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92 Cards in this Set

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Oral CHO digestion in monogastrics: mechanisms and what they do

Mastication - decreases particle size and increases area for enzyme digestion


Salivary amylase - Converts starch to maltose and smaller oligosaccharides

In which species does Amylase has a minor role in CHO digestion?

Pigs and Dogs

Corpus and Fundus CHO Digestion for monogastrics: mechanisms and how they work

Salivary amylase converts starch to maltose and smaller oligosaccharides (*important in pigs)



(amylase rapidly inactivated by low pH)

Intestinal CHO digestion in monogastrics

Pancreatic amylase converts remaining starch and polysaccharides to monosaccharides

What percentage of starch breakdown occurs in the:


Oral cavity?


Corpus/Fundus?


Intestines?

Oral: ~5%



Corpus/Fundus: ~30%



*Remainder in the intestines

Phases of intestinal digestion

Luminal phase



Membranous phase

Luminal Phase:


-Where are the enzymes active?


-What occurs during this phase (overview)?

Enzymes active in gut lumen



Large polymers like starch and protein digested


by digestive enzymes from salivary, gastric and pancreatic glands

Membranous Phase:


-Where are the enzymes active?


-What occurs during this phase (overview)?

Enzymes active at surface of gut



Small polymers like polysaccharides and peptides digested by digestive enzymes synthesized in enterocytes and attached to apical membrane

Specific starch digestion phases in the intestine

Pancreatic Phase



Mucosal Phase



Delivery Phase

What occurs during pancreatic phase?

alpha-amylase from pancreas breaks down starch into glucose (first goes through a-dextrine, maltotriose, maltose)


Lactase breaks down lactose into galactose and glucose

What occurs during mucosal phase?

Glucose is taken up into intestinal epithelium by the transporter: SGLT1 on brush border



Glucose can also move through paracellularly (paracellular diffusion)

What happens in delivery phase?

Glucose in the epithelial cell undergoes metabolism for cell functions



Glucose gets transported out of cell and into the portal circulation through the transporter: GLUT2

Where does the energy for the SGLT1 come from?

Na-K ATPase transporter

Name sodium-glucose co-transporters

SGLT1


SGLT2


SGLT3

SGLT1:


-Found in which major tissues?


-Functions?

Kidney, Intestine



Glucose reabsorption in intestine and kidney

SGLT2:


-Found in which major tissues?


-Functions?

Kidney**



Low affinity but high selectivity for glucose

SGLT3:


-Found in which major tissues?


-Functions?

Small Intestine, Skeletal muscle



Glucose activated Na+ channel

Facilitative Glucose Transporters: name the important ones

GLUT1, GLUT2, GLUT4, GLUT5

GLUT1:


-Found in which major tissues?


-Functions?

Ubiquitous: RBCs, Brain, Eye, Mammary



Basal glucose uptake and transport across blood tissue barrier

GLUT2:


-Found in which major tissues?


-Functions?

Liver, Kidney, Pancreas, Small Intestine



High capacity, low-affinity transport

GLUT4:


-Found in which major tissues?


-Functions?

Muscle, Fat, Heart



Insulin-regulated transport in muscle and fat

GLUT5:


-Found in which major tissues?


-Functions?

Intestine, Kidney, Testis



Fructose transport

What are CHOs good for in Ruminants

Major energy source


-50% of grain fed to animals


-60-70% total diet in dairy cattle

Main functions of CHOs in ruminants?

Energy for microbes and host


Maintain a healthy GIT

CHO fermentation productions in ruminants?

VFAs: Acetate, Proprionate, Butyrate

Ruminal digesta fractions and what they contain

1. Fibrous raft - high density of microbes


2. Liquid fraction - shuttles saliva & fermentation end products in and out


3. Boundary layer against lumen surface - bidirectional fluid exchange


4. Soupy Material - provides cud and material for omasum

Where is soupy material found?

Ventral and cranial sacs

Define: Fermentation

A slow, digestive process of anaerobic digestion by microbial enzymes

Synergy between host and microbes: what does each provide the other?

Host provides environment (substrate, H20, pH, redox conditions, slow digesta flow)



Microbes convert indigestible material into useful products for host (VFAs, CH4, NH3, CO2, Microbial cells and LCFA)

What are the requirements for fermentation?

1. Substrate (regular supply of new feed)


2. Microbes (suitable numbers and types)


3. Mixing and propulsion (helps fermentation)


4. Fermentation end products (steadily removed)


5. Stable intraruminal conditions

What are stable intraruminal conditions?

Optimum temperature: 37'C


Osmolality: 300 mOsm


pH: 6.4


Anaerobic conditions: most microbes are strictly anaerobic; -ve oxidation reduction potential

Rumen protozoa: digestion and fermentation

-Engulf feed particles, digest and store CHO, proteins and fat


-Ingest bacteria


-Produce some VFAs and NH3


-Slow digestion of rapidly fermentable starches and proteins

Rumen protozoa decrease significantly when?

High grain diets are fed and pH <5.5

Advantages of rumen protozoa

1. Store starch particles, thereby preventing rapid degradation by amylolytic bacteria


2. Reservoir of microbial protein


3. Provide host with protein, stored starch and PUFA when digested

Types of rumen bacteria based on location

1. Free-living in the liquid phase


2. Loosely/firmly associated with feed particles


3. Associated with rumen epithelium


4. Attached to surface of protozoa and fungi

Types of rumen bacteria based on fermentation

1. Primary bacteria



2. Secondary bacteria

Primary bacteria:


What do they do?


Examples?

Directly break down digesta


-Cellulytic (18h doubling time, slow metabolism, Opt. pH ~6.5)


-Amylolytic (<4h doubling time, Opt. pH 5.5-6.8)

Secondary bacteria:


What do they do?


Examples?

Feed on by-products of primary bacteria (16h doubling time, Optimum pH 6.2-6.8)


Propionate bacteria - utilize lactate


Mathanogenic bacteria - utilize H2

Process of rumen bacterial attachment to plants

1. Free bacteria move to fibrous substrate


2. Initial non-specific adhesion on cut surfaces (electrostatic/ionic)


3. Specific adhesion (ligands/adhesins on bacterial surface)


*Proliferation and colonization on feed

What happens to cellulose digestion if unsaturated fat is fed?

It leads to decreased cellulose digestion due to interference of bacterial attachment to substrate

Benefits of bacterial attachment to plants

1. Brings enzyme & substrate together


2. Protects enzymes from proteases in rumen


3. Allows bacteria to colonize the digestible surface of feed particles


4. Retention in the rumen to prolong digestion


5. Reduces predatory activity of protozoa

Function of protozoa

Ingest and digest feed particles producing VFA, CO2 and NH3



Also keeps bacteria in check

Protozoal storage

Feed particles like CHO, fat and protein to prolong digestion

Location of protozoa

Both liquid and solid phases

Number and size of protozoa

10^4 - 10^6 cells/gm of rumen contents


~51% of microbial volume

pH sensitivity of protozoa

Highly pH sensitive so they decreases in number on high grain diets

Function of bacteria

Ferment CHO, fat and protein to produce VFA, CO2 and NH3

Bacterial storage

Very limited/no storage capacity

Location of bacteria

Free living in rumen fluids, or


Loosely/firmly attached to feed particles, or


Attached to rumen epithelium (mainly fungi for fibre digestion)

Number and size of bacteria

10^10 - 10^12 cells/gram of rumen contents


~40% of microbial volume



*much smaller in size than protozoa

pH sensitivity of bacteria

Some strains are pH resistant

In a high forage: low concentrate diet, which VFAs are produced and relative quantity?



In a low forage: high concentrate diet, which VFAs are produced and relative quantity?

Mainly acetic acid, some acetic acid, the least butyric acid



Mainly propionic acid, some acetic acid, the least butyric acid



*butyric acid stays constant

Which VFA is the gluconeogenic one?

Propionate

How are VFAs transported from rumen fluid into the epithelial cells?

1. Simple diffusion (butyrate)


2. HCO3-/SCFA- antiporter


3. Lactate/H+ symporter

What happens in the rumen epithelial cell after VFAs enter?

Some HSCFA get broken down into SCFAs and then into KETONES

Main transporter for ketones from rumen epithelial cell into the blood?

MCT1

Methods of VFA absorption into the blood (across basolateral membrane)?

1. Simple diffusion (HSCFAs)


2. Cl-/SCFA- antiporter


3. HCO3-/SCFA- antiporter


4. MCT1

VFA disassociation curve

4 stages of VFA synthesis

Hydrolysis


Glycolysis


VFA synthesis


Microbial protein synthesis

Precursors for:


Acetate


Butyrate


Propionate

Phosphenol pyruvate



Acetyl CoA



Oxaloacetate & Lactate

Amount of Ruminal epithelial metabolism of VFAs and what it produces

90% Butyrate --> Ketone bodies (alimentary ketogenesis)



70% Prpionate --> lactate + CO2 + amino acids



30% acetate

Energy production, in ATP/mol, for each VFA

Acetate: 10



Propionate: 18



Butyrate: 27

Which VFAs are not used for net glucose synthesis?

Acetate and Butyrate

What does acetate provide?

Carbon source for fatty acids in adipose and mammary gland

What does propionate provide?

Glucose


Stimulates INSULIN secretion


5% converted to lactate

What does butyrate provide?

Carbon source for fatty acids in mammary gland


Stimulates INSULIN and GLUCAGON secretion


Critical for rumen papillae growth

What is Parakeratosis?



What are events leading up to it?

Excessive keritinization of the epithelium



Increase in fermentable CHO feeding initially causes sloughing of stratum corneum leading to parakeratosis and formation of stellate ulcers

Major type of bacterium in animals fed high grain diets

Amylolytic

Examples of Ruminal bacteria that rapidly ferment starch/soluble sugars

Selenomas ruminantium


Streptococcus bovis


Lactobacillus species

Describe S. ruminantium

Dominant organism that makes up 22-51% of culturable bacteria in the rumens of high-grain diet animals

Describe S. bovis

A facultative anaerobe that has explosive growth in response to availability of fermentable CHO especially when animal unadapted to high grain


Has a rapid growth rate and rapidly degrades cereal grain starches

Lactic acid production by S. bovis causes what?

Decrease in ruminal pH which inhibits growth rates of most ruminal bacteria


This causes acid-tolerant Lactobacilli to predominate

Describe lactobacilli

Predominant organism in acidotic rumens


Lactic acid producing!

Sequellae of rumen acidosis

Rumenitis (stellate ulcers)


Liver abscesses (F. Necrophorum)


Diarrhea due to increased osmolality of fluids


Laminitis


Sudden death from dehydration, acidosis, endotoxemia

Glycogenesis - Glycogenolysis: Liver vs. Muscle

Liver has glucose-6-Pase enzyme to produce glucose


Muscles don't have enzymes to sythesize glucose from lactate so glycolysis occurs and lactate then transported into liver


*Liver takes up lactate and undergoes gluconeogenesis to produce glucose

Rate limiting enzymes for glycogenesis

Glycogen synthetase

Rate limiting enzymes for glycogenolysis

Glycogen phosphorylase


Glucose-6-Phosphatase (G-6-Pase_

What happens during Cori cycle?

Lactate from muscle is transported into liver via blood - Gluconeogenesis from lactate in liver - glucose returned to muscle via blood

Sources for gluconeogenesis for ruminants

Propionate


Amino acids


Lactate


Glycerol

In ruminants, gluconeogenesis meets ________ of total glucose needs

75-90%

Gluconeogenesis sources in carnivores

Amino acids

Gluconeogenesis sources during anaerobic exercise

Muscle lactate (Cori cycle)

Plasma glucose differences between ruminants and carnivores

50-60mg/dl in ruminants (very stable levels)



100mg/dl in carnivores (fluctuations after meals)

Principle types of Hypoglycemia

1. Insufficient gluconeogenesis & glycogen stores


2. Mesenchymal tumors


3. Glycogen storage diseases


4. Hyperinsulinemia

Insufficient gluconeogenesis and glycogen stores most common in? why?

Ruminants during pregnancy and lactation


Neonatal pigs



Adrenal cortex/anterior pituitary deficiency


Liver diseases

Why do Mesenchymal tumours cause hypoglycemia?

Inhibits glucagon

Hyperinsulinemia: how does it occur (pathway)? Name phenomenon?

Somogyi overswing


Insulin overdose - hypoglycemia - increase glucagon and cortisol secretion - hyperglycemia and glucosuria

Hyperinsulinemia in dogs

Organic: Islet tumours



Functional: Insulin secretion normal at fasting, but hypersecretion after CHO ingestion

Principle types of hyperglycemia

Diabetes Mellitus


-Type 1: juvenile or IDDM


-Type 2: adult onset or NIDDM


-Other types

What causes Type 1 DM

Primary insulin deficiency


Beta-cell failure (autoimmune disorder)


Common in dogs and cats

What causes Type 2 DM

Primary insulin resistance


Beta-cell exhaustion and atrophy


Typical in humans, less common in dogs and cats


Early lactation cows can have it too

Other types of DM

Gestational diabetes


Diestrus diabetes