Absorption of Nutrients�&�Applied Physiology

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Dr. Amar Chaudhary, ^{DVM, MS}

Assistant Professor

Department of Physiology and Biochemistry

Agriculture and Forestry University,

Rampur, Chitwan, Nepal

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Forces Governing Absorption

Absorption is the process by which nutrients from digested food move across the intestinal lining and enter: Blood stream or

lymphatic system

The main forces governing absorption are:

• Diffusion:
• The passive movement of molecules from an area of higher concentration to an area of lower concentration
• This occurs mainly for small molecules like oxygen, carbon dioxide, and some nutrients like fatty acids
• Facilitated Diffusion:
• A form of passive transport where molecules move across the membrane with the help of specific carrier proteins(Glucose transporter proteins family subtypes) without the need for energy
• For example, glucose and amino acids enter cells via facilitated diffusion.
• Active Transport:
• Requires energy (ATP) to move molecules against their concentration gradient (from lower to higher concentration)
• This is crucial for the absorption of certain nutrients like sodium, potassium, and glucose in the small intestine.
• Osmosis:
• The movement of water molecules from an area of low solute concentration to an area of high solute concentration
• This process helps maintain the balance of fluids during nutrient absorption
• Endocytosis/Pinocytosis:
• The process by which larger molecules or particles (e.g., lipids, large proteins) are engulfed by the cell membrane and brought into the cell
• This is an energy-dependent process

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Places of Absorption

• Mouth :
• limited absorption occurs, in human alcohol or certain medication
• Stomach:
• In non ruminant limited extent absorption occurs in human such as alcohol and certain drugs
• In Ruminant: Ruminal epithelium particularly

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Jejunum:

The middle section, where the majority of nutrient absorption takes place

The presence of villi (finger-like projections) and microvilli (on epithelial cells) increases the surface area for absorption

Ileum:

The final part of the small intestine, which is responsible for absorbing any remaining nutrients, including vitamin B12 and bile salts

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Mechanism of Nutreint Absorption

• Carbohydrates:
• In ruminants, carbohydrates are fermented into VFAs in the rumen, which are absorbed across the rumen wall into the bloodstream
• These VFAs are the main energy source for ruminants
• Glucose
• Glucose and galactose are absorbed via secondary active transport with Na⁺ through the sodium-glucose linked transporter (SGLT1) in the apical membrane of enterocytes

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• Fructose is absorbed via facilitated diffusion through the GLUT5 transporter

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• These monosaccharides then enter the basolateral membrane of enterocytes and are transported into the bloodstream via GLUT2 transporters

Mechanism of Nutreint Absorption

Proteins:

• Microbial proteins
• Produced in the rumen are a significant source of protein for ruminants
• These proteins are absorbed in the small intestine
• Bypass proteins
• Which escape fermentation in the rumen, are digested in the abomasum and small intestine, where they are broken down into amino acids for absorption
• Amino acids and small peptides
• Amino acids are absorbed through sodium-dependent active transport systems
• The Na⁺/K⁺ pump maintains a gradient for sodium to enter the cell
• Peptides (di- and tripeptides) are absorbed via PepT1 (a proton-dependent transporter)
• After absorption, amino acids or small peptides enter the bloodstream via facilitated diffusion through various amino acid transporters in the basolateral membrane

Mechanism of Nutreint Absorption

Fats:

• Fats are partially broken down in the rumen by microbial lipases, but the majority of digestion and absorption of fats (as fatty acids & monoglycerides) occurs in the small intestine
• Fat absorption in ruminants is similar to that in non-ruminants, where it involves the formation of micelles, but it is influenced by the prior microbial breakdown of fats in the rumen
• These lipids, along with bile salts, form micelles that facilitate the transport of fats across the intestinal membrane
• Once inside the enterocyte, fatty acids and monoglycerides are re-esterified to form triglycerides and packaged into chylomicrons, which enter the lymphatic system before being released into the bloodstream
• Micelles transport lipids to the enterocyte membrane, where the lipids diffuse into the cell
• Inside the enterocyte, free fatty acids and monoglycerides are re-esterified into triglycerides and incorporated into chylomicrons
• Chylomicrons are transported via the lymphatic system into the bloodstream, bypassing the liver initially

Water and Electrolytes

Absorption of Electrolytes and Water

• Water Absorption:
• Water is absorbed primarily in the small intestine (90%) and the large intestine (10%).
• Osmosis is the primary mechanism for water absorption, driven by the movement of solutes (e.g., Na⁺, glucose) across the enterocyte membranes.
• Aquaporins, especially AQP1 and AQP3, facilitate water transport across the cell membrane.
• Electrolyte Absorption in the Small Intestine:
• Sodium (Na⁺): Actively absorbed via the Na⁺/K⁺ ATPase pump in the basolateral membrane, and through Na⁺-dependent co-transporters (like SGLT1 for glucose).
• Chloride (Cl⁻): Often absorbed via Na⁺/Cl⁻ cotransport.
• Potassium (K⁺): Absorbed passively due to concentration gradients, with some active transport in the ileum.
• Calcium (Ca²⁺): Active transport via TRPV6 channels, facilitated by vitamin D.
• Water and Electrolyte Coupled Transport:
• In the intestine, Na⁺ and water are absorbed together, maintaining fluid balance.
• This process is often coupled with nutrient absorption (e.g., glucose absorption driving water and sodium uptake).

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�Absorption of Minerals�

Mechanisms of Absorption:

• Sodium (Na⁺):
• Absorbed via active transport using the Na⁺/K⁺ ATPase pump
• Calcium (Ca²⁺):
• Absorbed in the small intestine via calcium-binding protein (CBP) in response to vitamin D
• It enters through TRPV6 channels(Transient Receptor Potential Vanilloid)
• Iron (Fe²⁺):
• Absorbed in the duodenum via DMT1 (divalent metal transporter), often facilitated by ascorbic acid (vitamin C)
• Magnesium (Mg²⁺):
• Absorbed through TRPM6 channels
• Phosphate (PO₄³⁻):
• Absorbed via Na⁺/PO₄ cotransporters
• Potassium (K⁺):
• Absorbed mainly via passive diffusion due to concentration gradients

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Mechanism of Nutreint Absorption

• Fat-Soluble Vitamins:
• Vitamins A, D, E, and K are absorbed along with dietary fats through the same mechanism as fat absorption
• They are incorporated into micelles and absorbed into the enterocytes, where they are incorporated into chylomicrons for transport
• Water-Soluble Vitamins:
• Vitamin C and B-vitamins are absorbed primarily by sodium-dependent active transport or facilitated diffusion.
• For example, ascorbic acid (vitamin C) is absorbed via SVCT1 (sodium-dependent ascorbate transporter).
• B12 absorption requires intrinsic factor, which binds to vitamin B12, allowing absorption via a receptor-mediated endocytosis mechanism in the ileum.

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Intestinal Transport of Electrolytes and Water

• Mechanisms of Intestinal Electrolyte Transport:
• Na⁺ absorption:
• Driven by active transport via the Na⁺/K⁺ ATPase pump in the basolateral membrane
• Na⁺ is transported across the apical membrane through various Na⁺-dependent cotransporters

e.g., SGLT1(Sodium-Glucose Linked Transporter 1) for glucose

• Chloride (Cl⁻):
• Often transported with sodium or via Cl⁻/HCO₃⁻ exchangers
• Potassium (K⁺):
• Transported by Na⁺/K⁺ ATPase pumps and through passive diffusion due to the electrochemical gradient

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• Water Transport:
• Water absorption is coupled with Na⁺ absorption (osmotic coupling)
• The SGLT1 co-transport system not only facilitates glucose and sodium absorption but also drives water absorption

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Ulcer in Animals(Gastric ulcer)

• Physiology of Gastric Ulcers:
• Gastric ulcers are lesions that develop on the stomach lining, typically in the fundus or pyloric region
• They occur due to an imbalance between aggressive factors (like hydrochloric acid and pepsin) and protective factors (like mucus, bicarbonate, and blood flow)
• Causes:
• Stress (transport, disease, etc.)
• Dietary factors (highly fermentable carbohydrates, poor-quality roughage)
• Infection (e.g., Helicobacter pylori in humans, similar pathogens in animals)
• Nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., aspirin, ibuprofen)

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Ulcer in Animals( gastric ulcer)

• Clinical Signs:
• Loss of appetite
• Abdominal pain (guarding or rolling in cattle)
• Dehydration
• Weight loss
• Vomiting (in severe cases)
• Colic (pain in the abdomen)
• Diagnosis:
• History and clinical signs
• Endoscopy to visualize ulceration
• Blood tests showing elevated levels of gastrin or reduced blood pH in severe cases
• Treatment:
• Antacids (H2 blockers like ranitidine)
• Proton pump inhibitors (omeprazole)
• Antibiotics if there’s an infection (e.g., Helicobacter)
• Stress management (environmental and dietary adjustments)

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Ruminal Acidosis

• Physiology of Ruminal Acidosis:
• Ruminal acidosis is a condition caused by excessive production of lactic acid in the rumen
• It results from the rapid fermentation of highly fermentable carbohydrates, leading to a drop in ruminal pH

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• Causes:
• Excessive grain or concentrate feeding (high starch, low fibre)
• Abrupt dietary changes (especially high grain intake)

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Ruminal Acidosis

• Clinical Signs:
• Reduced appetite
• Diarrhoea
• Abdominal distention
• Laminitis (in severe cases)
• Dehydration, lethargy, and potentially death if untreated
• Diagnosis:
• Clinical signs and history of diet
• Rumen fluid analysis (pH <5.5)
• Blood tests showing acidosis (low blood pH)
• Treatment:
• Rumen alkalizers (e.g., sodium bicarbonate)
• Slow reintroduction of fibre into the diet
• Probiotics to stabilize ruminal flora
• Intravenous fluids for rehydration and correction of acidosis

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Urea Toxicity

• Physiology of Urea Toxicity:
• Urea is a nitrogenous compound excreted in urine but can also be used in animal feed as a protein supplement
• Urea toxicity occurs when urea is consumed in excess and converted to ammonia, which exceeds the liver’s detoxification capacity
• Causes:
• Feeding urea in high amounts.
• Poor mixing of urea with feed.
• Sudden changes in urea levels or improper rumen adaptation

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Urea Toxicity

• Clinical Signs:
• Watery or mucous stool
• Dehydration (sunken eyes, dry mucous membranes)
• Loss of appetite
• Fever (if caused by infection)
• Diagnosis:
• History and clinical signs.
• Faecal examination for pathogens (e.g., cultures, PCR).
• Blood tests to assess dehydration and electrolyte imbalances.
• Treatment:
• Oral rehydration solutions (electrolyte supplementation).
• Antibiotics if bacterial infection is diagnosed.
• Probiotics (helpful in restoring gut flora).
• Antidiarrheals (e.g., kaolin-pectin mixtures).
• Supportive care (fluid therapy and monitoring).

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Protected Nutrients

• Protected Nutrients:
• These are nutrients that are chemically or physically protected to resist ruminal degradation, allowing them to pass into the small intestine for absorption
• Examples:
• Protected fats (calcium salts of fatty acids), protected proteins (heat-treated or coated proteins), and protected amino acids (methionine, lysine)
• Function:
• Enhance nutrient absorption in the small intestine
• Prevent the loss of essential nutrients in the rumen
• Improve growth, milk production, and reproductive efficiency
• Enzymes in Feed:
• Enzymes are used in animal feeds to improve nutrient digestibility
• Types of enzymes:
• Proteases
• amylases
• cellulases
• lipases
• Applications:
• Increase the digestion of fibrous material (cellulases in ruminants)
• Improve starch and protein digestion (amylases, proteases in non-ruminants)
• Aid in nutrient utilization and overall feed efficiency

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Antibiotics in Feed

• Purpose of Antibiotics in Animal Feed:
• Growth Promotion:
• Antibiotics can enhance feed conversion rates and promote weight gain
• Disease Prevention:
• Prevent subclinical infections and reduce the need for therapeutic antibiotics
• Common Antibiotics Used:
• Tetracyclines, Penicillin, Sulfonamides, Ionophores (e.g., monensin for rumen microbial management)
• Concerns and Regulations:
• Antibiotic resistance: Overuse of antibiotics can lead to resistance
• Withdrawal times: Ensure proper withdrawal periods before slaughter or milk collection
• Regulations: Many countries have banned certain antibiotics in feed for growth promotion

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Probiotics and prebiotics in Animal Feed

Probiotics:

• Definition:
• Live microorganisms that, when administered in adequate amounts, confer health benefits to the host

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• Mechanism of Action:
• Restore or maintain a balanced microbial flora in the gut
• Enhance gut health and immune function

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• Common Probiotics:
• Lactobacillus spp., Bifidobacterium spp., Saccharomyces cerevisiae (yeast), Enterococcus spp.

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Probiotics and prebiotics in Animal Feed

Prebiotics:

• Definition:
• Non-digestible food ingredients that selectively stimulate the growth or activity of beneficial microorganisms in the gut

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• Common Prebiotics:
• FOS (fructooligosaccharides), MOS (mannanoligosaccharides), Inulin

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• Applications:
• Probiotics:
• Improve gut health, prevent diarrhoea, and enhance nutrient absorption.
• Prebiotics:
• Support beneficial microbial populations, enhance immune function, and improve digestion.
• Synbiotics:
• A combination of probiotics and prebiotics

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