Ketosis 2011 samiei

Dr A. Samiei
Dairy Cow Nutrition (Ph.D(

Milk
production
Milk
production
STRESS
COW HEALTH and
PRODUCTIVITY
HomeostasisHomeostasis
CalvingCalving

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

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

When are cows leaving
herds
25% of culls leave before 60 DIM
Stewart et al., 2001

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

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

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

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

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.

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

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
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

Adipose
Tissue
NEFA
TG
NEFA
CPT
BETA-OXIDATION
TG
VLDL
Liver
CO2 Ketone
Bodies
Fatty
Liver
Peroxisomes
Mitochondria
- Insulin
+ Stress
Hormones
Glucagon, Epinephrine,
Somatotropine

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

65%
Propionate and AA
15-20%
Lactate
(endogenic/diet)
Glycerol
(lipases FA)
Deficit of 500 g/d Glucose
Protein (Muscle)

0
2500
2000
1500
1000
500
+21-21 0
Energy needed
Energie available
Glucoseg/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.

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

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]

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

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

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 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

NEFAconce
Days from parturition
Underwood 1998

LIVER
TG
NEFA NEFA
Peroxysomes
Mitochondries
Acetyl-CoA
Keton
Bosies
TG
CO2
Propionate
KETOSIS
STEATOSIS
!!
!!

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)

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

Position )μmol/L) βHBA
Normal Less than 1000
Uncertain 1000to 1400
Sub-clinical ketosis ≤1400
Clinical ketosis ≤3200
Dr G. Oetzel, Wisconsin University

Uncertain 1000to 1200
Sub-clinical ketosis ≤1200
Clinical ketosis ≤2600
Dr T. Duffield, Guelph University

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.

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).

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%)

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.

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

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

0
1
2
3
4
5
6
7
8
PercentKetosis
1 2 3 >3
Parity
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 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

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
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

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
ImmuneFunction(%Controls)ImmuneFunction(%Controls)
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
TG
TG
GLUCONEOGENESIS
TG
TG
TG

TG
TG
TG
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

• 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%.

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

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(.

0
5
10
15
20
25
30
35
40
45
50
Low High Low
Diet Energy Density
Surface area (mm2( Absorption rate (mmol/min(

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.

302520151050-5-10-15-20-25
5
10
15
20
25
30 Control
Force Fed
DMIkg/d
Force-feeding prepartum cows via
rumen cannula
Bertics et al., 1992

0
5
10
15
20
25
30
LiverTriglycerides,
%DM
-17 1 28
Force Fed
Control
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)

0
0.5
1
1.5
2
2.5
3
3.5
4
umol/h*gwetweight
-21 1 21 65
Propionate Alanine

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%

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, 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)

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(

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

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
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%

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).

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

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

Adipose Tissue
Triacylglycerol
HSL
Diacylglycerol
Monoacylglycerol
NEFA
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, 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)

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 ， lys
oPC ）
(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
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.

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

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

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

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)

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

↓ Lipolysis, ↓ gluconeogenesis
↓ supply of NEFA’s to liver
↓ transport of NEFA’s into mitochondria
insulin:glucagon ratio
Result is ↓ ketogenesis

IV over ~ 5 min
Not SC
tissue necrosis,
abscesses
Rapid resolution
of clinical signs
↑ milk yield
May relapse (~2d(

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

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

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

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

Prevalence of healthy cows (milk BHB < 100 mmol/l) after treatment with Catosal
P. Sarasola and B. Schmidt

A. Samiei
Ph.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

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

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

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

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

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

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

AN EVALUATION OF Β-HYDROXYBUTYRATE
IN MILK AND BLOOD FOR PREDICTION OF
SUBCLINICAL KETOSIS IN DAIRY COWS

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

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

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

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

EFFECTS OF ENERGY LEVEL, BUTYRIC
SILAGE AND BODY CONDITION SCORE
ON INCIDENCE OF SUBCLINICAL
KETOSIS IN DAIRY COWS

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

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

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

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

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

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

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

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

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

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

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

Ketosis 2011 samiei

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