±0.33b 7.06±0.37b Ca 1.30±0.14a 0.78±0.1b 0.9±0.11ab 0.98±0.17ab 0.95±0.04ab 1.27±0.24a 1.19±0.12ab 0.86±0.05b 0.83±0.06b 0.89±0.06ab P 0.18±0.008dc 0.14±0.007d 0.20±0.01bc 0.25±0.01ab 0.22±0.008abc 0.26±0.04a 0.20±0.008bc 0.22±0.01abc 0.23±0.01abc 0.24±0.005ab
    • 145. Item Dairy farms 1 2 3 4 5 6 7 8 9 10 pH 3.71±0.01b 3.57±0.03b 3.55±0.03b 4.04±0.1a 3.80±0.05ab 3.78±0.05ab 3.67±0.05b 3.69±0.09b 3.74±0.04b 3.56±0.03b Lactic acid 3.68±0.36bc 3.11±0.31c 8.06±2.60a 6.38±0.98ab 4.01±0.57bc 3.67±o.50bc 4.33±0.47bc 3.78±0.35bc 5.04±0.47bc 8.70±2.22a Acetic acid 4.09±0.67 3.70±0.27 3.86±0.29 3.45±0.26 4.39±1.08 4.05±0.31 3.52±0.37 3.78±0.40 4.72±0.1 3.68±0.45 Propionic1 0.38±0.02cd 0.56±0.09bc 1.47±0.23a 0.26±0.01cd 0.23±0.05d 0.00 0.82±0.16b 0.72±0.16b 0.34±0.02cd 1.45±0.2a Butyric acid 0.00 0.38±0.07b 0.00 1.01±0.31a 0.53±0.09ab 0.00 0.00 0.95±0.07ab 0.00 0.00 L:A2 1.02±0.1b 0.85±0.1b 2.07±0.59a 1.89±0.32a 0.97±0.06b 0.94±15b 1.23±0.15b 1.03±0.12b 1.06±0.08b 2.300.32a 1 Propionic acid 2 Lactic acid to acetic acid ratio
    • 146. pH DM Lactic Acetic Propionic Butyric Lactic:Acetic pH 1 DM -0.1985 1 Lactic -0.0198 0.2227 1 Acetic 0.0236 -0.1855 0.0944 1 Propionic -0.2772 0.3295* 0.4532** 0.1200 1 Butyric 0.4692* -0.0173 0.0631 0.0254 0.0490 1 Lactic:Aceti c 0.0660 0.2683 0.8782** 0.3271 0.4397** 0.9528 1
    • 147. Farm BCS±SD Day -3 Day 3 Day 14 Day 28 1 3.35±0.38a 3.10±0.38ab 2.70±0.33bc 2.35±0.29c 2 3.05±0.21a 2.80±0.21ab 2.55±0.21bc 2.40±0.14c 3 3.65±0.34a 3.40±0.34ab 3.15±0.34ab 2.90±0.42b 4 3.90±0.22a 3.65±0.22a 3.25±0.25b 2.90±0.42b 5 3.50±0.73 3.25±0.73 2.95±0.78 2.65±0.74 6 3.40±0.38a 3.25±0.38ab 2.75±0.31c 2.50±0.25c 7 3.25±0.35a 3.05±0.33ab 2.70±0.33bc 2.40±0.29c 8 3.70±0.37a 3.45±0.37a 2.85±0.22B 2.25±0.25C 9 3.90±0.22a 3.70±0.21a 3.40±0.14b 3.25±0.18b 10 4.25±0.25a 4.00±0.25a 3.50±0.18b 3.10±0.29c
    • 148. Parameter Estimate Standard Error Chi-Square Intercept -32.5690 12.6824 6.59* Butyric Silage 0.7481 0.7481 0.78ns NEL 21.9917 9.3095 5.58* BCS -0.6073 0.8483 0.51ns CP -0.1773 0.2117 0.70ns NFC -0.0493 0.1045 0.22ns Milk Yield 0.1357 0.0796 2.90ns SCK (%) = α + 21.99 NEL
    • 149. Butyric acid concentration in silage: 0.72% Corn silage consumed in TMR: 21 kg (asfed) or 5.43 kg (DM) Butyric acid per cow/day consumed was: 5.43 × 0.72% = 39g
    • 150. EFFECTS OF NON-FIBER CARBOHYDRATE OF DIET AND GLYCO-LINE SUPPLEMENTATION ON SUBCLINICAL KETOSIS IN DAIRY COWS
    • 151. Groups Treatments I 35%NFC, 0g PG II 35%NFC, 150g PG III 35%NFC, 300g PG IV 40%NFC, 0g PG V 40%NFC, 150g PG VI 40%NFC, 300g PG
    • 152. NFC 35% NFC 40% Effect, P value PG0 PG150 PG300 PG0 PG150 PG300 NFC PG NFC × PG BHBA 769±100a 786±109a 816±103a 625±99ab 576±82ab 513±69b 0.0044 0.9364 0.6873 Glucose 43±1.55c 49±1.38ab 47±1.59b 48±1.57b 51±1.94ab 52±1.61a 0.0045 0.0028 0.5409 Milk yield 28±0.49d 32±0.54c 33±0.74c 34±0.48bc 35±0.48b 38±0.59a >0.0001 >0.0001 0.0609
    • 153. `` UNIVERSITI PUTRA MALAYSIA

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