REGULATION OF VOLUNTARY FEED INTAKE Flashcards

1
Q

Reasons for intervention

A
  1. RESTRICTION OF FEED INTAKE E.g. breeding animals, obese animals etc.;
  2. INCREASE OF FEED INTAKE E.g. high lactating dairy cows, broiler chicks, sick animals etc.
    - Effect of body condition on feed intake: setting up the required body condition (e.g. dairy cows, pregnant sows etc.).
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2
Q

PREDICTION OF THE FEED INTAKE

A

Significance - setting up the nutrient density of diets made for monogastric animals,
- setting up the nutrient density of daily rations made for ruminants

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3
Q

Factors affecting feed intake. 1. Native status

A
  • The role of feed energy („animals eat for calories)”:
    e.g. rabbits, laying hens, rodents: self regulation of feed intake according to the energy density of feeds  =>possibility of ad libitum feeding;
  • other factors e.g. 
    Na, 
    ruminants: gastrointestinal capacity =>continuous and selective grazing,
  • predators: overeating, social effects, energy investment.
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4
Q

Factors affecting feed intake. 2. Effect of Domestication

A

E.g. swine: having been selected for body weight gain = selection for higher feed intake, =>they lost the ability of regulation according to the feed energy, 
hand feeding is required

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5
Q

Types of regulation

A

I. QUALITATVE REGULATION (What to eat?) - taste (human, swine, rat); - smell, adaptation (cats); - physical form (birds); - imitation (sheep, poultries); - enviousness, jealousy (dogs, cats).
II. QUANTITATIVE REGULATION (How much to eat?)
II/1. Short term control
II/2. Long term control
Both of them are regulated by the a) central nervous system, and by the b) peripheral signals.

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6
Q

II/1. Short term control (homeostatic control)

A

Role: - assurance of the homeostasis;
Central Nervous System (Hypothalamus):
- regulation of feed intake,
- regulation of reproduction (sexual steroids); Hypothalamic peptides:
- anabolic peptides => increase the feed intake (e.g. neuropeptide Y (NPY) – „central hunger peptide”),
- catabolic peptides =>decrease the feed intake (e.g. corticotrophin-releasing hormone /CRH/).

Peripheral signals

  1. Positive feedbacks: increase the feed intake e.g. Stomach  GHRELIN („peripheral hunger peptide”);
  2. Negative feedbacks: decrease the feed intake (gastrointestinal peptides) e.g. small intestine  Cholecystokinin (CCK).

Some other factors:
1)Physical factors (especially in ruminants):
capacity of the gastrointestinal tract, bulkiness, passage; 2)Chemical factors:
- blood glucose: in monogastric animals,
- blood volatile fatty acids (VFA): ruminants, rabbit,
- blood amino acid level: in all animal species,
- blood pH, osmotic pressure of blood (tap water),
- body temperature, temperature of the feed,
- higher feed intake =>increased heat production (ruminants – digestion work) etc.

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7
Q

II/2. Long term control (homeorhetic control)

A

Role: - assurance of the normal body weight, E reserves, body composition for longer periods (e.g. pregnancy, lactation etc.); high body fat content ≠ obesity (pl. bear, seal, migrating birds etc.).
Central Nervous System (Hypothalamus):
like in the short term control - regulation of feed intake, - regulation of reproduction (sexual steroids); Hypothalamic peptides: like in the short term control
- anabolic peptides=>increase the feed intake (e.g. neuropeptide Y (NPY) – „central hunger peptide”),
- catabolic peptides => decrease the feed intake (e.g. corticotrophin-releasing hormone /CRH/).

Peripheral signals

  1. Negative feedback (decreased feed intake) (Leptin: „leptos” = lean, thin) Over condition => increased adipocytes => more LEPTIN (hormone) produced=>  reduces the secretion of NPY(anabolic peptide of hypothalamus) => feed intake decreases;
  2. Positive feedback (increased feed intake): the opposite of the previous process;

Prerequisites of this mechanism: presence of leptin receptors: hypothalamus, ovary, uterus etc.,
Practical importance: fatty cow syndrome!
LIPOSTATIC CONTROL of feed intake

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8
Q

Genetic Background

A
  1. OB/OB and OB/ob: enough leptin is produced; ob/ob: insufficient leptin production =>obesity;
  2. Leptin receptor mutant mice (db/db)  insufficient amount of leptin receptors =>obesity;
  3. Insufficient amount of CKK (decreases the feed intake) receptors =>obesity.
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