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Digestion and absorption of carbohydrates



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Digestion and absorption of carbohydrates

  1. 1. Student’s Corner Selected for publication Biochemistry For Medics
  2. 2. Topic: Digestion and Absorption of carbohydrates with clinical significance. Presented by : THOSADU RAMDU Pooja. Roll no. : 102.
  3. 3. CONTENTS Digestion of carbohydrates Absorption of carbohydrates Clinical significance
  4. 4. Carbohydrates present in the diet Disaccharides Monosaccharides Polysaccharides Starch Lactose Glucose Glycogen Maltose Fructose Sucrose Pentose In GIT, all complex carbohydrates are converted to simpler monosaccharide form which is the absorbable form.
  5. 5. Details of digestion of carbohydrates 2 Types of enzymes are important for the digestion of carbohydrates Amylases Disaccharidases Convert disaccharides to convert polysaccharides to disaccharides monosaccharides which are finally absorbed Salivary Maltase Amylase Sucrase-Isomaltase Pancreatic Amylase Lactase Trehalase
  6. 6. Digestion in mouth Digestion in stomach Digestion in small intestine
  7. 7. Digestion in the Mouth Digestion of Carbohydrate starts in the mouth, upon contact with saliva during mastication. Saliva contains a carbohydrate splitting enzyme called salivary amylase , also known as ptylin.
  8. 8. Action of ptylin (salivary amylase) • Location: mouth • It is α-amylase and requires Cl− ion for activation with an optimum pH of 6.7 (Range 6.6 to 6.8). • The enzyme hydrolyses α-1→ 4 glycosidic linkages deep inside polysaccharide molecules. • However, ptylin action stops in the stomach when the pH falls to 3.0.
  9. 9. Starch, Glycogen and dextrins (Large polysaccharide molecules) α- Amylase Glucose,Maltose and Maltotriose. (Smaller molecules)
  10. 10. Drawback • Shorter duration of food in mouth. • Thus it is incomplete digestion of starch or glycogen in the mouth
  11. 11. Digestion in the Stomach • There is no enzyme to break the glycosidic bonds in gastric juice. • However, HCl present in the stomach causes hydrolysis of sucrose to fructose and glucose. HCl Sucrose Fructose + Glucose
  12. 12. Digestion in Duodenum • Food bolus reaches the duodenum from the stomach where it meets the pancreatic juice. • Pancreatic juice contains a carbohydrate splitting enzyme, pancreatic amylase (amylopsin) similar to salivary amylase.
  13. 13. Action of pancreatic amylase • It is an α- Amylase • Optimum pH=7.1 • Like ptylin, it requires Cl− ion for its activity. • It hydrolyses α-1→ 4 glycosidic linkages situated well inside polysaccharide molecules. • Note: Pancreatic amylase, an isoenzyme of salivary amylase, differs only in the optimum pH of action. Both the enzymes require Chloride ions for their actions (Ion activated enzymes).
  14. 14. Reaction catalyzed by pancreatic amylase Starch/Glycogen Pancreatic Amylase Maltose/ Isomaltose + Dextrins and oligosaccharides
  15. 15. Digestion in Small Intestine Note: • Main digestion takes place in the small intestine by pancreatic amylase • Digestion is completed by pancreatic amylase because food stays for a longer time in the intestine.
  16. 16. What are Disaccharidases? • They are present in the brush border epithelium of intestinal mucosal cells where the resultant monosaccharides and others arising from the diet are absorbed. • The different disaccharidases are : 1) Maltase, 2) Sucrase-Isomaltase (a bifunctional enzyme catalyzing hydrolysis of sucrose and isomaltose) 3) Lactase
  17. 17. Reactions catalyzed by Disaccharidases Maltase • Maltose Glucose + Glucose Sucrase Isomaltase • Sucrose Isomaltose 3Glucose + fructose Lactase • Lactose Glucose + Galactose
  18. 18. Clinical significance of Digestion • Lactose intolerance is the inability to digest lactose due to the deficiency of Lactase enzyme. • Causes Congenital Acquired during lifetime Primary Secondary
  19. 19. Congenital Lactose intolerance • It is a congenital disorder • There is complete absence or deficiency of lactase enzyme. • The child develops intolerance to lactose immediately after birth. • It is diagnosed in early infancy. • Milk feed precipitates symptoms.
  20. 20. Baby with Lactose Intolerance
  21. 21. Primary Lactase deficiency • Primary lactase deficiency develops over time • There is no congenital absence of lactase but the deficiency is precipitated during adulthood. • The gene for lactose is normally expressed upto RNA level but it is not translated to form enzyme. • It is very common in Asian population. • There is intolerance to milk + dairy products.
  22. 22. Adult with lactose intolerance
  23. 23. Secondary lactase deficiency • It may develop in a person with a healthy small intestine during episodes of acute illness. • This occurs because of mucosal damage or from medications resulting from certain gastrointestinal diseases, including exposure to intestinal parasites such as Giardia lamblia. • In such cases the production of lactase may be permanently disrupted. • A very common cause of temporary lactose intolerance is gastroenteritis, particularly when the gastroenteritis is caused by rotavirus. • Another form of temporary lactose intolerance is lactose overload in infants. Secondary lactase deficiency also results from injury to the small intestine that occurs with celiac disease, Crohn’s disease, or chemotherapy. • This type of lactase deficiency can occur at any age but is more common in infancy.
  24. 24. Intestinal parasite Rotavirus (Giardia lamblia)
  25. 25. Clinical manifestations • In the form of abdominal cramps, distensions, diarrhea, constipation, flatulenc e upon ingestion of milk or dairy products Biochemical basis • Undigested lactose in intestinal lumen is acted upon by bacteria and is converted to CO2 , H2 , 2 carbon compounds and 3 carbon compounds or it may remain undigested.
  26. 26. • CO2 and H2 causes Distensions and flatulence • Lactose + 2C + 3C are osmotically active. • They withdraw H2O from intestinal mucosal cell and cause osmotic diarrhea or constipation because of undigested bulk. Abdominal distension Flatulence
  27. 27. Diagnosis • Two tests are commonly used: - • Hydrogen Breath Test • The person drinks a lactose- loaded beverage and then the breath is analyzed at regular intervals to measure the amount of hydrogen. Normally, very little hydrogen is detectable in the breath, but undigested lactose produces high levels of hydrogen. The test takes about 2 to 3 hours.
  28. 28. • Stool Acidity Test • The stool acidity test is used for infants and young children to measure the amount of acid in the stool. Undigested lactose creates lactic acid and other short chain fatty acids that can be detected in a stool sample. Glucose may also be present in the stool as a result of undigested lactose. • Besides these tests, urine shows- positive test with Benedict’s test, since lactose is a reducing sugar and a small amount of lactose is absorbed in the intestinal cell by pinocytosis and is rapidly eliminated through kidneys in to urine.(Lactosuria) • Mucosal biopsy confirms the diagnosis.
  29. 29. Management of lactose intolerance • Avoidance of dairy products. • Although the body’s ability to produce lactase cannot be changed, the symptoms of lactose intolerance can be managed with dietary changes. • Most people with lactose intolerance can tolerate some amount of lactose in their diet. Gradually introducing small amounts of milk or milk products may help some people adapt to them with fewer symptoms. • Partly digested dairy products can also be given.
  30. 30. • Lactose-free, lactose-reduced milk, Soy milk and other products may be recommended. • Lactase enzyme drops or tablets(Yeast tablets) can also be consumed. • Getting enough calcium is important for people with lactose intolerance when the intake of milk and milk products is limited. • A balanced diet that provides an adequate amount of nutrients—including calcium and vitamin D—and minimizes discomfort is to be planned for the patients of lactose intolerance.
  31. 31. Sucrase-Isomaltase deficiency • These 2 enzymes are synthesized on a single polypeptide chain,hence , their deficiencies coexist. • Signs and symptoms • Same as that of lactose intolerance. • Urine does not give +ve test with Benedict’s test because of sucrose(Non reducing sugar). • History confirms the diagnosis. • Most confirmatory test is mucosal biopsy.
  32. 32. Absorption of carbohydrates 3 mechanisms Facilitated Active transport Passive diffusion diffusion/Carrier mediated
  33. 33. Features Passive diffusion Facilitated diffusion Active transport Concentration Down the Down the Against a gradient concentration concentration concentration gradient from high to gradient from high to gradient from low to low. low. high Energy expenditure none none Energy expenditure is in the form of ATP Carrier protein/ Not required required required transporter Speed Slowest mode Fast Fastest mode Note: Glucose is a polar molecule. It cannot pass through lipid bilayer of cell.
  34. 34. Glucose transporters Glucose transporters Na+ 2 types Na+ independent dependent transporter transporter Also called Also called SGLT GLUT
  35. 35. Na+ dependent transporter • Type of co-transport • 2 binding sites on the transporter, one for Na+ and other for glucose. • Na + binding is important because after Na + binding, conformational changes occurs so that glucose can bind. • Na + is transported across cell membrane, down the concentration gradient and glucose goes against a concentration gradient. • ATP is spent at the level of Na-K ATPase pump to expel Na out. • Both glucose and galactose are absorbed by a sodium- dependent process. • They are carried by the same transport protein (SGLT
  36. 36. Figure- Showing the co transport of Glucose, mediated by SGLT- 1/2. SGLT-1 are present on the intestinal cells while SGLT-2 are present on the proximal renal tubular cells.
  37. 37. 3 reasons for expulsion of sodium 1) Na + is osmotically active, causes osmotic flow to cells, leading to osmolysis. 2) Na + concentration has to be kept minimal to maintain the downward gradient. 3) Na + is inhibitory to many enzyme actions.
  38. 38. Energy released is Solvent Downward captured for transport of gradient of glucose against a conc. drag Na+ Gradient. releases absorption energy Na expelled This type of out through absorption Na-K is called ATPase solvent drag pump. Energy is consumed at the level of ATP Water 3 sodium carries are expelled dissolved out and 2 K glucose with are it internalised The Na removed to paracellular spaces exerts osmotic pressure that causes flow of water to intracellular spaces
  39. 39. Clinical significance • In deficiency of SGLT- 1, glucose is left unabsorbed and is excreted in feces. Galactose is also malabsorbed. • In deficiency of SGLT- 2, the filtered glucose is not reabsorbed back, it is lost in urine, causing glycosuria.
  40. 40. • Solvent drag is not the main mechanism of glucose absorption but is important after a carbohydrate rich diet. • Absorption of galactose is faster than glucose. • In kidney, reabsorption of filtered glucose takes place by a similar mechanism, i.e, it is also a co-transport with Na. The transporter is SGLT- 2. • In intestine, it is SGLT- 1.
  41. 41. Na+ independent transporters • Used for facilitated transport. • These transporters are numbered from 1 to 14 GLUT. • In the intestine, GLUT 2 are present towards the serosal surface of intestinal epithelial cells and GLUT 5 are present towards the luminal surface.
  42. 42. Location of GLUT 2 and GLUT 5 in intestine
  43. 43. Diagram showing absorption of monosaccharides
  44. 44. Purpose of GLUT 5 and GLUT 2 >Mainly responsible for pouring all the > For the transportation of absorbed glucose into blood. fructose.(least affinity for glucose). >GLUT 2 transporter transports all >Fructose is mainly transported by absorbed glucose to blood. It is down a facilitated diffusion. concentration gradient. >By GLUT 5, fructose moves down the >Transporter is present but there is no gradient and the process is faster than energy expenditure. passive diffusion. >Pentoses are absorbed by passive >Energy is not consumed. diffusion which is a very slow process.
  45. 45. Factors affecting rate of absorption of Monosaccharides • The absorption is faster through intact mucosa. The absorption is decreased if there is some inflammation or injury to the mucosa. • Thyroid hormones ↑ the rate of absorption of glucose. • Mineralocorticoid,i.e Aldosterone ↑ the rate of absorption.
  46. 46. • Vitamin B6,B12, pantothenic acid, folic acid are required for absorption of glucose. • With advancing age, rate of absorption declines. • Note: Insulin has no role in the absorption of monosaccharide like glucose.
  47. 47. Uptake of glucose in peripheral cells • Mechanism: facilitated diffusion. • There are 7 important glucose transporter for uptake of glucose into special cells. • They have been numbered from 1 to 7 (GLUT 1 to GLUT 7). • They are biologically important.
  48. 48. Tissue specific Tissue distribution Functions Clinical significance glucose transporter GLUT-1 Present in almost all Na-independent Cancer cells express (great affinity for cells with an high level of GLUT-1, glucose) abundance in RBC. so they can internalize more of glucose, which is used as a source of energy for rapidly dividing cells. GLUT-2 Present in intestine, Releases insulin by Diabetes Mellitus. (low affinity for liver and pancreas. movement of glucose glucose, it can into β-cells of transport only when pancreas. there is glucose load (Acts as a sensor for in the body) the release of insulin by pancreas.) Promotes uptake of glucose in liver cells, lowering down blood glucose.
  49. 49. GLUT 3 Brain cells, all other Cancer cells express cells of body high level of GLUT- 3, so they can internalize more of glucose, which is used as a source of energy for rapidly dividing cells GLUT 4 Adipose tissue, The only skeletal muscles, transporters which cardiac muscles are under the influence of insulin. Insulin promotes uptake of glucose in the tissues by mobilizing the transporters to the cell surface whenever there is high glucose concentration in the blood.
  50. 50. GLUT 5 Intestine at the Mainly for the (least affinity for luminal surface, transport of fructose glucose) testicles, seminal vesicles GLUT 6 Non-functional transporter product of a pseudogene. No role in absorption of glucose in peripheral cells. GLUT 7 Surface of Transportation of endoplasmic glucose across the reticulum membrane of endoplasmic reticulum. SGLT 1 Kidney, intestine For the absorption of In cases where SGLT 1 glucose. is deficient, glucose is left unabsorbed and is excreted in faeces. SGLT 2 Kidney For the re-absorption If deficient, filtered of glucose. glucose is not re- absorbed and is lost in urine.
  51. 51. References • Biochemistry for medics • Lecture notes • Sciencephotolibrary
  52. 52. Thank you for your attention  Silence is a source of great strength !