Tissue Support Flashcards

1
Q

Why is there a lag in DMI behind milk yield?

A

90% uptake of glucose production in mammary glands, >75% Metabolizable Protein intake going towards mammary gland
overall: negative energy balance >100% NE output as milk/ fetus energy
therefore use body reserves for nutrients to support demand

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2
Q

What’s insulins normal role?

A

stimulate lipogenesis in adipose and protein synthesis in muscle tissue

  • inhibits hydrolysis of TAG + protein
  • stimulate glucose uptake into tissues
  • inhibits oxidation of FA’s
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3
Q

what causes insulin resistance in onset of lactation + why?

A

Growth Hormone because allows favouring towards nutrient partitioning into milk

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4
Q

Mammary lactose synthesis causes what to drop?

A

plasma glucose and insulin

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5
Q

Adipose lipolysis increases resulting in what to rise?

A

plasma NEFA

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6
Q

what suppresses Dmi?

A

elevtated NEFA

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7
Q

where are NEFA oxidized?

A

liver

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8
Q

with elevated NEFA what happens to the liver?

A

partially oxidized NEFA > BHB because elevated NEFA cause fatty liver resulting in less active liver tissue

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9
Q

what does bST do?

A

a GH that enhances cell proliferation, incr insulin resistance in adipose tissue

  • acetyl coA carboxylase causing FA synthase in mammary gland higher than fat tissue
  • protein synthesis in mammary gland
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10
Q

incr insulin causes acetate to do what ?

A

incr lipogenesis in adipose tissue

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11
Q

Insulin > GH

A

due to fed non lactating sheep have higher acetate uptake (higher fat uptake)
- fed lactating have decreased acetate uptake but still more than fasted non lactating

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12
Q

low producing cows have higher what than high producing cows?

A

plasma insulin- due to high producing cows have higher insulin resistance

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13
Q

high producing cows have higher what than low producing cows?

A

GH - due to incr insulin resistance for nutrient partitioning before calving

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14
Q

whats ketosis?

A

metabolic acidosis due to hyperketonemia + hypoglycemia

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15
Q

how does ketosis occur?

A

due to negative energy balance before calving causing low blood glucose, cows use body fat stores to utilize for energy. this occurs by incr NEFA from FA stores which are partially oxidized in liver due to elevated amounts. therefore BHB (ketone) produced.. in combination with low plasma glucose and insulin (from GH resistance) leads to hyperketonemai, acidosis..

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16
Q

why is injecting insulin bad for ketosis?

A

stimulates more glucose uptake into tissue but cow needs in blood stream to burn off NEFA and BHB

17
Q

how do treat high NEFA and BHB?

A

treat with glucose - glycol drench, glucocorticoid

18
Q

Ketosis Prevention

A

encourage DMI through cow comfort, bunk management and proper ration(less sorting)

  • niacin + choline (help transort FA)
  • monensin- produce more propionate
  • peripartum drenching- start into lactation
19
Q

How to catch subclinical ketosis?

A

measure NEFA if >5uM then catch prevent before BHB rise above >1.4mM

20
Q

Why is propylene glycol drench helpful with ketosis?

A

2 alcohol ends, giving propionic acid (propionate) which produces glucose and helps burn off NEFA and BHB

21
Q

When losing how much BW makes a cow ketotic prone?

A

0.75 BCS in first 8 weeks post partum