Transcript Summarizing the metabolic disease as a main influence on

Summarizing the metabolic
diseases as a main influence on
reproductive failure
Paola Amodeo
Regional Breeders Association of Lombardy
Crema– Italy
S.A.T.A. Bovine Nutrition Specialist
[email protected]
Can genetical selection of dams &
sires stop the fertility downbound
trend?
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It can help but it is surely not the
main drive
Management and nutrition have
still a lot to do and say about it
October 25-26 2011
Dott. Paola Amodeo - SATA Bovine Specialist
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Strong milk producers have worse
fertility?
It is all a management challenge
October 25-26 2011
Dott. Paola Amodeo - SATA Bovine Specialist
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Why should we care?
Post partum involuntary culling
Days in milk
(even more expensive for first calving cows)
More costs:
Dead cows and
urgent cullings
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Better culling value,
voluntary culling
Dott. Paola Amodeo - SATA Bovine Specialist
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Why should we care?
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Transition cow metabolic diseases
lead to reproductive failure
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We must search for the causes of
such diseases and losses
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Cow comfort (housing, space,
grouping)
Environmental (heat stress)
Nutritional : mainly related to NEB in
the transition period
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Seems to be a very important area
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Dairy Cow Transition
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We are not dealing with macroscopic and
gross nutrition mistakes on animal
requirements or on macro and micro
mineral umpairing as it used to be
Now the problem is more subtle and
maybe more sneaky
At the moment it is the main area on
which all researchers and nutritionists are
concentrating their efforts
October 25-26 2011
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Strong physiological changes from dry
cow (pregnancy) to lactation
Suppression of appetite
Immune system Suppression
Higher risk for fatty liver, DA, RP, Ketosis and
milk fever + masitis and metritis (infectuous)
Fertility
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culling risk
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Main Goal:
Control fat mobilization through the
transition period to decrease DMI
depression and immune suppression
from high non esterified fatty acids
(NEFA)
Latest theory of feed intake control to
formulate diets for transition cows
(M.S.Allen and B.J. Bradford – Michigan
State University)
October 25-26 2011
Dott. Paola Amodeo - SATA Bovine Specialist
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Hepatic Oxidation Theory (HOT)
Food intake is controlled by fuels
oxidation in the liver through a
system of connections to the
hepatic vagus nerve
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Firing rate of the nerve determined by liver
oxidation of fuels wich produces ATP:
Higher firing rate= hunger
 Lower firing rate= satiety
 Higher ATP= more oxidation=lower firing
rate=satiety
We still do not know how ATP concentration
influences firing rate of hepatic vagus nerve
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October 25-26 2011
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Fuels for oxidation in ruminants are:
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Fatty acids (from diet and/or body reserves)
Propionate (by microbial fermentation)
Lactate (by muscles and gut tissues from
glucose)
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Amino acids
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(from protein degradation)
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…Fatty acids…
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NEFA from body fat mobilization
(readily oxidized) suppress DMI in
the transition period
Fat mobilization is affected by
plasma insulin concentration
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High insulin = fat synthetis
Low insulin = fat mobilization
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But plasma Insulin decreases by 50%
in the pre calving weeks
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Lower insulin=more fat mobilization=
higer NEFA
Moreover we have a decreased tissue
sensitivity to insulin (insulin resistance )
Lower glucose utilization (which remains
constant despite declining of feed intake) so
use of NEFA by muscles increases
October 25-26 2011
Dott. Paola Amodeo - SATA Bovine Specialist
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…At calving..
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Plasma glucose concentration drops
dramatically at calving
Plasma insulin and insulin tissue
sensitivity remain low
Plasma NEFA concentration remain high
for several weeks Ketones in plasma
DMI decreases
Risk of fatty liver
no new glucose production
No insuling produced in the pancreas
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Mechanism of intake regulation according
to the hepathic oxidation theory
Allen et al 2009
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NEFA and transition diseases risk
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High NEFA in the 2 weeks before calving is
associated with
2 to 4 times increased risk of LDA (Cameron et al,
1998; LeBlanc et al, 2005; Opsina et al, 2010)
1.8 times increased risk of retained placenta (RP)
(LeBlanc et al 2004)
2 times increased of culling before 60 days in milk
(DIM) and 1.5 times increased risk of culling over
the whole lactation (Duffield et al, 2005)
Reduced milk yield (Carson, 2008; Opsina et al,
2010)
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Dott. Paola Amodeo - SATA Bovine Specialist
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BHBA and Transition diseases
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Subclinical ketosis (BHBA > 1200 – 1400
mol/L) in early lactation is associated with
3 to 8 times increased risk of LDA
(Duffield, 1997; Geishauser et al, 2000b;
LeBlanc et al 2005)
Decreased probability of pregnancy at
first AI (Walsh et al, 2008)
Decreased milk production (Duffield,
2009)
Increased duration and severity of
mastitis (Suriyasathaporn, 2000
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Suggested herd goals for NEFA and
Ketons
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AVOID NEB!
(Negative Energy Balance)
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It suppresses immune function
It promotes metabolic disorders
It potentially explaines the relationship
between infectious and non infectuous
transition disorders
Important role of inflammation response
in infectuous diseases as well as
metabolic disorders (B.Bradford-Kansas State
University)
October 25-26 2011
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Inflammation Response
from infectuous disorders
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Activated immune cells release of nitric oxide,
prostaglandins and citokines
Citokines stimulate systemic inflammatory responses
(>Temp,<DMI)
Citokines activate production of acute phase proteins
(haptoglobin and serum Amyloid A by the liver
•Mammary and uterin infections
Local and systemic inflammation
•Coliform Mastitis
Endotoxines, cytokines and acute phase
proteins
•Metritis
High plasma haptoglobin prior to clinical signs of metritis
These non specific inflammatory responses promote
development of metabolic disorders by decrease in DMI
and unpair
metabolic
functions
Dott. Paola
Amodeo - SATA
Bovine Specialist
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October 25-26 2011
Inflammation-based pathogenesis of
transition cows disorders
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Wide evidence of link between inflammation and
transition disorders, unpaired repro efficiency,
lower plasma calcium concentrations
Metabolic Disorders derive also from
inflammation caused by
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Infections (se above)
Oxidative stress (lipids meet ROS (reactive oxigen
species) and produce lipid peroxides
Endotoxins from the gut (sub acute ruminal acidosis?
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Consequences of such inflammation
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Disruption of normal metabolism
Induction of metabolic diseases
Suppression of immune function
by oxidative stress which damages
lipids, proteins and DNA of immune
cells
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…in summary….
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A combination of insults including
infection, chronic inflammation in
obese cows an lipid peroxide
formation promotes systemic
inflammation during transition
Inflammation impairs immune
function making cows more
susceptible to infectuous disorders
and to metabolic disorders
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…what can we do?
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Antioxidants: Vit E and Selenium
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Contribute to ROS neutralization (both)
Decrease production of inflammatory
cytokines (only Vit E)
Effects on immune function (only Vit E)
Raccomended doses
VIT E = 1500 UI/d in close-up cows
 Organic Selenium (if deficient) 0,3 ppm/d
(FDA limit)
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…what can we do?
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Antioxidant Beta Carotene
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Its concentration dicreases during
transition
Recommended dose 600mg/d
Can replace Vit A in transition
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…what can we do?
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Metabolic modifiers: PPAR
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Agonists of peroxisome receptors
Decrease Plasma NEFA concentration
Promote fatty acid oxidation in liver
Limit triglyceride accumulation and
production of lipid peroxides
NOT APPROVED!
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…what can we do?
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Choline
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Limits peroxides formation by
decreasing plasma NEFA and clearing
triglycerides from the liver
In the rumen protected form it may
contribute to immune functions
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…what can we do?
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Anti inflammatory agents: NSAIDs
(non-
steroid anti-inflammatory drugs)
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Prevention of hypoglicemia
Effective at reducing body temperature
Do not consistently improve recovery from
infections
Better activity against metabolic disorders
Aspirin: lower production of haptoglobine
Future research needed
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Nutritional strategies for Transition
cows
Late lactation and far off Dry Cows
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Limit mobilization of body fat by
controlling BCS during late lactation
Feed high NDF, low energy in dry
cows
Feed low concentration of high
fermentable starch in dry cows
October 25-26 2011
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Nutritional strategies for Transition
cows
Close-up
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Feed high fill, moderate energy diets
in close-up cows (Drackley, Overton)
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control energy intake
reduce fat depots
sustain plasma glucose through calving
increase amount of ruminal digesta
which dicreases risk of DAs
increase bufferuing capacity (acidosis)
increase acetate production, dicreases
propionate production
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Nutritional strategies for Transition
cows
Close-up
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Correct choice of forages
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Low potassium content if grasses
Not too high NDF fermentability
Wheat straw has a slow rumen passage and
slows down diet passage rate (mat) also
increasing digesta retention
FATs: should not be fed
Can depress feed intake and increase fat
oxidation
Exception: Ω3???? Perhaps antiinflammatory
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Overall goals for energy intake of both
far-off and close-up cows
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Far off cows (dry off until ~ 3 weeks precalving
 ~18 Mcal of NEL per day
Close-up cows (last 3 weeks before calving)
 ~19 Mcal of NEL per day
Vary energy density of diets based upon group DMI
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If energy intake low, increasing energy density may help
If energy intake too high, bulk up the diet to control
energy intake
The ONLY way to minimize management/facilityinduced variation in feed intake among cows is to
ensure that the group is FULLY FED
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Drakley’s guidelines for dry cow diets
2006
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Drakley’s guidelines for closee-up cow diets
2006
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Low K only
NEL, Mcal/lb
0.66 to 0.68
NEL, Mcal/kg
1.45 to 1.50
Metabolizable protein, g/d
1100 to 1200
NFC, %
30 to 34
Starch, %
17 to 20
Dietary Ca, g/d
100
Dietary Ca, %
0.90
Dietary P, %
0.30 to 0.35
Mg, %
0.40 to 0.42
Cl, %
0.3
K, %
< 1.3
Na, %
0.10 to 0.15
S%
0.20
Added Se, ppm (organic)
0.3
Vitamin A (IU/d) 100000
Vitamin D (IU/d) 30000
Vitamin E (IU/d)
1800
Full anionic
140
1.2
0.8 to 1.2
< 1.3
0.3 to 0.4
100000
30000
1800
Prefer use of organic trace elements, including organic Se
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Nutritional strategies for Transition
cows
Fresh cows (0-14 days post partum)
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Avoid highly fermentable starch
sources (high propionate production
stimulation of oxidation of Acetyl CoA suppress
feed intake)
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Dry Corn is best
(provide glucose precursors
and less propionate)
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As gut fills begins to dominate feed
a less filling and more fermentable
diet
October 25-26 2011
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Next problem….
How can we move
from theory to
practice?
Thanks for the attention
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