Trastornos metabólicos y nutricionales - vet.unicen.edu.ar · sÍndrome de vaca gorda (vaca lechera) cetosis (vaca lechera) toxemia de la preÑez (oveja) obesidad perros y gatos)

Trastornos metabólicos y nutricionales

Cuando nosotros alimentamos a los animales que atendemos o criamos, somos responsables de los trastornos nutricionales

La nutrición es una disciplina cuantitativa: nutrientes aportados en la ración nutrientes requeridos por el animal

Los trastornos nutricionales y metabólicos ocurren por un desequilibrio entre los dos términos de esta ecuación

Sólo podemos entender los trastornos y evitarlos o intervenir para corregirlos si conocemos los principios que guían la nutrición de los animales en diferentes estados fisiológicos y los métodos de formulación de raciones

I nformación Técnica

Factores a tener en cuenta antes de sobrepoblar

5 El Boletín de Semex España

Primavera 2012

S

obre el papel, las cuentas son claras, cuantas

más vacas, mayor dilución del coste fijo que supo-

nen las instalaciones, la sala de ordeño y la maquinaria

y por tanto mayor beneficio.

Aumentando el número de cabezas de ganado, preten-

demos aumentar la producción y así el nivel de ingre-

sos de nuestra operación.

Sin embargo, al igual que en cualquier unidad de pro-

ducción, ir demasiado lejos en cuanto al número de ani-

males para el que está preparada nuestra instalación

puede suponer una disminución en la productividad del

ganado a corto, medio o largo plazo, que hay que eva-

luar detenidamente para estar seguros de trabajar con

el óptimo económico en cuanto a tamaño del rebaño

con el que producimos.

El mayor reto consiste en poder cuantificar, aunque sea

de forma aproximada, la repercusión de nuestro nivel de

sobrepoblación sobre las distintas variables que determi-

nan la productividad de nuestro rebaño, estas son:

• Producción• Eficiencia (respecto al nivel de ingestión de materia

seca)

• Rendimiento reproductivo• Salud: sobre todo posparto, de pezuñas y de ubre

Para ello, se impone la necesidad de monitorizar dete-

nidamente a nivel de explotación las distintas variables

a lo largo del tiempo para comprender a ciencia cierta

como responde el ganado frente a los distintos cam-

bios, y en concreto respecto a los referentes al nivel de

población.

Por desgracia, pese a la amplia bibliografía existente

respecto a “cow confort” en general, y a sobrepoblación

en particular, no existe en muchos casos un consenso

claro a la hora de establecer unas pautas concretas,

pero sobre todo de cuantificar la repercusión económi-

ca de la sobrepoblación en aspectos diversos, por

varias razones:

• Por lo general, los estudios tienden a ceñirse a un

periodo de tiempo limitado, que obviamente no es

extrapolable a la realidad histórica de una explota-

ción, en que las condiciones de sobre población se

mantengan indefinidamente. Es por ello por lo que

en muchos casos se omiten los efectos de la sobre

población a más largo plazo.

• Tampoco el número de animales por grupo deestudio, por lo general de 15 a 40, responden siem-

pre a la realidad de muchas explotaciones, que por

razones obvias trabajan con grupos de más de 100

animales, en los que la interacción social es más

compleja, las labores de mantenimiento más difíci-

les, la duración del ordeño es mayor…

• Los estudios tienden a centrarse sobre todo en

repercusiones a nivel de producción, periodo diario

de descanso, número de interacciones agresivas,

patrón de comportamiento alimentario, mucho

menos en lo referente a salud animal (posparto,

podal y de ubre), y apenas nada sobre rendimiento

reproductivo – condición corporal y sobre la eficien-

cia de la ingestión, por lo que creemos que por lo

general omiten como decimos los efectos más alargo plazo del nivel de sobre población.

Por Bernat Sales Nogueras. Veterinario y asesor del Grupo AhedoEnfermedades relacionadas con alteraciones en el aporte y en el metabolismo de la energía

DIABETES Y CETOACIDOSIS (PERROS Y GATOS)

SÍNDROME DE VACA GORDA (VACA LECHERA)

CETOSIS (VACA LECHERA) TOXEMIA DE LA PREÑEZ (OVEJA)

OBESIDAD PERROS Y GATOS)

BAJA CONDICIÓN CORPORAL (VACA DE CRÍA)

Balance de energía (E)

Δ TEJIDO MAGRO Proteína & Agua

Δ TEJIDO GRASO TAG de depósito

Meses

Crecimiento fetal crecimiento fetal Producción de leche Reservas corporales de E Consumo de alimento Parto

Secado Lactancia temprana Lactancia media Lactancia tardía Secado

Balance de energía (E) negativo enflaquecimiento

Condiciones extremas

Balance de energía (E) positivo obesidad

Condiciones extremas


Ingesta de E = Requerimientos de E (Necesidades de E) Equilibrio energético

Ingesta de E > Requerimientos de E => Balance E positivo

Ingesta de E < Requerimientos de E < 0 => Balance E negativo ¿Cómo cuantificamos?

Decisiones sobre la oferta de energía

0

+

-

0

+

-

0

+

-

¿Qué es?

Cambios en balance de E

Δ Peso corporal

Δ Composición química corporal

No se mide con balanza sino con la condición corporal

Δ TEJIDO MAGRO Proteína : Agua 1:3,5

Δ TEJIDO GRASO TAG de depósito

Δ Contenido de energía corporal

Proteína = 23 MJ/kg Magro = 5,1 MJ/kg

Grasa = 39 MJ/kg

Δ NO PROPORCIONALES

¿Cómo se expresa?

ideal falto de peso muy flaco exceso de peso obeso

Condición corporal: puntaje en relación a la forma que tienen ciertas zonas del cuerpo de los animales, previamente definidas

Ver presentación de condición corporal (esta en la página de Pato III)

Consumo de E = Requerimientos de E

E mantenimiento (reposo) + E actividad + E feto y placenta + E leche+ E retenida tejidos corporales + E fibras EM EA EG EL ET EF

E consumida con el alimento (dieta)

EM + EA + EG + EL + ET + EF

Balance de energía (E) ¿Cómo se calcula ?

Consumo de E


Carbohidratos (17 MJ/kg o 4,2 Mcal/kg)

Proteínas (23 MJ/kg o 5,5 Mcal/kg)

Lípidos (39 MJ/kg o 9,3 Mcal/kg)

Digestibilidad

E digestible

E heces

Contenido de E de los nutrientes

Consumo de E = Requerimientos de E

E mantenimiento (reposo) + E actividad + E feto y placenta + E leche+ E retenida tejidos corporales + E fibras EM EA EG EL ET EF




EM + EA + EG + EL + ET + EF Requerimientos de E

440 kJ /d/kg peso 0,75 EM

105 kcal/d/ kg peso 0,75 EM

1 caloría= 4,184 Joules

masa tejido magro edad sexo

(castración) peso = 100 kg

peso 0,75 = 31.6 kg

EM= 13.9 MJ/d

-

+

Costo de funciones de mantenimiento de estructura y servicios orgánicos

Estructura Equilibrio iónico de membranas

Síntesis proteica Síntesis de lípidos

Servicios

Actividad cardíaca y tono vascular Filtración y reabsorción renal

Respiración Actividad hepática

Tejido nervioso

30-40 9-12 2-4

9-11 6-7 6-7 5-10 10-15

% metabolismo basal


440 kJ /kg peso 0,75 EM

Horizontal

27-30 J / m / kg peso

2,13 J/kg peso/m

Vertical

1,2 m/s (4,3 km/h)

2,49 J/kg peso/m 1,8 m/s (6,5 km/h)

2,93 J/kg peso/m 2,4 m/s (8,6 km/h)

EM= 13.9 MJ/d

peso = 100 kg

3 km a 6,5 km/h

2,49 J/kg peso/m

7470 J/kg peso

EA = 747000 J EA = 0,75 MJ

E= 14,65 MJ/d

Blaxter, 1989

Producción de calor de un hombre que camina a diferentes velocidades sobre un terreno nivelado

peso = 70 kg

EM = 7,4 KJ/min 22 KJ/min 3 x EM

12,5 KJ/min 1,7 x EM

EM = 10,6 MJ/d

Blaxter, 1989



Horizontal: 2-4 J / m / kg peso

Vertical: 25-30 J / m / kg peso 54 g/kg 38 g/kg 32 g/kg

kg leche / día

lactosa 16 MJ/kg

grasa 39 MJ/kg

proteína 23 MJ/kg

0,864 MJ/l + 1,48 MJ/l + 0,736 MJ/l = 3,08 MJ/l

peso = 650 kg peso 0,75 = 121 kg

EM = 53 MJ/d

k-lactación1 ≅ 0,65

4,7 MJ/l

10 l/d 47 MJ/d

20 l/d 30 l/d 40 l/d 94 MJ/d 141 MJ/d 188 MJ/d

100 MJ/d 1,9 x EM

147 MJ/d 2,8 x EM

194 MJ/d 3,7 x EM

241MJ/d 4,5 x EM

1 K-lactación = eficiencia de uso de la energía



Horizontal: 2-4 J / m / kg peso

Vertical: 25-30 J / m / kg peso tejido magro tejido graso

Condición corporal

54 g/kg 38 g/kg 32 g/kg

kg leche / día

Energía MJ/d

semanas

grasa

proteína

Cambios en las tasas de deposición de energía de grasa y proteína durante el crecimiento

proteína : agua :: 1,0 : 3,5 Tejido magro

Proteína: 23 MJ/kg

Grasa: 39 MJ/kg

La relación entre retención o pérdida de energía y retención o pérdida de peso no siempre es directa ni simple de predecir: depende del contenido de grasa del cuerpo y de la proporción de tejido graso y tejido magro que se retenga o se pierda

Proteínas Lípidos

Carbohidratos

Tejido Magro: 5,1MJ/kg

E proteína > E grasa E grasa > E proteína

Peso vivo (kg) Peso vacío (kg)* Grasa (kg) Proteína (kg) Agua (kg) Agua/Proteína Minerales (kg) Energía (MJ/kg)

kg % 320 285 22 8 58 20 191 67 3,4 14 5 6,3

kg % 380 339 54 16 62 18 206 61 3,4 17 5 10,4

kg % 440 391 94 24 67 17 215 55 3,2 15 4 13,4

Composición corporal y condición corporal - Escala 1-9 (1-5)

2 (1,5) 4 (2,5) 6 (3,5)

* peso vacío = peso corporal menos contenidos del tubo digestivo

Consumo de E

E retenida en tejidos (ET)

magro grasa proteína : agua 1,0 : 3,5

E Mantenimiento

E Actividad

(E absorbida ~ E digestible)

E heces


E Lactación E Gestación

Consumo de E



E Mantenimiento

E Actividad


E heces


E consumida - Requerimiento E = 0 Equilibrio energético

Adulto Alimentación a requerimientos


Consumo de E



E Mantenimiento

E Actividad


E heces


Adulto

E consumida - Requerimiento E > 0 exceso de peso

Obesidad

condición corporal

Sobrealimentación


E consumida - requerimientos E ≠ 0

> 0 -> exceso de peso

< 0 -> pérdida de peso

Obesidad

BALANCE DE ENERGÍA

Cambio en condición corporal

Mayor condición corporal

Enflaquecimiento - Emaciación

Menor condición corporal

Exceso de grasa corporal suficiente para causar o contribuir a la presentación de enfermedades

20-25 % de exceso de peso en forma de grasa corporal

Obesidad

baja tolerancia al ejercicio dificultad respiratoria enfermedad cardiovascular osteoartritis diabetes tipo II (insulino independiente) reducción de la espectativa de vida

enfermedades asociadas

Consumo de E



E Mantenimiento

E Actividad


E heces


Adulto

E consumida - Requerimiento E > 0 exceso de peso

Obesidad

condición corporal

reducción de peso


E consumida - requerimientos E ≠ 0

> 0 exceso de peso

< 0 pérdida de peso

Obesidad

BALANCE DE ENERGÍA

Cambio en condición corporal

Mayor condición corporal

Enflaquecimiento - Emaciación

Menor condición corporal

Consumo de E



E Mantenimiento

E Actividad


E heces


E consumida - Requerimiento E < 0 pérdida de peso

Adulto

condición corporal

?

Subalimentación


Condición corporal 1-9 (1-5)

3 (2) 4 (2,5) 5 (3)

6 (3,5) 7 (4)

Tasa de

preñez %

43 61 83 93

Intervalo entre partos

d

414 381 364 364

Aumento peso

ternero kg/d

0,73 0,79 0,84 0,84

Condición corporal de la madre, reproducción y crecimiento de las crías

Intervaloparto-celo

d

89 70 60 52 31

Edad destete ternero

d

190 223 240 240

Peso destete ternero

kg

170 208 230 230

20 Nº8 - Octubre 2009

Cavidad menos pronunciada alrededor de la encoladura. Presencia de algo de tejido adiposo. Extremos de costillas algo redondeados. Insuficientes reservas corporales. Luego del parto bajará su estado corporal y se comprometerá su performance reproductiva y lactancia. Anestro superficial.

2

FLACA

TUBEROSIDADESCOXAL E ISQUIATICA

ESPACIO COXALISQUION

BASE DE COLA

SEMEJANTE A CC1 AUNQUE MENOS

PRONUNCIADAS

3

21Nº8 - Octubre 2009

Cuadernillo técnico - IPCVA

Desaparece cavidad alrededor de la cola. Presencia de tejido adiposo no exagerado en esa superficie. Extremos de costillas cortas cubiertas, aunque palpables con leve presión. Estado próximo al ideal en estado post parto. Buena reserva que va a estar asociada a vacas cíclicas y de buena lactancia. Carga justa por hectárea de campo.

3

PROMEDIO



BASE DE COLA

LIGERAS DEPR ESIONES LIGERA FOSA

22 Nº8 - Octubre 2009

Aparición de mayor tejido adiposo cubriendo toda la pelvis, costillas cortas invisibles y difíciles de palpar. Estado ideal aunque será antieconómico. Vacas cíclicas. Excelente lactancia. Buenos índices de preñez, pero es indicativo de baja carga por hectárea.

4

GORDA



BASE DE COLA

SUPERFI CIES REDONDEADAS

5

CC = 3 (2) CC = 5 (3) CC = 7 (4)

Condición corporal 1-9 (1-5)

https://es.slideshare.net/jonescoleen/learn-to-score-body-condition-for-dairy-cows

Condición Corporal

CETOSIS Y CETOACIDOSIS

Insuficiente provisión de glucosa o

precursores de glucosa o insuficiente captación

celular de glucosa

Excesiva condición corporal y alta

movilización de lípidos

Cuerpos cetónicos BOH butirato Acetoacetato

Glucosa

Ácidos Grasos no esterificados

DIABETES (PERROS Y GATOS)

SÍNDROME DE VACA GORDA

(VACA LECHERA) CETOSIS (VACA LECHERA) TOXEMIA DE LA PREÑEZ (OVEJA)

insulina Triglicéridos plasma

Glucosa o = Glucosa


EM = 440 kJ /kg peso 0,75

peso = 650 kg peso 0,75 = 121 kg

EM = 53 MJ/d

4,7 MJ/ leche

10 l/d 47 MJ/d

20 l/d 30 l/d 40 l/d 94 MJ/d 141 MJ/d 188 MJ/d

100 MJ/d 1,9 x EM

147 MJ/d 2,8 x EM

194 MJ/d 3,7 x EM

241MJ/d 4,5 x EM

INSULIN-LIKE GROWTH FACTOR-I IN DAIRY COWS 933

16......- .......-.-----.....-............-...-...... 43 5 7 9 11WEEKS POSTPARTUM

•-' - NEB •./" .-'- PEB • / -"",/'J ··-- --- -."/

, "'" I"'-J_-'

60l

80J.......l:)

E 120"-en..=.. 100

6w(k::o

5.5zo

5 f-azou

4.5 >-aoCD

••• ...... I--28

3 5 7 9 11WEEKS POSTPARTUM

Figure 2. Changes in OM intake (... - -.) and bodycondition score during the first 12 wk postpartum.Data from cows in positive (PEB) and negative energybalance (NEB) were pooled (n = II). Asterisks indicate thefllst mean that differs from wk I (·P<.05); from wk 2("P<.05); or from wk 3 (···P<.05).

Figure 3. Changes in concentration of insulin-likegrowth factor-' (IGF-I) in serwn during the first 12 wkpostpanum for cows in positive (PEB) (_. n = 5) ornegative energy balance (... - -., n =6). Asterisk indicatesmean differs (·P<.05) from wk I in NEB cows and wk 4 inPEB cows.

body condition score did not change (P>.IS)(Figure 2). Change in body condition scorefrom wk I to wk 12 did not differ between PEBand NEB cows (-.6 ± .4 and -1.S± .4, respec-tively).

Serum Insulln·Uke Growth Factor-I

ciated with estrus compared with only 16.7%for the NEB cows (Figure 4) (P<.IS). Duringthe second postpartum estrous cycle, estrus wasobserved prior to ovulation in 80% of PEBcows and 66.7% of NEB cows (b. 15).Average weekly concentration of progester-

one in serum was 4.56 ± .36 nglml during the12-wk study and did not differ (b. IS) between

1 2ESTROUS CYCLE POSTPARTUM

Figure 4. The percentage of cows in negative (NEB)(open bar) and positive energy balance (PEB) (shaded bar)exhibiting estrus during their fllSt and second estrous cyclespostpartum. Asterisk indicates mean differs from NEB(P<.I5).

Cows in PEB had greater (P<.IS) concentra-tions of IGF-I in serum than did NEB cows(102.5 ± 10.6 nglml vs. 78.8 ± 9.7 nglml;Figure 3). Concentrations of IGF-I in serumalso changed (P<.OOl) with weeks postpartum.The IGF-I concentrations in serum of PEBcows increased between wk 4 and 5, whereasno change occurred after 3 wk postpartum inNEB cows (Figure 3).

Ovarian and Estrous Activity

Interval to first postpartum ovulation (24.4 ±2.3 d, as assessed by the first rise in serumprogesterone concentration >1.5 nglml), and in-tervals to first and second estrus (41.9 ± 6.6 dand 58.2 ± 5.4 d) did not differ between PEBand NEB cows. In addition, days to frrst ovula-tion (range 14 to 39 d) was not correlated toaverage EB during the I2-wk study (r = .278,b.I5, n = II). However, 60% of the frrstpostpartum ovulations in PEB cows were asso-

lfl 100::>a::I-

80l:)

z 60I-m

40wtil

20ou0

o NEB

o PEB

*:!.,l,:'i:

,',::::'

I "'!;.,

Journal of Dairy Science Vol. 73, No.4, 1990

932 SPICER ET AL.

TABLE 2. Me;an components (± SE) of energy balance calculations for cows in negative (NEB) or positive energy balance(PEB).

NEB PEB

Body weight. kgNet energy for maintenance, Mcal/dOM intake. kg/dNet energy intake. McalldMilk yield. kg/dMilk fat. %Milk SNF. %Milk energy, Mcal/dEnergy balance. I Mcal/d

X715.911.0823.136.8538.63.588.9427.46-1.69

SE27.7.35.8US3.0.18.17I.SSa.66c

X662.110.4423.237.0933.13.688.8023.233.43

SE29.7.37.91.453.3.18.191.66b.71d

a,bwithin a row, means differ (P<.lO).c.dWithin a row, means differ (P<.OOI).lCaiculated as net energy intake - (net energy for maintenance + milk energy).

45 B

Body Weight andBody Condition Scores

Average weekly BW during the 12-wk studywas 692 ± 29 kg (range 526 to 815 kg) and didnot differ (P>.15) between PEB and NEB cows(Table 2). Also, BW did not change (P>.IS)with weeks postpartum. However, BW changebetween wk 1 and 12 differed (P<.lO) betweenPEB and NEB cows (30.5 ± 14.3 and -5.6 ±13.1 kg, respectively).Average weekly body condition score during

the 12-wk study was 4.8 ± .1 (range 2.0 to 7.0)and did not differ (P>.15) between PEB andNEB cows. Average weekly body conditionscore decreased (P<.OOI) from 5.8 ± .1 on wk Ito 4.6 ± .1 on wk 5 postpartum, after which

PEB and NEB cows (fable 2). In both groups,milk yield changed (P<.OOI) with week post-partum (Figure 1B). Cows in PEB group had apeak milk yield of 36.0 ± 11.1 kg/d during wk3 of lactation compared with 40.6 ± 10.2 kgldduring wk 6 for NEB cows (P>.15) (FigureIB). The 4% FCM did not differ (P>.15) be-tween PEB (31.1 ± 2.5 kg/d) and NEB (36.0 ±2.2 kg/d) cows.Average daily DM intake during the

12-wk study was 23.3 ± .8 kg/d (range 13.7 to29.1 kg/d) and did not differ between PEB andNEB cows (P>.IS) (Table 2). Daily DM intakeincreased (P<.OOI) from 18.2 ± .6 kg/d duringwk 1 to 25.6 ± .5 kg/d (maximum) in wk 12postpartum (Figure 2).NEB••

6

Figure I. Changes in energy balance (panel A) and milkyield (panel B) during the first 12 wk postpartum for cowsin positive (PEB) (_. n = 5) or negative energy balance(NEB) (II- . -•• n =6). Panel A: Asterisks indicate mean ofPEB cows for that week differs (·P<.IO. ··P<.05) frommean of NEB cows. Panel B: Asterisks indicate first meanwithin group thaI differs from wk I (·P<.05) or from wI. 2(··P<.05).

-0......... 40Ol.:>!........ 35o--l30

>-25


G -10'"wi3 -14.L..,.----....... .......-----3 5 7 9 11

WEEKS POSTPARTUM

Journal of Dairy Science Vol. 73, No.4. 1990

932 SPICER ET AL.

TABLE 2. Me;an components (± SE) of energy balance calculations for cows in negative (NEB) or positive energy balance(PEB).

NEB PEB

Body weight. kgNet energy for maintenance, Mcal/dOM intake. kg/dNet energy intake. McalldMilk yield. kg/dMilk fat. %Milk SNF. %Milk energy, Mcal/dEnergy balance. I Mcal/d

X715.911.0823.136.8538.63.588.9427.46-1.69

SE27.7.35.8US3.0.18.17I.SSa.66c

X662.110.4423.237.0933.13.688.8023.233.43

SE29.7.37.91.453.3.18.191.66b.71d

a,bwithin a row, means differ (P<.lO).c.dWithin a row, means differ (P<.OOI).lCaiculated as net energy intake - (net energy for maintenance + milk energy).

45 B

Body Weight andBody Condition Scores

Average weekly BW during the 12-wk studywas 692 ± 29 kg (range 526 to 815 kg) and didnot differ (P>.15) between PEB and NEB cows(Table 2). Also, BW did not change (P>.IS)with weeks postpartum. However, BW changebetween wk 1 and 12 differed (P<.lO) betweenPEB and NEB cows (30.5 ± 14.3 and -5.6 ±13.1 kg, respectively).Average weekly body condition score during

the 12-wk study was 4.8 ± .1 (range 2.0 to 7.0)and did not differ (P>.15) between PEB andNEB cows. Average weekly body conditionscore decreased (P<.OOI) from 5.8 ± .1 on wk Ito 4.6 ± .1 on wk 5 postpartum, after which

PEB and NEB cows (fable 2). In both groups,milk yield changed (P<.OOI) with week post-partum (Figure 1B). Cows in PEB group had apeak milk yield of 36.0 ± 11.1 kg/d during wk3 of lactation compared with 40.6 ± 10.2 kgldduring wk 6 for NEB cows (P>.15) (FigureIB). The 4% FCM did not differ (P>.15) be-tween PEB (31.1 ± 2.5 kg/d) and NEB (36.0 ±2.2 kg/d) cows.Average daily DM intake during the

12-wk study was 23.3 ± .8 kg/d (range 13.7 to29.1 kg/d) and did not differ between PEB andNEB cows (P>.IS) (Table 2). Daily DM intakeincreased (P<.OOI) from 18.2 ± .6 kg/d duringwk 1 to 25.6 ± .5 kg/d (maximum) in wk 12postpartum (Figure 2).NEB••

6

Figure I. Changes in energy balance (panel A) and milkyield (panel B) during the first 12 wk postpartum for cowsin positive (PEB) (_. n = 5) or negative energy balance(NEB) (II- . -•• n =6). Panel A: Asterisks indicate mean ofPEB cows for that week differs (·P<.IO. ··P<.05) frommean of NEB cows. Panel B: Asterisks indicate first meanwithin group thaI differs from wk I (·P<.05) or from wI. 2(··P<.05).

-0......... 40Ol.:>!........ 35o--l30

>-25


G -10'"wi3 -14.L..,.----....... .......-----3 5 7 9 11

WEEKS POSTPARTUM

Journal of Dairy Science Vol. 73, No.4. 1990

10,5 kg MS/d 16 kg MS/d 21 kg MS/d 26 kg MS/d dieta (DIVMS 0.7)

Movilización de tejidos corporales en las primeras semanas de lactancia

Balance energético negativo

Movilización de tejidos corporales en las primeras semanas de lactancia

1) Requerimientos E > E consumida Balance E negativo

2) Requerimientos de nutrientes específicos por la glándula mamaria, a tasas que no pueden ser cubiertas por la absorción de nutrientes desde el tubo digestivo.

Lactosa, Glicerol, NADPH

Ácidos grasos de cadena corta y media ( C4 - C14)

50 % Ácidos grasos de cadena larga (1/3 C16 y 2/3 C18)

glucosa

BHO butirato

Ácidos grasos

Aminoácidos Proteínas de la leche (lactosa, via gluconeogénesis)

El aporte de estos nutrientes depende de la función hepática y de la condición corporal

Hormona de Crecimiento

Tejido Adiposo

Tejido muscular

Lipogénesis insulino dependiente

Lipólisis mediada por β adrenérgicos

Utilización de glucosa

PLASMA AGNE

Consumo de E



E Mantenimiento

E Actividad


E heces


E Lactación

E consumida - Requerimiento E < 0 pérdida de peso y

condición corporal

Lactancia temprana

Meses



Condición corporal deseada

Cambio de la condición corporal durante la lactancia en vacas lecheras

Producción Hepática (B-OH-Butirato)

Utilización tisular

AGNE

B-OH-Butirato

Acetoacetato

Acetil-CoA

KREBS

Movilización de lípidos

PLASMA B-OH-Butirato

Intermediarios (Oxalacetato, Cetoglutarato)

Glucosa / Amino ácidos

Producción Hepática Cuerpos cetónicos

(B-OH-Butirato)

AGNE


B-OH-Butirato

Acetoacetato

Acetil-CoA

KREBS


PLASMA

Glucosa

Amino ácidos Propionato


Glándula mamaria

Ácidos grasos C4 a C14

Lactación Utilización tisular


B-OH-Butirato

Acetoacetato

Acetil-CoA

KREBS


Glucosa

PLASMA

Amino ácidos

Producción Hepática Cuerpos cetónicos

(B-OH-Butirato)

AGNE

Propionato

Lactación


Glándula mamaria

Ácidos grasos C4 a C14


BOH butirato (mM)

Semanas de lactancia Parto

≅ 1,0 - 1,2 cetosis subclínica

≅ 2,9 -3,0 cetosis clínica

≅ 0,3 – 0,5

Concentración sanguínea de BOHbutirato (mM)

Producción de leche (kg/d)

Balance E

Consumo

Semana de lactancia

Prod

ucció

n de

lech

e (k

g/d)

Curvas de lactancia en vacas Holstein pertenecientes a poblaciones con cuatro clases diferentes de concentración de acetona en plasma(?)

Ácidos grasos no esterificados

Oxidación cuerpos cetónicos

Formación de TAG

Síntesis de apo-proteínas

Síntesis de VLDL

VLDL

BOHB

Ácidos grasos no esterificados

Oxidación cuerpos cetónicos

Formación de TAG

Síntesis de apo-proteínas

Síntesis de VLDL

VLDL

TGA en hepatocito

BOHB

Bobe y col., Journal Dairy Science 87:3105 (2004) Acceso libre en http://www.journalofdairyscience.org

Categorías de hígado graso en vacas lecheras

REVIEW: FATTY LIVER IN DAIRY COWS 3111

Table 9. Association of fatty liver with health status in dairy cows.

Disorder Association1 Reference

Displaced abomasum +++ Wada et al., 1995; Rehage et al., 1996Impaired immunoreactivity ++ Wentink et al., 1997; Zerbe et al., 2000Ketosis +++ Grohn et al., 1987; Veenhuizen et al., 1991Laminitis + Fronk et al., 1980; Rehage et al., 1996Mastitis ++ Morrow et al., 1979Metritis ++ Haraszti et al., 1982; Heinonen et al., 1987Milk fever + Higgins and Anderson, 1983; Grohn et al., 1987Retained placenta + Haraszti et al., 1982; Heinonen et al., 1987

1The number of + represents slight, moderate, or strong detrimental association of fatty liver. The strengthof association increases with increasing concentrations of triacylglycerol.

Milk production, health status, and reproductive per-formance of dairy cows with fatty liver can be decreasedfor weeks after concentrations of liver TAG decreaseback to baseline concentrations (Veenhuizen et al.,1991; Breukink and Wensing, 1997), which suggeststhat fatty liver is associated with long term histological,metabolic, and hormonal changes. Accumulation ofTAG in liver reverses slowly (Veenhuizen et al., 1991)and probably has only minor long term negative associ-ations with the liver itself because liver cells can regen-erate within days. The detrimental associations of fattyliver with other tissues, however, are probably longerterm and less reversible.

Immunological Pathology of Fatty Liver

The incidence of fatty liver is strongly associated withthe incidence of other metabolic disorders, especiallyketosis and displaced abomasum (Table 9) becausethese metabolic disorders have in common that the cowseither are or will be in a severe negative energy balance.Accumulation of liver lipids in cows also is associatedwith increased length and severity of infectious dis-eases such as mastitis (Hill et al., 1985) and metritis(Haraszti et al., 1982). The incidence and severity ofinfectious diseases are increased somewhat in the peri-partal period, even without the presence of fatty liver(Goff and Horst, 1997), because immune functions aresuppressed and concentrations of proinflammatory cy-tokines such as tumor necrosis factor-alpha (TNF!)are increased (Ametaj et al., 2002).

Different aspects of the immune response are sup-pressed in cows with fatty liver (Breukink and Wensing,1997; Suriyasathaporn et al., 2000). The lower cellularcytotoxicity and reactive oxygen species generation ofpolymorphonuclear cells in blood suggest a decreasedcapacity for phagocytosis by polymorphonuclear cellsand macrophages in cows with fatty liver (Zerbe et al.,2000). The lower IgG concentrations after tetanus tox-oid immunization (Wentink et al., 1997) and the lowerinterferon production in blood leukocytes (Szuster-Cie-

Journal of Dairy Science Vol. 87, No. 10, 2004

sielska et al., 1995) suggest that cows with fatty liverhave decreased capacity to release some of the inflam-matory mediators. The lower concentrations of leuko-cytes, lymphocytes, eosinophils, monocytes, and matureneutrophils in blood (Morrow et al., 1979; Reid et al.,1986), the decreased lymphoproliferative response aftertetanus toxoid immunization (Wentink et al., 1997),and the lower number of membrane antigens on thesurface of polymorphonuclear cells (Zerbe et al., 2000)suggest a decreased capacity of blood leukocytes to mi-grate into the infected mammary gland.

The decreased clearance of endotoxins (Breukink andWensing, 1997) and the increased concentrations of theacute phase proteins haptoglobulin and serum amyloidA, which are synthesized in the liver (Ametaj et al.,2002; Katoh, 2002), suggest that accumulation of liverlipids can affect the immune response directly by alter-ing the ability of the liver to synthesize and degradecompounds involved in the immune response (Shi etal., 2001; Katoh, 2002). It is more likely, however, thatliver lipid accumulation is associated indirectly witha decreased immune response by its association withchanges in metabolic hormones, metabolites, and com-pounds, which affect immune functions (Breukink andWensing, 1997; Suriyasathaporn et al., 2000). Elevatedconcentrations of BHBA and NEFA have compromisedthe immune response in vitro (Suriyasathaporn et al.,2000), and IGF-I stimulates neutrophil function (Zhaoet al., 1993). Because lipoproteins protect various spe-cies of nonruminants against endotoxin-induced toxic-ity (Harris et al., 2000), it can be assumed that de-creased lipoprotein concentrations in blood also are det-rimental to the immune response.

Conversely, inflammatory responses could be part ofthe etiology of fatty liver and other periparturient disor-ders (Ametaj et al., 2002; Furll and Leidel, 2002; Katoh,2002). Liver lipid accumulation can be preceded by in-creased concentrations of the proinflammatory cytokineTNF! (Ametaj et al., 2002), which increase insulin re-sistance and plasma concentrations of haptoglobulinand serum amyloid A (Katoh, 2002). Haptoglobin binds

Bobe y col., Journal Dairy Science 87:3105 (2004) Acceso libre en http://www.journalofdairyscience.org

Asociación de hígado graso con la salud en vacas lecheras.

Consumo de E



E Mantenimiento

E Actividad


E heces


E Lactación

E consumida - Requerimiento E > 0 Ganancia de peso y

condición corporal

Lactancia media y tardía

Meses



Condición corporal deseada

Cambio de la condición corporal durante la lactancia en vacas lecheras

Discusión de un experimento de nutrición de vacas lecheras (Douglas et al., Journal of Dairy Science, 2006) 47 vacas Holstein, con una condición corporal al secado de 3,0 puntos, fueron divididas en dos grupos y alimentadas, desde el secado hasta el parto (60 días) con diferentes cantidades de una misma dieta de secadao o preparto. Esta dieta de secado o preparto, estaba compuesta por silo de alfalfa (50%), silo de maiz (25%), maíz partido (15%), expeler y cáscara de soja (9,3 %, para aumentar el contenido de proteína y fibra degradable) y un núcleo mineral (Concentración de energía =10 MJ EM/kg materia seca). El grupo Control, recibió esta dieta ad libitum (≅160 % de los requerimientos). El grupo Restringido, recibió la misma dieta pero en menor cantidad, como para cubrir solo el 80% de los requerimientos. La dieta preparto estaba formulada para proveer la cantidad necesaria de energía como para que una vaca de 650 kg de peso, con un consumo de 12 kg/d (1,85 % del peso), pudiese cubrir los requerimientos de mantenimiento materno y crecimiento fetal y, además, conseguir una ganancia de 36 kg de peso (o ≅ 0,6 puntos de condición corporal) durante el período de secado. Después del parto los dos grupos de animales recibieron la misma dieta de lactancia (o dieta post parto) ad libitum.

47 vacas Holstein

grupo Control ad libitum

160% requerimientos

-9

postparto

grupo Restringido 80% requerimientos

preparto

0 16

grupo Control ad libitum

grupo Restringido ad libitum

Dieta preparto Dieta post parto

semanas en relación al parto

Mediciones Consumo de materia seca de la dieta, cambios en el peso corporal, cambios en la condición corporal, producción de leche y de grasa de leche, concentración plasmática de glucosa, insulina, ácidos grasos no esterificados y beta-OH-butirato, y contenido de triglicéridos en hígado (biopsia).

Esquema del experimento

DIETARY FAT AND FEED RESTRICTION FOR DRY COWS 2147

Figure 1. Intakes of DM (panel A) and NEL (panel B; calculatedaccording to NRC, 2001) for cows fed diets for ad libitum DMI (!;n = 23) or restricted DMI ("; n = 24) during the dry period. PanelA: Prepartum largest SEM = 0.5 kg/d; postpartum largest SEM = 0.9kg/d. For prepartum data, effects of prepartum intake (P < 0.0001),week (P < 0.0001), and the interaction of prepartum intake ! week (P< 0.0001) were significant. For postpartum data, effects of prepartumintake (P < 0.028) and week (P < 0.0001) were significant. The interac-tion of prepartum intake ! week was not significant (P = 0.13). PanelB: Prepartum largest SEM = 0.8 Mcal/d; postpartum largest SEM =1.7 Mcal/d. For prepartum data, effects of prepartum intake (P <0.0001), week (P < 0.0001), and the interaction of prepartum intake! week (P < 0.0001) were significant. For postpartum data, effects ofprepartum intake (P < 0.044) and week (P < 0.0001) were significant;the interaction of prepartum intake ! week was not significant(P = 0.16).

despite different prepartum diets or BCS (Garnsworthyand Topps, 1982).

Regardless of the energy source used in the dry perioddiets, BW during the dry period tended (P = 0.08) to begreater for A cows (Table 3). Although BW increasedfor both A and R groups, cows fed A gained BW at agreater rate during the dry period until 3 wk beforecalving (Figure 3B; intake ! week, P < 0.02). The plateauand slight loss of BW for A cows during the last 3 wkmay reflect decreased DMI and gut fill as well as somemobilization of body tissue. These changes also mayhave been influenced by the greater number of twinbirths in A groups than in R groups (4 vs. 1; Table 4).Mean BW gains over the entire dry period were 56.2,46.7, 27.9, and 18.9 kg for CA, FA, CR, and FR groups,respectively. Estimated BW gain attributable to fetalgrowth during the dry period is 35 to 40 kg (NRC, 2001).

Journal of Dairy Science Vol. 89 No. 6, 2006

Figure 2. Daily intakes of DM (panel A) and NEL (panel B; calcu-lated according to NRC, 2001) during the transition period (21 dbefore to 21 d after parturition) for cows fed diets for ad libitum DMI(!; n = 23) or restricted DMI ("; n = 24) during the dry period. PanelA: Prepartum largest SEM = 0.6 kg/d; postpartum largest SEM = 1.0kg/d. For prepartum data, effects of prepartum intake (P < 0.0001),day (P < 0.0001), and the interaction of prepartum intake ! day (P< 0.0001) were significant. For postpartum data, effects of prepartumintake (P < 0.017) and day (P < 0.0001) were significant, but theinteraction of prepartum intake ! day was not significant (P = 0.19).Panel B: Prepartum largest SEM = 0.8 Mcal/d; postpartum largestSEM = 1.9 Mcal/d. For prepartum data, effects of prepartum intake(P < 0.0001), day (P < 0.0001), and the interaction of prepartum intake! day (P < 0.0001) were significant. For postpartum data, effects ofprepartum intake (P < 0.035) and day (P < 0.0001) were significant,but the interaction of prepartum intake ! day was not significant(P = 0.20).

Because calf birth weights were not significantly differ-ent among treatment groups (Table 3), R cows musthave mobilized more maternal tissues to support fetaldevelopment during the dry period. Peripartum pat-terns of BW loss were similar to those of BCS; cowsfed A during the dry period lost significantly more BWduring the 3 wk before and after calving, but both Aand R groups reached similar nadirs in BW during thefirst 6 wk postpartum. Likewise, 175% (Rukkwamsuket al., 1998) to 270% (Kunz et al., 1985) greater postpar-tum BW losses have been reported for cows that wereoverfed to promote BW gain prepartum compared withcows limit-fed to maintain or lose BW prepartum.

Although mean milk production was about 2 kg/dhigher during the first 105 d of lactation for cows fedR than for those fed A during the dry period (Table 3),

Gráficos 1 y 2. Consumo de Materia Seca (DMI) y de Energía (NEL intake) desde el secado, hasta la 16ta semana de lactancia (Gráfico 1) y desde el día 21 antes del parto hasta el día 20 postparto (Gráfico 2)

Semana en relación al parto Día en relación al parto

Gráfico 1 Gráfico 2

grupo Restringido = 80 % requerimientos preparto grupo Control = ad libitum (160% requerimientos preparto)


Figure 4. Milk yield (panel A), content of fat in milk (panel B),and milk fat yield (panel C) for cows fed diets for ad libitum DMI(!; n = 23) or restricted DMI ("; n = 24) during the dry period. PanelA: Largest SEM 1.8 kg/d. The effect of week was significant (P <0.0001). Effects of prepartum intake (P < 0.21) and the interactionof prepartum intake ! week (P < 0.21) were not significant. Panel B:Largest SEM = 0.16%. The effects of week (P < 0.0001) and theinteraction of prepartum intake ! week (P < 0.0001) were significant.Panel C: Largest SEM = 0.07 kg. The effects of week (P < 0.0003)and the interaction of prepartum intake ! week (P < 0.031) were sig-nificant.

The lower prepartum intakes of DM and NEL for Rcows resulted in significantly lower prepartum concen-trations of glucose (Table 5, Figure 5) and insulin (Table5) in plasma. Neither variable was affected by diet com-position. The difference in glucose concentration be-tween A and R cows confirms that energy status differedsubstantially between intake levels. In contrast, Kunzet al. (1985) reported that glucose concentrations weresimilar between groups of cows that were either overfedor limit-fed to requirements during the dry period. Ruk-kwamsuk et al. (1998) also reported similar glucose


concentrations at 1 wk before calving for dry cows of-fered feed for ad libitum or restricted intakes but didnot measure glucose concentrations throughout the re-striction period. Differences between these studies andthe present study may have resulted because our cowswere limit-fed below requirements rather than to meetrequirements as in the other studies (Kunz et al., 1985;Rukkwamsuk et al., 1998).

As calving approached, concentrations of glucose(Figures 5 and 6) and insulin (Figure 6) in plasma de-creased for all treatment groups. Grum et al. (1996)reported similar patterns for peripartum glucose con-centrations; others have reported transient increasesin glucose and insulin concentrations at calving fol-lowed by marked decreases after parturition (Vazquez-Anon et al., 1994; Kunz et al., 1985; Rukkwamsuk etal., 1998). Differences among studies may reflect differ-ences in peripartal DMI. Regardless, the significantdecreases in DM and NEL intakes during the prepartumtransition period by cows fed A during the dry periodin our study probably resulted in the more rapid de-creases in plasma glucose (intake ! day, P < 0.02) andinsulin (intake ! day, P < 0.0001; Figure 6). After calv-ing, glucose and insulin concentrations were not differ-ent among treatments (Table 5), although the interac-tion of prepartum intake ! diet ! week was significant(Figure 5A). The interaction resulted mainly from thesharp drop of plasma glucose for cows in the FA groupat wk 2; the reason for this decrease is unknown.

As expected, R cows had significantly higher concen-trations of NEFA in plasma throughout the dry periodthan did A cows (Table 5, Figure 5B), in which NEFAbegan to increase only during the last 2 wk before calv-ing. Similar trends were reported by Kunz et al. (1985)for cows that were limited to maintenance intakes dur-ing the final 70 d of gestation and by Grum et al. (1996)for cows fed a high-roughage, fat-supplemented dietrelative to groups that consumed greater than requiredamounts of NEL. The concomitantly lower concentra-tions of glucose and insulin in plasma resulting fromfeed restriction throughout the dry period would beassociated with moderately higher rates of adipose tis-sue TG mobilization to support energy needs, and wasreflected in the sustained loss of BCS throughout thedry period (Figure 3). Concentrations of BHBA inplasma (Table 5, Figure 5C) did not differ significantlyamong treatment groups during the dry period; thedifference between R and A did not achieve statisticalsignificance (P < 0.14). During the last week beforecalving, NEFA concentration increased more for cowsfed A during the dry period (Figure 6C). In contrast toour data, dry cows fed to 67 or 100% of energy require-ments for a short period (from d 30 to 10 before expected

DOUGLAS ET AL.2148

Figure 3. Body condition score (panel A) and BW (panel B) forcows fed diets for ad libitum DMI (!; n = 23) or restricted DMI (";n = 24) during the dry period. Panel A: Prepartum largest SEM =0.08; postpartum largest SEM = 0.07. For prepartum data, effects ofprepartum intake (P < 0.024), week (P < 0.0001), and the interactionof prepartum intake ! week (P < 0.05) were significant. For postpar-tum data, effects of week (P < 0.0001) and the interaction of prepartumintake ! week (P < 0.0001) were significant. Panel B: Prepartumlargest SEM = 14 kg; postpartum largest SEM = 13 kg. For prepartumdata, the effect of prepartum intake approached significance (P <0.08), and the effects of week (P < 0.0001) and the interaction ofprepartum intake ! week (P < 0.018) were significant. For postpartumdata, effects of week (P < 0.0001) and the interaction of prepartumintake ! week (P = 0.007) were significant.

the difference did not achieve statistical significance(P = 0.20). The higher postpartum DM and NEL intakesfor cows previously restricted while dry would be ex-

Table 4. Frequency1 of health conditions and twinning in cows fed control (C) or fat-supplemented (F) dietsat ad libitum (A) or restricted (R) intakes during the dry period

Prepartum diet and intake Effect of diet Effect of intake

Condition CA CR FA FR !2 P !2 P

Displaced abomasum 2 0 3 0 0.18 0.67 5.84 0.02Retained placenta 3 3 2 2 0.62 0.43 0.01 0.94Metritis 2 3 0 0 5.83 0.01 0.18 0.67Mastitis 1 2 1 2 0.003 0.96 0.67 0.41Ketosis 3 1 1 0 2.16 0.14 2.16 0.14Milk fever 2 3 2 0 1.67 0.20 0.22 0.64Total metabolic andinfectious conditions 13 12 9 4 — — — —

Hoof and leg problems 2 2 0 3 0.07 0.94 0.90 0.36Twins 1 0 3 1 0.07 0.94 0.61 0.46

1Number of cows with at least one incidence; cows may have had more than one condition.


pected to support higher milk production. Contents andyields of milk fat did not differ between treatments(Table 3) but decreased as lactation progressed (Figure4; week, P < 0.001). However, a significant interactionof intake ! week (P < 0.001) indicated that cows fedA while dry had higher milk fat contents during theimmediate postpartum period (Figure 4B); milk fat con-tent then declined to values similar to those of R cows.Higher milk fat content during the first 4 wk postpar-tum may have resulted from the lower DMI postpartumand greater losses of BCS postpartum for cows fed ei-ther diet at A intake while dry. Greater rates of bodyfat mobilization increase milk fat because of greateruptake and incorporation of NEFA (Palmquist et al.,1993). Similar trends were observed for milk fat yield(Figure 4C). Neither the content nor yield of CP in milkwas different among treatment groups (Table 3).

The incidences of health problems during the experi-ment are reported in Table 4; !2 analysis suggestedthat only the incidence of metritis was affected by diet,with incidences lower (P < 0.01) for cows fed F thanthose fed C. Because the incidences of retained placentaand mastitis were not affected by treatment, it is un-clear why metritis might have been less prevalent forcows fed F. The incidence of displaced abomasum wasthe only disorder affected significantly by intake, withfewer occurrences for cows fed either diet for R intakeduring the dry period (Table 4). Greater occurrence ofdisplaced abomasum may reflect the lower DMI post-partum for cows fed A prepartum. The number of twinbirths tended to be greater for cows fed F, and wasnumerically greater for cows fed A than R. Deletingcows that calved with twins from the data set did notchange direction or interpretation of results for produc-tion and metabolic variables; consequently, they werekept in the analysis. The small number of cows pertreatment and the large amount of variation thataccompanies peripartal health data demand that thesedata be interpreted with caution.

Gráficos 3 y 4. Condición corporal (BCS), peso corporal (BW), producción de leche (Milk), y contenido (Milk fat, %) y producción de grasa de leche (Milk fat, kg/d) desde el secado hasta la 16ta semana de lactancia.

Semana en relación al parto Semana en relación al parto

Gráfico 3

grupo Restringido = 80 % requerimientos preparto grupo Control = ad libitum (160% requerimientos preparto)

Gráfico 4


Figure 5. Concentrations of glucose (panel A), NEFA (panel B),and BHBA (panel C) in plasma from cows fed control (diamonds) orfat-supplemented (triangles) diets for ad libitum DMI (filled symbolsand solid lines) or restricted DMI (open symbols and broken lines)during the dry period. Panel A: Prepartum largest SEM = 1.9 mg/dL; postpartum largest SEM = 1.9 mg/dL. For prepartum data, effectsof prepartum intake (P < 0.0002) and week (P < 0.0001) were signifi-cant, and the interaction of prepartum intake ! week (P < 0.06)approached significance. For postpartum data, the effects of week (P< 0.0001) and the interaction of prepartum intake ! diet ! week (P< 0.041) were significant. Panel B: Prepartum largest SEM = 0.066mM; postpartum largest SEM = 0.098 mM. For prepartum data, theeffects of prepartum intake (P < 0.0001), week (P < 0.0001), and theinteraction of prepartum intake ! week (P < 0.039) were significant.For postpartum data, effects of prepartum intake (P < 0.040) andweek (P < 0.0001) were significant, and the interaction of prepartumintake ! diet ! week (P = 0.073) approached significance. Panel C:Prepartum largest SEM = 0.5 mg/dL; postpartum largest SEM = 1.4mg/dL. For prepartum data, the effects of week (P < 0.0001), theinteraction of prepartum intake ! week (P < 0.004), and the interac-tion of prepartum diet ! week (P < 0.010) were significant. For postpar-tum data, effects of prepartum intake (P < 0.045), week (P < 0.0001),the interaction of intake ! week (P < 0.0001), and the interaction ofprepartum intake ! diet ! week (P = 0.040) were significant.


Figure 6. Concentrations of glucose (panel A), insulin (panel B),and NEFA (panel C) in plasma during the transition period (21 dbefore to 21 d after parturition) from cows fed diets for ad libitumDMI (!; n = 23) or restricted DMI ("; n = 24) during the dry period.Panel A: Largest SEM = 1.8 mg/dL. Effects of prepartum intake (P< 0.005), day (P < 0.0001), the interaction of prepartum intake ! day(P < 0.014), and the interaction of prepartum diet ! day (P < 0.016)were significant, and the interaction of prepartum intake ! diet !day (P < 0.092) approached significance. Panel B: Largest SEM =0.67 !IU/mL. The effects of prepartum intake (P < 0.020), day (P <0.0001), and the interaction of prepartum intake ! day (P < 0.0001)were significant. Panel C: Largest SEM = 0.11 mM. The effects ofday and the interaction of prepartum intake ! day were significant(P < 0.0001).

cows that were previously fed R while dry had greatercholesterol concentrations throughout the first 15 wkof lactation (Table 5), which probably resulted from thehigher postpartum DMI. Prepartum diet did not affectpostpartum cholesterol concentration.

Despite the lower CP intakes for R cows during thedry period, no differences were observed for the concen-tration of total protein in plasma (Table 5). Plasma

DOUGLAS ET AL.2152

Figure 7. Concentration of BHBA in plasma during the transitionperiod (21 d before to 21 d after parturition) from cows fed control(diamonds) or fat-supplemented (triangles) diets for ad libitum DMI(filled symbols) or restricted DMI (open symbols) during the dry pe-riod. Largest SEM = 1.9 mg/dL. The effects of prepartum intake (P< 0.020), day (P < 0.0001), the interaction of prepartum intake ! day(P < 0.0001), and the interaction of prepartum intake ! diet ! day(P = 0.050) were significant.

total protein is decreased during protein malnutrition(Swenson, 1993). Total protein steadily decreased(week, P < 0.0001) during the last 4 wk of gestationregardless of dietary treatment, but concentrations re-turned to those observed during the early dry periodby 3 to 4 wk postpartum (data not shown). Similarpatterns for plasma total protein during the transitionperiod following energy restriction during the dry pe-riod were reported by Kunz et al. (1985). Plasma ureaN concentrations did not differ between A and R groupsduring the dry period (Table 5). Plasma concentrationsof urea N steadily decreased as calving approached(week, P < 0.0001); a significant interaction of diet !week (P < 0.02) indicated that cows fed F during thedry period had higher urea N early in the dry periodbut lower urea N by calving (Figure 8B). The interactionof prepartum intake ! diet was significant for urea Npostpartum (Table 5), although we cannot explain sucha response. Plasma concentrations of urea N increasedas lactation progressed (week, P < 0.0001; Figure 8B).

Increased NEFA concentrations in blood have beenassociated with increased risk for development of fattyliver and, subsequently, for development of other peri-partum metabolic disorders including ketosis (Grum-mer, 1993; Bobe et al., 2004). Interestingly, cows thatwere restricted-fed while dry had significantly lowerconcentrations of total lipid (intake ! day, P < 0.01) andTG (intake ! day, P < 0.01) in the liver at 1 and 21d postpartum (Figure 9) despite chronically elevatedconcentrations of NEFA throughout the dry period. TheNEFA concentrations in R cows during the dry period


Figure 8. Concentrations of total cholesterol (panel A) and ureaN (panel B) in plasma from cows fed control (!; n = 23) or fat-supplemented ("; n = 24) diets during the dry period. Panel A: Prepar-tum largest SEM = 5.3 mg/dL; postpartum largest SEM = 7.6 mg/dL. For prepartum data, effects of prepartum intake, prepartum diet,week, and the interaction of prepartum diet ! week were significant(P < 0.0001). For postpartum data, effects of prepartum intake (P <0.004) and week (P < 0.0001) were significant. Panel B: Prepartumlargest SEM = 0.76 mg/dL; postpartum largest SEM = 0.74 mg/dL. Forprepartum data, the effects of week (P < 0.0001) and the interaction ofprepartum diet ! week (P < 0.030) were significant. For postpartumdata, only the effect of week (P < 0.0001) was significant.

were not high enough to cause hepatic TG accumulation(Drackley et al., 2001). Both A and R cows had markedincreases of NEFA immediately before parturition.These data agree with previous observations that liverlipid accumulation occurs in the presence of increasedplasma concentrations of NEFA at calving (Gerloff etal., 1986; Skaar et al., 1989; Vazquez-Anon et al., 1994).However, TG contents at d 1 for A cows were approxi-mately double those of R cows. Peak NEFA concentra-tions (at d 2; Figure 6C) were similar between A andR cows, but NEFA remained elevated for longer in Acows. Grum et al. (1996) suggested that chronicallyincreased NEFA and low insulin during the dry periodled to increased oxidative enzymes in liver and de-creased esterification activity for NEFA, which couldlead to decreased TG accumulation.

Concentrations of TG in liver tissue from cows pre-viously fed F tended (P < 0.10) to be lower than from

0.3

1.2

0.7

1.5

grupo Restringido = 80% requerimientos preparto grupo Control = ad libitum (160% requerimientos preparto)

mM

ol

Gráficos 5 y 6. Concentración de glucosa (glucose), insulina (insulin), ácidos grasos no esterificados (NEFA) y beta hidroxibutirato (BHBA) en plasma desde el secado hasta la 16ta semana de lactancia.

Gráfico 5

Gráfico 6


Figure 9. Concentrations (wet weight basis) of total lipid (panelA), triglyceride (TG; panel B), and glycogen (panel C) in liver fromcows fed diets for ad libitum DMI (!; n = 23) or restricted DMI (";n = 24) during the dry period. Panel A: Largest SEM = 0.58%. Theeffects of prepartum intake (P < 0.001), day (P < 0.0001), and theinteraction of prepartum intake ! day (P < 0.001) were significant.Panel B: Largest SEM = 0.67%. The effects of prepartum intake (P< 0.001), day (P < 0.0001), and the interaction of prepartum intake! day (P < 0.001) were significant. Panel C: Largest SEM = 0.28%.The effects of day (P < 0.0001) and the interaction of prepartumintake ! day (P < 0.016) were significant.

cows fed C; at d 1 postpartum TG concentrations were6.6, 5.0, 3.6, and 2.8% of wet weight for cows previouslyfed CA, FA, CR, and FR, respectively. Others have re-ported increases in plasma concentrations of NEFAwith dietary fat supplementation prepartum and sug-gested a greater risk for development of fatty liver(Skaar et al., 1989). However, the present data and ourpreviously published data (Douglas et al., 2004), as well


as data from others (Doepel et al., 2002), indicate noincreased hepatic lipid accumulation due to dietary fat.Effects of prepartum fat supplementation on postpar-tum intake and production have been unremarkable(Skaar et al., 1989; Salfer et al., 1995; Douglas et al.,2004). Doepel et al. (2002) compared low-energy dietswith diets in which energy density was increased byaddition of 2.2% tallow and decreased forage-to-concen-trate ratio during the last 21 d before parturition. Al-though they reported improvements in postpartumDMI, energy balance, and liver TG content with higherenergy diets, the small number of cows per treatmentand the fact that cows were fed differently during latelactation and the early dry period depending on BCSmake comparison with our results difficult.

Liver glycogen contents (Figure 9C) were not statisti-cally different among treatment groups. Concentra-tions of glycogen in liver decreased dramatically at d 1postpartum regardless of prepartum intake or sourceof dietary energy and then increased to concentrationsobserved at dry-off by d 65 (day, P < 0.0001). However,a significant interaction of prepartum intake ! day indi-cated that cows fed A had higher hepatic concentrationsof glycogen than did R cows at 21 d before calving (Fig-ure 9C). Glycogen concentrations in liver were similarbetween intake groups at d 1 postpartum but then wereslightly greater for R cows than A cows by d 21, whichmay reflect the greater postpartum DMI by R cows.Similar peripartal changes in liver glycogen concentra-tions were reported by Grum et al. (1996).

We interpret our data to indicate that a lower overallplane of nutrition prepartum compared with overfeed-ing results in markedly less accumulation of total lipidand TG in the liver after parturition. Diet (i.e., theaddition of fat in replacement for NFC) had a smallerimpact on peripartal TG accumulation in liver. To-gether with results of Douglas et al. (2004), our dataindicate that the marked decrease in hepatic lipid accu-mulation observed in the study of Grum et al. (1996)was predominantly caused by the decreased energy andnutrient intakes prepartum for cows fed the high-fat,low-NFC diet in that study rather than by fat supple-mentation per se. In that study, the fat-supplementedgroup had lower DMI and lost BCS; in contrast, cowsfed the lower energy density control diet consumed nearrequirements and cows fed a higher energy diet con-taining more grain consumed >145% of energy require-ments and yet both accumulated more liver TG thanthe fat-supplemented cows (Grum et al., 1996).

The mechanisms responsible for the reduction of peri-partal liver lipid accumulation observed with lower en-ergy intake during the dry period are not fully knownor understood. Rukkwamsuk et al. (1998) and Drackley(1999) concluded that the decreased hepatic TG accu-


Figure 9. Concentrations (wet weight basis) of total lipid (panelA), triglyceride (TG; panel B), and glycogen (panel C) in liver fromcows fed diets for ad libitum DMI (!; n = 23) or restricted DMI (";n = 24) during the dry period. Panel A: Largest SEM = 0.58%. Theeffects of prepartum intake (P < 0.001), day (P < 0.0001), and theinteraction of prepartum intake ! day (P < 0.001) were significant.Panel B: Largest SEM = 0.67%. The effects of prepartum intake (P< 0.001), day (P < 0.0001), and the interaction of prepartum intake! day (P < 0.001) were significant. Panel C: Largest SEM = 0.28%.The effects of day (P < 0.0001) and the interaction of prepartumintake ! day (P < 0.016) were significant.

cows fed C; at d 1 postpartum TG concentrations were6.6, 5.0, 3.6, and 2.8% of wet weight for cows previouslyfed CA, FA, CR, and FR, respectively. Others have re-ported increases in plasma concentrations of NEFAwith dietary fat supplementation prepartum and sug-gested a greater risk for development of fatty liver(Skaar et al., 1989). However, the present data and ourpreviously published data (Douglas et al., 2004), as well


as data from others (Doepel et al., 2002), indicate noincreased hepatic lipid accumulation due to dietary fat.Effects of prepartum fat supplementation on postpar-tum intake and production have been unremarkable(Skaar et al., 1989; Salfer et al., 1995; Douglas et al.,2004). Doepel et al. (2002) compared low-energy dietswith diets in which energy density was increased byaddition of 2.2% tallow and decreased forage-to-concen-trate ratio during the last 21 d before parturition. Al-though they reported improvements in postpartumDMI, energy balance, and liver TG content with higherenergy diets, the small number of cows per treatmentand the fact that cows were fed differently during latelactation and the early dry period depending on BCSmake comparison with our results difficult.

Liver glycogen contents (Figure 9C) were not statisti-cally different among treatment groups. Concentra-tions of glycogen in liver decreased dramatically at d 1postpartum regardless of prepartum intake or sourceof dietary energy and then increased to concentrationsobserved at dry-off by d 65 (day, P < 0.0001). However,a significant interaction of prepartum intake ! day indi-cated that cows fed A had higher hepatic concentrationsof glycogen than did R cows at 21 d before calving (Fig-ure 9C). Glycogen concentrations in liver were similarbetween intake groups at d 1 postpartum but then wereslightly greater for R cows than A cows by d 21, whichmay reflect the greater postpartum DMI by R cows.Similar peripartal changes in liver glycogen concentra-tions were reported by Grum et al. (1996).

We interpret our data to indicate that a lower overallplane of nutrition prepartum compared with overfeed-ing results in markedly less accumulation of total lipidand TG in the liver after parturition. Diet (i.e., theaddition of fat in replacement for NFC) had a smallerimpact on peripartal TG accumulation in liver. To-gether with results of Douglas et al. (2004), our dataindicate that the marked decrease in hepatic lipid accu-mulation observed in the study of Grum et al. (1996)was predominantly caused by the decreased energy andnutrient intakes prepartum for cows fed the high-fat,low-NFC diet in that study rather than by fat supple-mentation per se. In that study, the fat-supplementedgroup had lower DMI and lost BCS; in contrast, cowsfed the lower energy density control diet consumed nearrequirements and cows fed a higher energy diet con-taining more grain consumed >145% of energy require-ments and yet both accumulated more liver TG thanthe fat-supplemented cows (Grum et al., 1996).

The mechanisms responsible for the reduction of peri-partal liver lipid accumulation observed with lower en-ergy intake during the dry period are not fully knownor understood. Rukkwamsuk et al. (1998) and Drackley(1999) concluded that the decreased hepatic TG accu-

Gráfico 7. Concentración de triacilglicérido en hígado (Liver TG %) desde 60 días antes del parto hasta 60 días despuñes del parto.

grupo Restringido = 80% requerimientos preparto grupo Control = ad libitum (160% requerimientos preparto)

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