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