Alimentary Ch5

• Study notes below:

Liver

• Primary functions include storage, metabolism, and bile synthesis.
• Receives nutrient-rich deoxygenated blood from the gut.
• Also receives oxygenated blood from the hepatic artery.
• Branches supply every hepatocyte.
• External lobation occurs; converges and drains back to the caudal vena cava.
• Arrangement allows easy exchange of blood supply and bile canaliculi.
• Bile flows through canaliculi to the portal triad.
• Accumulation of hepatocytes and vessels in the liver; has a "mockled" appearance.

Sinusoid

• A specialized, fenestrated, leaky capillary between lines of hepatocytes.
• Allows easy diffusion between hepatocytes and blood.
• Blood flows from the portal triad to the central vein, merges with the portal vein, then to the caudal vena cava towards the art.

Portal Triad

• Artery: thick-walled and round in shape.
• Vein: thin-walled and irregularly shaped.
• Bile duct is lined with simple columnar epithelium; modifies bile with water.

Hepatocyte

• Smooth ER facilitates cholesterol conversion to bile acids.
• Has detergent properties: both hydrophilic and hydrophobic regions.
• Takes up phospholipids and cholesterol from cell membranes.
• Bile salts: attaches sodium.
• Draws water, duct wall cells then produce bile.
• Drugs and toxins: excreted through liver.
• Bilirubin: a non-functional pigment produced from RBC turnover.
• Green in color.
• Testing liver function by testing bilirubin lv.

Gall Bladder

• Stores and concentrates bile.
• Lined by simple columnar epithelium
• Glandular.

Pancreas

• Endocrine function: hormone production.
• Islets of Langerhans: islands within a "sea" of acini.
• Alpha cells produce glucagon.
• Glycogenolysis
• Beta cells produce insulin.
• Glycogenesis.
• Delta cells produce somatostatin.
• Growth inhibiting
• Decreases HCl production, slowing down digestion.
• PP cells produce pancreatic polypeptide.
• Exocrine function: enzyme production.
• Pancreatic duct: lined by stratified cuboidal epithelium that is protective and secretory.
• Exocrine secretions merge into the main pancreatic duct.
• Opens at the major duodenal papilla.
• Duct of Santorini: opens at the major duodenal papilla, present in both dogs and cats.
• Duct of Wirsung: opens at the minor duodenal papilla, present in dogs but not cats.

Blood Glucose Levels

• Normal blood glucose levels: 4.5-5.5 mM.
• Higher blood glucose.
• After a CHO meal: ~7mM.
• In diabetes: 10-12 mM.
• Lower blood glucose during starvation: 3-4 mM.
• Ruminant blood lv: 2-3 mM.

Parasympathetic Nervous System

• Insulin release: occurs after a meal, decreases blood glucose lv, stimulates storage and use of fuel.
• Glycogen deposition in muscle and liver.
• Glycolysis in liver: produces substrate for fatty acid synthesis.
• Increased protein synthesis (especially in muscle) with excess amino acids becoming metabolic intermediaries, indicating a fed state.
• Glucagon release: occurs during fasting, increases blood glucose lv, with the liver as the main target organ.
• Release of stored fuel.
• Glycogenolysis and gluconeogenesis in liver results in glucose entering the blood.
• Hormone-sensitive lipase in adipose tissue: converts CHO to fat for metabolism.

Regulation of Glucose Uptake

• Transporters (1-5) regulate uptake based on glucose concentration and tissue type.
• GLUT 1 & 3: present in all cells, Km (substrate concentration at half-max transport rate) ~ 1-5 mM, leading to basal slow uptake.
• GLUT 2: present in pancreatic beta cells (insulin) and hepatocytes, Km ~ 15-20 mM, leading to uptake during hyperglycaemia.
• GLUT 4: present in muscle and adipocytes, active when insulin is present, Km ~ 5 mM.
• Internalized within cell vesicles.
• Insulin induces vesicles to fuse with plasma membrane, increasing rapid glucose uptake.
• Cycling: GLUT 2 uptake of glucose into beta cells and hepatocytes, leading to insulin release.
• GLUT 4: Expression on muscle & fat cells, uptake is accelerated, storage of glycogen and glycerol/glycolysis to synthesize fatty acids.

Ketogenesis

• Occurs only in hepatocytes and requires specific enzymes.
• A process that occurs in the liver when carbohydrate availability is very low, by-product of fat breakdown.
• Fat and carb breakdown leads to acetyl CoA entering Krebs cycle.
• During fasting: fat breakdown predominates causing accumulation of acetyl CoA.
• Increased production from mobilized fatty acids undergoing beta oxidation.
• Decreased usage due to increased energy charge (ATP from beta oxidation), gluconeogenesis depleting intermediates of Krebs cycle, inhibited.
• Ketone bodies are produced.
• 4-C: 3-hydroxybutyrate, acetoacetate.
• 3-C: acetone.

Ketone Body Usage

• Fatty acids do not cross the blood-brain barrier but ketone bodies do.
• Krebs cycle converts them back into acetyl CoA.
• Fasting response increases energy production > glucose.
• RBCs use glycolysis.
• Help maintains blood glucose lv.
• Fuel brain
• Excessive production leads to ketoacidosis.
• Decreases pH, is poisonous.
• Severe metabolic disease:
• Ruminant production disease.
• Severe diabetes.
• Starvation.
• Presence can be tested through urine tests.

Muscle Metabolism

• Stores glucose.
• Resting state: uses gluconeogenesis (fatty acid).
• Insulin / adrenaline (sympathetic): increases blood glucose lv.

Lipidosis: Fatty Degeneration

• Liver accumulates lots of fat.
• Caused by:
• Increased fatty, increasing blood lv.
• Starvation: fat is mobilized , others stored as more neutral fat.
• Overeating: more energy intake > expenditure during non activity.
• Metabolic diseases: alternate pathway for energy production, ketogenesis, chronic diabetes, etc.
• Decreased fatty acid use.
  • Hypoxia (X O2).
  • Toxin: pregnancy toxaemia (sheep: twin lambs), acetonemia (high yield diary cow, shortly after parturition).

Appearance

• Liver:
  • Increase in size.
  • Tan / yellowish.
  • Slight pressure → rupture.
• Kidney cortex: paler.
• Heart: flabby, w/ streaks.
• Microscopic:
  • Fat compromise function, reducing space and blood flow
  • fat globle in blood
  • Nucleus pushed to periphery
• Glycogen infiltration has the symptoms of no alternation.
• In-born error: Inherited defect of key metabolic enzyme occurs in rare cases.
  • excess Glycogen Accumulation Storage Disease
  • Defect of phosphorylase
  • Can carry out gluconeogenesis
  • → Defect glucose 6-phosphatase More Serious → No glucose due to severe hypoglycemia. Only in liver defect

Ruminant Digestion & Metabolism

• Herbivore fermentation involves microorganisms that digest cellulose and other plant carbohydrates.
• Occurs primarily in the foregut or hindgut.
• Features a slow food transit to extract maximun nutrients.
• Steady conditions through constant feed intake & pH controled with saliva.
• Cellulose digestion: 3 stages of glycolyses.
• Extracellular microbial enzyme: complex → simple sugar.
• Intracellular microbial enzyme: simple sugar → pyruvate.
  • Volatile fatty acid:
• Acetate: 60-70% (4-C, make 2 acetyl CoA, increased w/ roughage).
• Butyrate: 10-15% (4-C, make 2 acetyl CoA).
• Forms long chains
• Much lower blood glucose lv. Bovaer feed to limit reduce CH4 emission.
• Increase glucose lv in goats through oxaloactetate which help make them more pronate.
• Some ananomals have better ruminant by pass protein, heated soybean.
• metabolic profile can lead to ketosis.

Protein Digestion in Rumen: Involves Microbial Action

• Proteinaceous nitrogen compound (e.g., urea) → amino acids.
• Broken down, amino acids are absorbed.
• Manufacture essential amino acids, thrive on the low diet.
• Manufacture vitamins in gut.
• Deal w/ higher glucose diet due to deal with more glucose.
• Deamination → VFA & NH3 production.
• Rumen microbes: use NH3 for microbial processes
• N-based Digestion and Metabolism (N-Cycling)
• Urea from saliva is recycled, influencing nitrogen metabolism.
• Foregut versus Hindgut Fermenters
• Foregut:
  • Material passes from the rumen to the abomasum.
    • Involves monogastric stomach and intestine
    • Slurry, protein-rich broth.
• Hindgut: fermentation happens after GIT tract.
  • Only digestion of fermentation, rabbit ingest post digestive
• Higher protein is quality diet such as energy.

Ruminant Abdomen & Bloat (Ruminal Tympany)

• Bloat occurs when excess gas leads to abnormal enlargement of the rumen and impaired eructation.
• Bloat distension involves : cardiac sphincter oesophagus.
• Distention is observed only of the LHS, enlarged non smmetrically .Compressing lungs and cause respiratory distress.
• Occurs Left paralumbar fossa of the body.
• Recumbent position cannot stand.
• Types
• Bloat is formed gas
• Gas production in rumen is small
• Fluid Blockage
• High diet
• Froathy bloat small coalesence can not eticutae.