Ketosis 2011 samiei
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Transcript of Ketosis 2011 samiei
Dr A. SamieiDairy Cow Nutrition (Ph.D)
Milk production
STRESSCOW HEALTH and PRODUCTIVITY
HomeostasisHomeostasis
Calving
Metabolic stressDigestive stressAbusive cow
handlingPoor sanitationCalvingMilk production
STRESSCOW HEALTH andPRODUCTIVITY
Abusive cow handling
Digestive stress
Poor sanitation
Milk fever
DAMastitis
CalvingMilk production
Metabolic stress
STRESSCOW HEALTH andPRODUCTIVITY
When are cows leaving herds
25% of culls leave before 60 DIM
Stewart et al., 2001
StudyDohooMarkusfeldBigras-PoulinGrohnn2,8755600220473368
Milk Fever-1.55.63.8
Metritis18.2-10.72.3
Mastitis16.8-24.25.4
Ketosis1716.63.36RP8.619.47.74.8
Cystic Ovary10.4-56.8
Thomas Geishauser
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
PregnantNonlactating
NonpregnantLactating
ExtremeCHALLENGE
0
5
10
15
20
25
30
35
day relative to calving
lb of
dry
matt
er/d
ayParturition
Bertice 1992
Days Relative to Calving
Balance NEl, Mcal/day(NEl intake - NEl expanded) Drop in
DMI
-21 -14 -7 0 7 14 21
Colostrum & milksynthesis
-15
-10
-5
0
5
Grummer, 1995
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
Blood estrogen might be responsible for the depression in feed intake
before parturition.
Injection of estradiol-17β reduced feed intake in lactating cows.
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)
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.
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.
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
Overall, increases plasma glucose levels.
Liver Muscle Adipose tissue
XAdiposeTissue Free fatty
acidsLiver
Ketone BodiesInsulin
Pancreas
Mechanism for prevention of ketosis due to excess ketone body production that can lead to ketoacidosis
Liver Adipose tissue
Protein Hormone
Similar structure to Insulin
Stimulates cell growth
Inhibits apoptosis
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
proteinkinase A
cellmembrane
EpinephrineGlucagon
HORMONES
cyclicAMP
ATP
ADP
= activation- = inhibition
TriacylglycerolFatty acid +
Diacylglycerol
OPHSL-a
proteinphosphatase
Pi
+ Insulin
- caffeine
Phospho-diesterase
AMP
+
Adenylylcyclase
(inactive form)
HSL-bOH
inactiveactive
+
+ insulin
AdiposeTissue
NEFA
TG
NEFA
CPT
BETA-OXIDATION
TG
VLDL
Liver
CO2 KetoneBodies
Fatty Liver
Peroxisomes
Mitochondria
- Insulin
+ Stress Hormones
Glucagon, Epinephrine, Somatotropine
Month
Phase 4Phase 4
Pha
se 1
Ph a
s e 1
Phase 6Phase 6P
hase
3P
hase
3Phase 5Phase 5
Pha
se 2
Pha
se 2Dry Matter IntakeDry Matter Intake
Body WeightBody Weight
Milk Milk ProductionProduction
Peak DMIPeak DMIPeak MilkPeak Milk Tail EndTail End
FreshFresh Far Off
Far Off
Close Up
Close Up
65%
Propionate and AA
15-20%
Lactate(endogenic/diet)
Glycerol (lipases FA)
Deficit of 500 g/d GlucoseProtein (Muscle)
0
2500
2000
1500
1000
500
+21-21 0
Energy neededEnergie available
Glu
cose
g/d
- 500 g/d
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.
PrepartumPostpartumincrease
Hepatic Blood Flow1140 l/h2099 l/h+ 84%
DMI9.8 kg/d14.1 kg/d+ 44 %
Liver Oxygen Utilization1619 mmol/h3159 mmol/h+ 95 %
Liver Metabolic Activity
4.4 mmol O2/g
8.6 mmol O2/g
X 2
MITOCHONDRION
cell membraneFA = fatty acidLPL = lipoprotein lipaseFABP = fatty acid binding protein
ACS
FABP
FABPFA
[3]
FABPacyl-CoA
[4]
CYTOPLASM
CAPILLARY
FAalbuminFA FA
FA
fromfatcell
FA
[1]
acetyl-CoA TCAcycle
-oxidation[6]
[7]
carnitinetransporter
acyl-CoA[5]
Overview of fatty acid degradation
ACS = acyl CoA synthetase
LPL
Lipoproteins(Chylomicrons or VLDL)
[2]
GLUCOSE
Triose - P
Pyruvic acid
GLYCEROL
Lactic acid MPG
Oxaloacetic acid Niacin
NiacinSuccinic acid
Transformation cycle
(Krebs)
EnergyPROPIONATE
B12
LIVER
RUMEN
PROPIONATE
BLOOD
Acetyl-CoA
Ketone body formation (ketogenesis) in liver mitochondria from excess acetyl CoA derived from the -oxidation of fatty acids
MITOCHONDRION
(excess acetyl CoA)
Hydroxymethylglutaryl CoA
HMG-CoA synthaseacetyl CoA
CoA
Acetoacetate
HMG-CoA-lyaseacetyl CoA
-Hydroxybutyrate
-Hydroxybutyratedehydrogenase
NAD+
NADH
Acetone
(non-enzymatic)
2 Acetyl CoAFatty acid-oxidation
Citric acid cycle
oxidation to CO2
Acetoacetyl CoACoA
Thiolase
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
MAMMARY GLAND
ADIPOSE TISSUELIVER
TG
FA
NEFA NEFA
MILK FAT
NEFAPeroxysomes
Mitochondria
Acetyl-CoAKeton Bodies
TGVLDL
CO2
Propionate1
2
3
(Drackley, 1997)
CPT-1
Apolipoprotein B, is the main protein in VLDL
NEFA
con
cent
ratio
n m
Eq/L
Days from parturition
Underwood 1998
LIVER
TG
NEFA NEFAPeroxysomes
Mitochondries
Acetyl-CoAKetonBosies
TG
CO2
PropionateKETOSIS
STEATOSIS
!!
!!
LIVER
TG
STEATOSIS
!!
TGTG
TG
TG
TG
TG
TG
TGTG
GLUCONEOGENESIS
TGTG
TG
NH3 UREA
TG
TGTG
Steatosis reduces liver capacity to metabolise ammonia to urea. Hy ammoniac concentration reduces glucose production of hepatocytes (Cadorniga-Valino, 1997; Strang, 1998)
BHBA
Ac
Monitoring Subclinical Ketosis
β-Hydroxybutyrate Concentration in Blood
Urine Ketone Body Test
Milk Ketone Body Test
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
Dr A. Samiei
Position)μmol/L( βHBA
NormalLess than 1000
Uncertain1000 to 1400
Sub-clinical ketosis ≥1400
Clinical ketosis ≥3200
Dr G. Oetzel, Wisconsin University
Position)μmol/L( βHBA
NormalLess than 1000
Uncertain1000 to 1200
Sub-clinical ketosis ≥1200
Clinical ketosis ≥2600
Dr T. Duffield, Guelph University
Position)μmol/L( βHBA
NormalLess than 600
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
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.
ββHBAHBA
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).
TestSensitivitySpecificity
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%)
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%)
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
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).
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 .
DisorderMean (%)Range (%)Milk fever7.20 to 44.1Displaced abomasum3.30 to 14Ketosis3.70 to 20Retained fetal membranes
90 to 22.6
Metritis12.80 to 66
Journal of Dairy Science Vol. 82, No. 11, 1999
0
5
10
15
20
25
30
Perc
ent K
etos
is
Dry '1-2 '3-4 '5-8 '7-8 '9-10Week Post-Calving
Duffield, et al., 1997. Can Vet J 38:713
012345678
Perc
ent K
etos
is
1 2 3 >3Parity
Duffield, et al., 1997. Can Vet J 38:713
ab aba b
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
Type I diabetes mellitus.
Blood insulin concentration is low
hypoglycemia due to a shortage of glucose precursors.
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
Grummer, 1993
5
10
15
20
25
Dry Matter IntakeKg/day
Weeks relative to calving0-1-2 1 2 3
200
400
600
800
1000
Non-EsterifiedFatty Acid um/l
30 -35%intakedepression
300%Increased fatmobilization
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
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 .
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 .
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 .
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.
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
BCS
FFA/NEFA
The average days of lactation.
Association between FFA (NEFA) values and BCS
FFA (NEFA), mmol/l BCS
Gergácz ey al, 2008
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
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
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 .
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)
Immune Function in Periparturient Cows as a Percentage of Control Steers
Week Around ParturitionWeek Around Parturition
Imm
une
Func
tion
(% C
ontr
ols)
Imm
une
Func
tion
(% C
ontr
ols)
Goff & Horst, JDS, 1997
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.
LIVER
TG
TGTG
TG
TG
TG
TG
TG
TGTG
GLUCONEOGENESIS
TGTG
TG
TG
TGTG
Fatty Liver
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
Reduction in milk yield ranged between 4-10 kg/day for clinical ketosis and 3 kg/day for subclinical ketosis .
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
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%.
2022242628303234363840
Con
cept
ion
rate
, %
< 3.0 3.0 - 4.0 4.0 - 4.5 >4.5Milk fat, Percent
Kristula, et al., 1995. Prev. Vet. Med 23:95
Nutritional Management
Propylin Glycol
Niacin
Rumen-Protected Choline
Rumen-Protected Methionine and Lysine
Monensin
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.
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).
05
101520253035404550
Low High LowDiet Energy Density
Surface area (mm2) Absorption rate (mmol/min)
725-kg Cow 570-kg HeiferFunction Pre Post Pre Post
Maintenance 11.2 10.1 9.3 8.5Pregnancy 3.3 --- 2.8 ---Growth --- --- 1.9 1.7Milk 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.
302520151050-5-10-15-20-255
10
15
20
25
30 ControlForce Fed
Day Relative to Calving
DM
I kg /
d
Force-feeding prepartum cows via rumen cannula
Bertics et al., 1992
0
5
10
15
20
25
30Li
ver T
rigly
cerid
es,
% D
M
-17 1 28
Day Relative to Calving
Force FedControl
Bertics et al., 1992
Fat content in liver of force-fed cows
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)
00.5
11.5
22.5
33.5
4
umol
/h *
g w
et w
eigh
t
-21 1 21 65
Propionate Alanine
GLUCOSE
Triose - P
Pyruvic acid Lactic acid MPG
Oxaloacetic acid Niacin
NiacinSuccinic acid
Transformation cycle
(Krebs)
EnergyPROPIONATE
B12
LIVER
RUMEN
MPG PROPIONATE
BLOOD
Acetyl-CoA
Transformation of the ingredientsin Propylene glycol into glucose…
Calcium propionate
50%
50%
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).
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, IU/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)
Effect of PG on Performance and Blood Metabolites of Cows
Item
Treatment Milk, kg/d
Insulin, IU/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)
32
34
36
38
40
42
1 2 3 4 5 6 7 8ماههایشیرواری
(kg)
شیرلید
تو
Treated Group Control Group
Propylene Glycol fed at 100g per dayfor 3 weeks pre- and 4 weeks post-calving1600 cow trial; Arizona
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 .
GLUCOSE
Triose - P
Pyruvic acid
GLYCEROL
Oxaloacetic acid Niacin
NiacinSuccinic acid
Transformation cycle
(Krebs)
Energy
LIVER
RUMEN
Butyric Acid
BLOOD
Acetyl-CoA
Transformation of the ingredientsin glycerol into glucose…
GLYCEROL
BLOOD
52%PROPIONATE
48%
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 .
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 .
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).
ComponentsGlyco-LineMPGGlocusaMPG35.514.76.78
Glycerol818.218.5Propionate Ca11.55.88.2
Propionic acid94.426.49Ca1.51.356.61
DM7365.779.45Produce Glucose 28512398.9
AdiposeTissue
NEFA
TG
NEFA
CPT
BETA-OXIDATION
TG
VLDL
Liver
CO2 KetoneBodies
Fatty Liver
Peroxisomes
Mitochondria
- Insulin
+ Stress Hormones
Reducing NEFA mobilization
Stimulating peroxisomal β-oxidation
Boosting VLDL synthesis
Stimulating mitochondrial β-oxidation
Adipose Tissue Triacylglycerol
HSL
DiacylglycerolMonoacylglycerolNEFA
Blood Compartment
Niacin-
Zinnet al., 1987and Santschiet al., 2005, data combined
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)
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)
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, M 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)
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.
apolipoprotein B (apoB )
Phospholipids
Cholestrol (FC)
Cholesteryl ester
Triglyceride (TG)
( PC , SM , lysoPC )
(CE)
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.
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
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
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)
Carnitine transports FA inside the mitochondria where they are burnt
to produce energy (β-oxidation).
Figure 2 (top). Activation of palmitate to palmitoyl CoA (step 4, Fig. 1) and conversion to palmitoyl carnitine
IntermembraneSpace
OUTERMITOCHONDRIALMEMBRANE
palmitoyl-carnitine
CoApalmitoyl-CoA
carnitine
Cytoplasm
palmitoyl-CoA
AMP + PPiATP + CoA
palmitate
CPT-I [2]
ACS[1]
CPT-I defects cause severe muscle weakness because fatty acids are an important muscle fuel during exercise.
Figure 2 (bottom). Mitochondrial uptake via of palmitoyl-carnitine via the carnitine-acylcarnitine translocase (CAT) (step 5 in Fig. 1).
Matrix
INNERMITOCHONDRIALMEMBRANE
Intermembrane Space
palmitoyl-carnitinecarnitine
CoApalmitoyl-CoA
CAT [3]
palmitoyl-carnitineCPT-II
carnitine
CoApalmitoyl-CoA[4]
CPT-I
CAT
IntermembraneSpace
OUTERMITOCHONDRIALMEMBRANE
palmitoyl-carnitine
CoA
carnitine
Cytoplasmpalmitoyl-CoA
AMP + PPiATP + CoA
palmitate
palmitoyl-CoA
Matrix
INNERMITOCHONDRIALMEMBRANE
[3]
palmitoyl-carnitinecarnitine
CoApalmitoyl-CoA[4]
CPT-I [2]
ACS[1]
CPT-II
Figure 3. Processing and -oxidation of palmitoyl CoA
matrix side
inner mitochondrialmembrane
2 ATP3 ATP
respiratory chain
recycle6 times
Carnitinetranslocase
Palmitoylcarnitine
Palmitoylcarnitine
Palmitoyl-CoA
+ Acetyl CoACH3-(CH)12-C-S-CoA
O
oxidationFAD
FADH2
hydration H2O
thiolase CoA
oxidation NAD+
NADH
Citricacid cycle 2 CO2
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.
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)
500 mls 50% dextrose IV (250g)
transient (<2hr) glucose, most lost
in urine
minimal input to daily glucose requirements
-60 0 60 120 180
Insulinng/ml
Glucosemg/dl
AAmg/dl
0
2
0
200
0
10
Lipolysis, gluconeogenesis supply of NEFA’s to liver transport of NEFA’s into mitochondriainsulin:glucagon ratio
Result is ketogenesis
IV over ~ 5 minNot SC
tissue necrosis, abscesses
Rapid resolution of clinical signs
milk yieldMay relapse (~2d)
Oral Propylene glycol (PG)8-14 oz as a drench SID-BID 3-5 drumen motility required for absorption
most absorbed rapidly from rumen as PGmetabolized in liver to glucose
peak conversion ~ 4 hrs, preinfusion levels ~12 hrsToxicity
appetite suppression, diarrhea
Shift glucose distribution and utilization blood glucose milk production
Stimulate appetiteUse in fatty liver controversial
unchanged or lipolyis and blood NEFA’sgood data lacking
Not in pregnant cows
Dexamethasone (Azium: Schering-Plough)5-20 mg IV or IM q 24 hr
Isoflupredone acetate (Predef 2X: Pharmacia-Upjohn)
10-20 mg IM q 24 hr May risk for hypokalemia (mineralocorticoid
activity)Administer in conjunction with dextroseCaution in cows with concurrent infectious disease
Monitor for relapses, other conditionsNicotinic acid
antilipolytic, increases blood glucosemode of action?, efficacy data lacking
Insulinantilipolytic, antiketogenichypoglycemia, so should be administered in
conjunction with glucose, glucocorticoidsgood data lacking
Prevalence of healthy cows (milk BHB < 100 mmol/l) after treatment with Catosal
P. Sarasola and B. Schmidt
A. SamieiPh.D Thesis
Universiti Putra Malaysia
Lack of knowledge in Ketosis in Iran
Diagnosis of Ketosis in herd
Poor nutritional management
Drop in milk yield after calving
Economical loss
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 .
PREVALENCE OF KETOSIS AND ITS CORRELATION WITH LACTATION
STAGE, PARITY, PEAK MILK YIELD AND REGIONS IN IRANIAN DAIRY COWS
VariablesMeanStandard DeviationMinimum
Maximum
Parity (n)2.641.5871
12
Lactation Stage (d)20.9112.2365
80
Glucose (mg/dl)52.919.94830
111
BHBA (µmol/L) 763.270.788100
4,900
Peak Milk Yield (kg)42.578.5781464
BHBAGlucoseLactation stageParityPeak milk yield
)µmol/L()mg/dl()day()n()kg(
Normal477±8c54±0.30a22±0.44a2.6±0.06a45±0.26a
SCK1780±37b48±0.90b17±0.90b2.8±0.13a35±.51b
Clinical3597±92a35±1.20c14±1.00b2.7±0.24a28±.97c
Source of VariationSum of SquaresdfFP
Region25.23124.67<0.0001
Parity2.0322.260.105
Lactation Stage5.11111.350.0008
Blood Glucose29.03164.44<0.0001
Peak Milk Yield80.541178.79<0.0001
Error443.27984
RegionsBHBAGlucoseLactation stageParityPeak milk yield
)µmol/L()mmol/L()day()n()kg(
Arak602±118cd53±1.20ab24±1.80ab1.8±0.16b39±1.00d
Qazvin730±87abcd54±1.40ab20±1.20abc2.6±0.19ab50±1.00a
Gorgan1056±119ab52±1.60ab21±1.30abc2.4±0.15ab37±1.00d
Isfahan654±44b 52±0.70ab 20±0.90abc3±0.12a47±0.60ab
Karaj688±62bcd54±0.70ab26±2.00a2.6±0.15ab41±0.70cd
Mashhad671±95bcd56±2.00a22±1.60abc2.7±0.30a44±1.00bc
Rey851±67abc55±0.70a22±0.70abc2.6±0.13ab40±0.70d
Sari1145±154a49±1.10bc10±0.50d2.7±0.18ab45±1.40bc
Semnan890±387abc46±1.60c18±2.20bc2.2±0.40ab41±1.60cd
Shahrekord926±164abc49±2.80bc16±1.60cd2.6±0.34ab46±2.00ab
Shiraz377±56d51±2.20ab17.5±2.00bc2.5±0.45ab40±1.20d
Tabriz571±121cd56±2.20a22±2.50abc3.1±0.47a47±1.70ab
Varamin743±45abcd53±0.60ab21±0.70abc2.5±0.12ab40±0.52d
RegionsKetosis SCK Clinical ketosis
(%)(%)(%)
Arak9.757.302.45
Qazvin12.008.603.40
Gorgan31.0023.657.35
Isfahan15.0012.602.40
Karaj11.119.002.11
Mashhad9.507.102.40
Rey21.2616.095.17
Sari28.6019.049.56
Semnan9.000.009.00
Shahrekord30.0030.000.00
Shiraz0.000.000.00
Tabriz9.509.500.00
Varamin17.8015.901.90
ParityLactation StageGlucoseBHBAPeak 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
AN EVALUATION OF Β-HYDROXYBUTYRATE IN MILK AND BLOOD FOR PREDICTION OF SUBCLINICAL KETOSIS IN DAIRY COWS
Plasma and milk factorsUnitMeanPlasma BHBA concentrationµmol/L 1234
Milk BHBA concentrationµmol/L 145
Plasma NEFA concentrationmEq/L 0.284
Milk yield 28dkg 29.5
Milk yield 60dkg 32
Fat percent%3.9
Protein percent%2.8
Plasma and milk factorsUnitNormalSCKPlasma BHBA concentrationµmol/L 7301600
Milk BHBA concentrationµmol/L 65203
Plasma NEFA concentrationmEq/L 0.3350.587
Milk yield 28dkg 3029
Milk yield 60dkg 3430
Fat percent%3.943.98
Protein percent%1.121.35
0102030405060708090
100
0 4.76 23.81 66.67
False Positive Rate (1- Specificity) (%)
True
Pos
itive
Rat
e (S
ensi
tivity
) (%
)
500
200
10050
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
Milk
Yie
ld (K
g)Non SCK
SCK
EFFECTS OF ENERGY LEVEL, BUTYRIC SILAGE AND BODY
CONDITION SCORE ON INCIDENCE OF SUBCLINICAL KETOSIS IN
DAIRY COWS
FarmMilk yield1BCS2BW3Pariety
110,0653.407163.8
210,5223.657904
311,0003.906674
49,8003.427294.4
510,5003.056334
69,6073.256644.4
710,3003.356384
811,1003.56573.6
910,6004.257403.6
109,9503.957044.4
1 Average milk yield during 305d2 Average body condition score at calving3 Average body weight at calving
FarmSCK (BHBA)Normal (BHBA)
12138±117ab853±48ab
21842±115b920±85a
31860±170b770±62abc
41923±118ab873±58a
51905±107b658±59bc
62085±100ab870±86a
71800±112b630±61cd
82286±95a834±77ab
91479±57c453±44d
102005±80ab910±70a
Item
Dairy farms
12345678910
DM56.95±5.54b49.75±2.12bc54.26±2.9b52.57±0.75bc51.98±1.73bc54.72±0.79b87.26±1.95a45.07±1.25c49.26±1.14bc55.96±0.91b
CP14.93±0.58a13.91±0.36ab11.56±0.58cd13.86±0.29ab14.57±0.62ab12.95±0.49bc13.16±0.28bc10.85±0.24d15.54±0.95a15.30±0.16a
NEL1.58±0.02ab1.50±0.04bc1.47±0.06c1.53±0.02abc1.53±0.006abc1.56±0.01abc1.50±0.009bc1.47±0.03c1.59±0.006a1.48±0.01c
NDF44.42±1.83a44.90±2.33a48.93±2.88a44.66±2.05a45.21±0.41a44.10±0.8a43.42±2.64a47.92±0.65a35.18±0.51b45.482.03a
ADF29.11±1.71bc23.32±2.57abc25.46±3.89a21.77±1.48abc21.83±0.39abc20.38±0.62abc25.18±2.17a23.75±0.55ab25.20±0.69a18.30±0.3c
NFC30.48±2.31b30.0±2.387b32.36±3.66b31.47±1.95b30.53±1.09b35.80±1.08ab30.76±2.35b29.65±0.78b41.15±0.52a34.75±1.91b
EE2.84±0.52a2.57±0.31a1.36±0.29cd1.11±0.09d1.51±0.11cd1.25±0.08d2.22±0.18abc2.22±0.35abc1.61±0.19bcd2.42±0.09ab
Ash7.31±0.31bc8.53±0.73ab5.76±0.61d8.88±0.26a8.18±0.53ab5.88±0.13cd8.06±0.26ab7.03±0.21bcd5.94±0.18cd7.30±0.34bc
Ca0.72±0.12ab0.65±0.05bc0.44±0.08c0.80±0.08ab0.82±0.05ab0.76±0.06ab0.76±0.03ab0.73±0.04ab0.80±0.02ab0.91±0.03a
P0.45±0.03ab0.30±0.03cd0.25±0.03d0.32±0.03cd0.35±0.03cd0.37±0.01bc0.31±0.038cd0.31±0.02cd0.38±0.02abc0.47±0.01a
ItemDairy farms
12345678910
DM23.17±1.35b22.55±0.72b28.86±0.5a24.12±0.8b28.12±2.3a28.03±0.33a25.62±1.15ab24.65±0.67ab25.65±0.67ab28.63±0.40a
CP7.86±0.2abc7.56±0.19abc6.92±0.1c7.78±0.19abc7.86±0.36abc8.25±0.07ab7.37±0.16bc7.47±0.16bc8.53±0.58a7.86±0.18abc
NEL0.97±0.02ab0.91±0.01abcd0.83±0.02cd0.92±0.03abcd0.82±0.04d0.85±0.01bcd0.96±0.009abc0.94±0.009abc1.02±0.08a0.91±0.20abcd
NDF58.30±0.68ab51.60±3.02b54.06±1.1ab62.05±3.24a56.45±0.43ab53.06±0.93ab54.25±5.30ab53.25±5.30ab51.85±1.8b55.96±0.48ab
ADF32.15±0.75ab30.25±0.47abcd27.66±0.9cd33.95±2.74a27.25±1.5d28.06±0.3bcd31.80±0.3abc30.80±0.3abc30.45±1.16abcd30.06±0.69abcd
NFC24.12±0.59c26.40±0.55abc30.58±0.89ab18.37±3.1c32.32±2.32ab31.69±0.9ab29.15±4.99ab26.30±0.50abc33.68±2.89a27.42±0.09ab
EE1.47±0.221.82±0.11.43±0.041.74±0.211.63±0.021.45±0.051.45±0.151.54±0.101.58±0.101.67±0.07
Ash8.15±0.44ab7.02±0.42b7.00±0.36b10.05±2.07a6.32±0.39b5.53±0.12b7.77±0.29ab7.67±0.29ab5.32±0.33b7.06±0.37b
Ca1.30±0.14a0.78±0.1b0.9±0.11ab0.98±0.17ab0.95±0.04ab1.27±0.24a1.19±0.12ab0.86±0.05b0.83±0.06b0.89±0.06ab
P0.18±0.008dc0.14±0.007d0.20±0.01bc0.25±0.01ab0.22±0.008abc0.26±0.04a0.20±0.008bc0.22±0.01abc0.23±0.01abc0.24±0.005ab
ItemDairy farms
12345678910
pH3.71±0.01b3.57±0.03b3.55±0.03b4.04±0.1a3.80±0.05ab3.78±0.05ab3.67±0.05b3.69±0.09b3.74±0.04b3.56±0.03b
Lactic acid3.68±0.36bc3.11±0.31c8.06±2.60a6.38±0.98ab4.01±0.57bc3.67±o.50bc4.33±0.47bc3.78±0.35bc5.04±0.47bc8.70±2.22a
Acetic acid4.09±0.673.70±0.273.86±0.293.45±0.264.39±1.084.05±0.313.52±0.373.78±0.404.72±0.13.68±0.45
Propionic1 0.38±0.02cd0.56±0.09bc1.47±0.23a0.26±0.01cd0.23±0.05d0.000.82±0.16b0.72±0.16b0.34±0.02cd1.45±0.2a
Butyric acid0.000.38±0.07b0.001.01±0.31a0.53±0.09ab0.000.000.95±0.07ab0.000.00
L:A21.02±0.1b0.85±0.1b2.07±0.59a1.89±0.32a0.97±0.06b0.94±15b1.23±0.15b1.03±0.12b1.06±0.08b2.300.32a
1Propionic acid 2Lactic acid to acetic acid ratio
pHDMLacticAceticPropionicButyricLactic:Acetic
pH1
DM-0.19851
Lactic-0.01980.22271
Acetic0.0236-0.18550.09441
Propionic-0.27720.3295*0.4532**0.12001
Butyric0.4692*-0.01730.06310.02540.04901
Lactic:Aceti
c
0.06600.26830.8782**0.32710.4397**0.95281
FarmBCS±SD
Day -3Day 3Day 14Day 28
13.35±0.38a3.10±0.38ab2.70±0.33bc2.35±0.29c
23.05±0.21a2.80±0.21ab2.55±0.21bc2.40±0.14c
33.65±0.34a3.40±0.34ab3.15±0.34ab2.90±0.42b
43.90±0.22a3.65±0.22a3.25±0.25b2.90±0.42b
53.50±0.733.25±0.732.95±0.782.65±0.74
63.40±0.38a3.25±0.38ab2.75±0.31c2.50±0.25c
73.25±0.35a3.05±0.33ab2.70±0.33bc2.40±0.29c
83.70±0.37a3.45±0.37a2.85±0.22B2.25±0.25C
93.90±0.22a3.70±0.21a3.40±0.14b3.25±0.18b
104.25±0.25a4.00±0.25a3.50±0.18b3.10±0.29c
ParameterEstimateStandard ErrorChi-Square
Intercept-32.569012.68246.59*
Butyric Silage0.74810.74810.78ns
NEL21.99179.30955.58*
BCS-0.60730.84830.51ns
CP-0.17730.21170.70ns
NFC-0.04930.10450.22ns
Milk Yield0.13570.07962.90 ns
SCK (%) = α + 21.99 NEL
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
EFFECTS OF NON-FIBER CARBOHYDRATE OF DIET AND GLYCO-LINE SUPPLEMENTATION ON SUBCLINICAL KETOSIS IN DAIRY COWS
GroupsTreatments
I35% NFC, 0g PG
II35% NFC, 150g PG
III35% NFC, 300g PG
IV40% NFC, 0g PG
V40% NFC, 150g PG
VI40% NFC, 300g PG
NFC 35%NFC 40%Effect, P value
PG0PG150PG300PG0PG150PG300NFCPGNFC ×
PG
BHBA769±100a786±109a816±103a625±99ab576±82ab513±69b0.00440.93640.6873
Glucose43±1.55c49±1.38ab47±1.59b48±1.57b51±1.94ab52±1.61a0.00450.00280.5409
Milk yield28±0.49d32±0.54c33±0.74c34±0.48bc35±0.48b38±0.59a<0.0001<0.00010.0609
``
UNIVERSITI PUTRA MALAYSIA