We Get To Discuss The Application Of This As It Pertains To ✓ Solved

We get to discuss the application of this as it pertains to

We get to discuss the application of this as it pertains to digestion. Let's say you are drinking a glass of milk. Milk contains sugars known as lactose. In most people the pathway for milk includes ingestion, digestion, absorption and elimination. Please explain this pathway in detail (when you get to digestion and absorption focus only on the molecule lactose). Next, how would the process change in someone who is lactose intolerant (they cannot digest lactose).

Paper For Above Instructions

Overview

Drinking a glass of milk initiates a multi-stage physiologic process: ingestion, digestion, absorption and elimination. This paper traces that pathway with a focus on the disaccharide lactose during the digestion and absorption stages, and then contrasts normal processing with the changes that occur in lactose intolerance.

1. Ingestion: Oral and Early Mechanical Processing

Ingestion begins when milk enters the oral cavity. Mechanical processing by the teeth and mixing with saliva form a bolus for swallowing. Salivary enzymes do not significantly hydrolyze lactose; instead, the oral phase primarily prepares the bolus and triggers reflexes that coordinate swallowing and gastric motility [1]. Milk then passes through the esophagus to the stomach, where churning and acid exposure begin to act on proteins and fats while largely sparing lactose, which is stable in gastric acid.

2. Digestion: Enzymatic Hydrolysis of Lactose

Most chemical digestion relevant to lactose occurs in the small intestine. Lactose is a disaccharide composed of one glucose and one galactose unit linked by a β-1,4-glycosidic bond. The small intestinal brush border expresses the enzyme lactase-phlorizin hydrolase (commonly called lactase) at the apical membrane of enterocytes in the jejunum and proximal ileum. Lactase cleaves lactose into its monosaccharide constituents (glucose and galactose) at the luminal surface; these monosaccharides are then available for absorption [2][3].

Mechanistically, lactase is a membrane-bound glycoprotein that hydrolyzes the β-1,4 bond, producing equimolar glucose and galactose. The activity of lactase is highest in infancy in species that consume milk and typically declines after weaning in many humans unless genetic lactase persistence alleles maintain expression into adulthood [4]. When lactase activity is adequate, nearly all ingested lactose is hydrolyzed at the brush border before it progresses further down the gut.

3. Absorption: Transport of Lactose-Derived Monosaccharides

Absorption refers to movement of digestion products from the intestinal lumen into the bloodstream. After brush-border hydrolysis, glucose and galactose are absorbed across enterocytes via the sodium-dependent glucose transporter 1 (SGLT1) on the apical membrane. SGLT1 couples sodium influx to monosaccharide uptake; monosaccharides then exit the enterocyte across the basolateral membrane via facilitated diffusion through GLUT2 into the portal circulation [5][6].

Because absorption depends on enzymatic cleavage first, intact lactose (the disaccharide) is poorly absorbed by enterocytes. Therefore, efficient lactase activity is essential for normal lactose-derived carbohydrate uptake and subsequent delivery of glucose and galactose to the liver and peripheral tissues for metabolism or storage [2][5].

4. Elimination: Transit and Fecal Output of Unabsorbed Components

If lactose is adequately digested and monosaccharides absorbed, little lactose is left to pass to the colon. Normal elimination involves water and indigestible residues being formed into feces for excretion. Unabsorbed monosaccharides are not a feature in normal digestion because they are absorbed earlier in the small intestine.

5. What Changes in Lactose Intolerance?

Lactose intolerance results when small intestinal lactase activity is insufficient to hydrolyze the amount of lactose ingested. Causes include primary adult-type lactase nonpersistence (genetic downregulation of lactase after infancy), secondary lactase deficiency due to mucosal injury (e.g., gastroenteritis, celiac disease, inflammatory bowel disease), or congenital lactase deficiency (rare) [3][7].

When lactase activity is low, lactose is not hydrolyzed in the proximal small intestine and therefore travels intact to the distal small bowel and colon. Two major consequences follow:

  • Osmotic effects: Unabsorbed lactose is osmotically active, drawing water into the intestinal lumen and causing loose stools or osmotic diarrhea.
  • Colonic fermentation: Colonic microbiota ferment lactose to short-chain fatty acids, hydrogen, methane and carbon dioxide. Fermentation products and gas cause bloating, flatulence, abdominal pain, and increased stool volume [8][9].

Symptoms typically occur within 30 minutes to a few hours after consuming lactose-containing foods and vary with the dose of lactose and residual lactase activity. Because glucose and galactose absorption is reduced, there is less immediate monosaccharide available for metabolic use, but systemic energy balance is normally maintained by other dietary components unless the diet is otherwise deficient.

6. Diagnostic and Clinical Implications

Diagnosis can be made by hydrogen breath testing (elevated breath hydrogen after lactose load), lactose tolerance blood testing (rise in blood glucose after lactose), stool acidity in infants, or genetic testing for lactase persistence alleles [10]. Management focuses on dietary modification (reducing lactose intake), use of lactose-free or lactose-reduced dairy products, enzyme replacement (oral lactase supplements), and fermented dairy products (yogurt with active cultures can have lower lactose and improved tolerance) [3][8]. In secondary deficiency, treating the underlying mucosal disease can restore lactase activity.

Conclusion

In a person with normal lactase activity, ingestion of milk leads to brush-border hydrolysis of lactose into glucose and galactose, efficient SGLT1-mediated absorption of these monosaccharides, and minimal colonic fermentation or symptoms. In lactose intolerance, insufficient lactase leaves lactose intact, causing osmotic diarrhea and colonic fermentation with gas and discomfort. Understanding the enzymatic and transport steps clarifies why enzyme deficiency — not inability to absorb monosaccharides — is the central problem in lactose intolerance, and it guides diagnostics and dietary or enzymatic interventions.

References

  1. Guyton AC, Hall JE. Textbook of Medical Physiology. 13th ed. Elsevier; 2016.
  2. Lehninger AL, Nelson DL, Cox MM. Lehninger Principles of Biochemistry. 7th ed. W.H. Freeman; 2017.
  3. Heyman MB. Lactose intolerance in infants, children, and adolescents. Pediatrics. 2006;118(3):1279–1286.
  4. Swallow DM. Genetics of lactase persistence and lactose intolerance. Annu Rev Genomics Hum Genet. 2003;4:119–138.
  5. Wright EM, Loo DD, Hirayama BA. Surprising versatility of Na+-glucose cotransporter SGLT1. Physiology (Bethesda). 2013;28(6):357–363.
  6. Rao SS. Physiology of the small intestine and fluid and electrolyte transport. In: Feldman M, Friedman LS, Brandt LJ, editors. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 10th ed. Elsevier; 2015.
  7. Lomer MC, Parkes GC, Sanderson JD. Review article: lactose intolerance in clinical practice—myths and realities. Aliment Pharmacol Ther. 2008;27(2):93–103.
  8. Vesa TH, Marteau P, Korpela R. Lactose intolerance. J Am Coll Nutr. 2000;19(2 Suppl):165S–175S.
  9. Di Stefano M, et al. Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment options. World J Gastroenterol. 2015;21(44):12383–12388.
  10. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Lactose Intolerance. U.S. Department of Health and Human Services. https://www.niddk.nih.gov/health-information/digestive-diseases/lactose-intolerance. Accessed 2024.

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