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LASTOSE AND
FRUCTOSE
INTOLERANCE
BY
N.SUGANDHI
Lactose
 Lactose is a disaccharides of β-D-galactose and β-
D-glucose in β(1,4)linkage.
 Human milk contain 200mmol/lit of lactose.
 It is digested by enzyme lactase to form glucose
and galactose in the brush border of the intestine.
Lactose intolerance
 Lactose intolerance is called lactase deficiency
and hypolactasia is the inability to digest and
metabolize lactase, a sugar found in milk.
 Lactose intolerance is not a allergy because it is
not an immune response but caused by lactase
deficiency.
 When dairy products are ingested, the lactose
reaches the digestive system and it is broken
down by lactase into the simple sugars, glucose
and galactose, which can them be absorbed into
the blood stream.
 Lactose intolerance occurs when due to deficiency
of lactase is not completely broken down and
consequently blood sugar level do not rise.
 Lactose intolerance is the dangerous condition can
cause severe discomfort. It may produce a wide
range of GI problems & abdominal pain.
 When lactose moves through the large intestine
without being properly digested it can cause
uncomfortable symptoms.
 LI can occur in any age group of people
Lactose containing food stuffs
 Fresh, skimmed, non-fat and condensed milk
 Cream
 Yoghurt
 Cheese
 Processed food
 Salad dressing etc.
Types of lactose deficiency
 primary lactase deficiency
 Secondary lactase deficiency
 Congenital lactase deficiency
Primary lactase deficiency
 It is also called primary hypolactasia.
 PTD is a genetically determined absence or
decreased in the enzyme.
 Those who experience classical symptoms
following excessive milk or lactase ingestion, can
be kept asymptomatic by limiting the intake of
milk prdts.
 PTD is abnormal in adulthood.
Secondary lactase deficiency
 It is also called acquired or transient lactase
deficiency or secondary hypolactasia.
 It is due to the small intestine mucosal disease,
abnormalities of brush border cells & transport
processes.
 It may be caused by acute gastroenteritis, celiac
disease, ulcerative colitis, cystic fibrosis,
kwashiorkor and malnutrition or other evnt
causes.
Congenital lactase deficiency
 It is also called primary congenital hypolactasia.
 It is a rare autosomal recessive genetic disorder
that prevents lactase expression from the first
feed.
 People with CLD cannot digest lactose from the
birth. This genetic defect is characterized by a
complete lack of lactose
 CLI is serious disorder in which the infants may
fail to thrive unless given lactose free formula
feed
Symptoms
 Abdominal bloating & cramps
 Flatulence
 Diarrhea
 Nausea
 Vomiting etc.
Diagnosis
 Dietary history of the patient who are
complaining flatulence, abdominal pain, diarrhea.
 Familial history of the patient
 Check whether the patient has underwent partial
gastrectomy and other related procedures.
 Test - stool acidity test
-hydrogen breath test
-blood sugar test
Treatment
 Avoiding lactose containing prdts
 Using alternative prdts such as plant-based milks
and derivatives are inherently lactose free : soy
milk, rice milk, almond milk, oat milk, coconut
milk etc.
Fructose
 Fructose is a simple ketonic monosaccharide
found in many foods such as fresh fruits and
honey, high fructose corn syrup & many
processed foods.
 Ingestion of large quantities of fructose or sucrose
is linked with many health complications.
 High fructose corn syrup consumption has
increased for more than 90% with an annual
consumption of fructose to have risen in fructose
malabsorption & fructose intolerance
Fructose metabolism
 After ingestion, fructose is converted into
fructose-1-phosphate in the liver by fructokinase.
 Deficiency of fructokinase cause essential
fructosuria a clinically benign condition
characterized by the excerition of unmetabolized
fructose in urine.
 Fructose-1-phosphate is metabolized by aldolase
B into dihydroxyacetone phosphate and
glyceraldehyde.
 HFI is caused of aldolase B result in an
accumulation of fructose-1-phosphate,& trapping
of phosphate
 The downstream effects of this enzyme black are
the inhibition of glucose production & reduced
regeneration of ATP.
Fructose malabsorption
 Some people cannot completely absorb fructose
in their small intestine.
 The undigested fructose is then carried to colon
where our normal bacteria rapidly devour it.
 In this process, the bacteria produces gases which
cause the intestine to swell.
 This is experience by the person as bloating,
cramping, gas and distention and diarrhea may
also occur due to the undigested praticals of
fructose.
Fructose intolerance
 Fructose intolerance is also known as hereditary
fructose intolerance, fructosemia, fructose
aldolase B deficiency.
 It is an inbron error of fructose metabloism
caused by a deficiency of the enzyme aldolase B
 Individual affected with HFI are asymptomatic
until they ingest fructose, sucrose, or sorbitol.
 If the fructose is ingested, the enzymatic block at
aldolase B cause an accumulation of fructose-1-
phosphate which, overtime result in the death of
liver cells
 This accumulation has downstream effect on
gluconeogenesis & regeneration of adenosine
triphosphate (ATP)
Symptoms
 Abdominal cramps
 Diarrhea or constipation
 Increased intestinal sounds
 Irritable bowel syndrome
 Gas production
 Reflux (acid taste in mouth)
 Nausea or vomiting
 Poor feeding
 Yellow skin or whites of the eyes
Diagnosis
 The only definitive way to ascertain if one is
suffering from HFI is to have one of two test.
 An enzymatic assay to determine aldolase
activity.
- The aldolase is obtained from patient liver
tissue in an invasive surgical procedure called
liver biopsy.
 A fructose tolerance test, fructose is injected
introvenously under controlled condition where
acute glucose, fructose & phosphate levels are
monitered.
 And hydrogen breathe test it is a method currently
used to diagnosis following ingestion of fructose,
the hydrogen concentration of the patients breathe
is measured at various time intervals.
Treatment
 Avoiding fructose, sucrose or sorbitol from diet to
avoid foods like honey, palm or coconut sugar,
high fructose corn syrup etc.
 Treatment with dietary supplements of xylose
isomerase may reduce the sympotoms of FI
 Xylose isomerase acts to convert fructose sugar to
glucose.
Thank you

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Lastose and fructose intolerance

  • 2. Lactose  Lactose is a disaccharides of β-D-galactose and β- D-glucose in β(1,4)linkage.  Human milk contain 200mmol/lit of lactose.  It is digested by enzyme lactase to form glucose and galactose in the brush border of the intestine.
  • 3. Lactose intolerance  Lactose intolerance is called lactase deficiency and hypolactasia is the inability to digest and metabolize lactase, a sugar found in milk.  Lactose intolerance is not a allergy because it is not an immune response but caused by lactase deficiency.  When dairy products are ingested, the lactose reaches the digestive system and it is broken down by lactase into the simple sugars, glucose and galactose, which can them be absorbed into the blood stream.
  • 4.  Lactose intolerance occurs when due to deficiency of lactase is not completely broken down and consequently blood sugar level do not rise.  Lactose intolerance is the dangerous condition can cause severe discomfort. It may produce a wide range of GI problems & abdominal pain.  When lactose moves through the large intestine without being properly digested it can cause uncomfortable symptoms.  LI can occur in any age group of people
  • 5.
  • 6. Lactose containing food stuffs  Fresh, skimmed, non-fat and condensed milk  Cream  Yoghurt  Cheese  Processed food  Salad dressing etc.
  • 7. Types of lactose deficiency  primary lactase deficiency  Secondary lactase deficiency  Congenital lactase deficiency
  • 8. Primary lactase deficiency  It is also called primary hypolactasia.  PTD is a genetically determined absence or decreased in the enzyme.  Those who experience classical symptoms following excessive milk or lactase ingestion, can be kept asymptomatic by limiting the intake of milk prdts.  PTD is abnormal in adulthood.
  • 9. Secondary lactase deficiency  It is also called acquired or transient lactase deficiency or secondary hypolactasia.  It is due to the small intestine mucosal disease, abnormalities of brush border cells & transport processes.  It may be caused by acute gastroenteritis, celiac disease, ulcerative colitis, cystic fibrosis, kwashiorkor and malnutrition or other evnt causes.
  • 10. Congenital lactase deficiency  It is also called primary congenital hypolactasia.  It is a rare autosomal recessive genetic disorder that prevents lactase expression from the first feed.  People with CLD cannot digest lactose from the birth. This genetic defect is characterized by a complete lack of lactose  CLI is serious disorder in which the infants may fail to thrive unless given lactose free formula feed
  • 11. Symptoms  Abdominal bloating & cramps  Flatulence  Diarrhea  Nausea  Vomiting etc.
  • 12. Diagnosis  Dietary history of the patient who are complaining flatulence, abdominal pain, diarrhea.  Familial history of the patient  Check whether the patient has underwent partial gastrectomy and other related procedures.  Test - stool acidity test -hydrogen breath test -blood sugar test
  • 13. Treatment  Avoiding lactose containing prdts  Using alternative prdts such as plant-based milks and derivatives are inherently lactose free : soy milk, rice milk, almond milk, oat milk, coconut milk etc.
  • 14. Fructose  Fructose is a simple ketonic monosaccharide found in many foods such as fresh fruits and honey, high fructose corn syrup & many processed foods.  Ingestion of large quantities of fructose or sucrose is linked with many health complications.  High fructose corn syrup consumption has increased for more than 90% with an annual consumption of fructose to have risen in fructose malabsorption & fructose intolerance
  • 15. Fructose metabolism  After ingestion, fructose is converted into fructose-1-phosphate in the liver by fructokinase.  Deficiency of fructokinase cause essential fructosuria a clinically benign condition characterized by the excerition of unmetabolized fructose in urine.  Fructose-1-phosphate is metabolized by aldolase B into dihydroxyacetone phosphate and glyceraldehyde.  HFI is caused of aldolase B result in an accumulation of fructose-1-phosphate,& trapping of phosphate
  • 16.  The downstream effects of this enzyme black are the inhibition of glucose production & reduced regeneration of ATP.
  • 17. Fructose malabsorption  Some people cannot completely absorb fructose in their small intestine.  The undigested fructose is then carried to colon where our normal bacteria rapidly devour it.  In this process, the bacteria produces gases which cause the intestine to swell.  This is experience by the person as bloating, cramping, gas and distention and diarrhea may also occur due to the undigested praticals of fructose.
  • 18. Fructose intolerance  Fructose intolerance is also known as hereditary fructose intolerance, fructosemia, fructose aldolase B deficiency.  It is an inbron error of fructose metabloism caused by a deficiency of the enzyme aldolase B  Individual affected with HFI are asymptomatic until they ingest fructose, sucrose, or sorbitol.  If the fructose is ingested, the enzymatic block at aldolase B cause an accumulation of fructose-1- phosphate which, overtime result in the death of liver cells  This accumulation has downstream effect on gluconeogenesis & regeneration of adenosine triphosphate (ATP)
  • 19. Symptoms  Abdominal cramps  Diarrhea or constipation  Increased intestinal sounds  Irritable bowel syndrome  Gas production  Reflux (acid taste in mouth)  Nausea or vomiting  Poor feeding  Yellow skin or whites of the eyes
  • 20. Diagnosis  The only definitive way to ascertain if one is suffering from HFI is to have one of two test.  An enzymatic assay to determine aldolase activity. - The aldolase is obtained from patient liver tissue in an invasive surgical procedure called liver biopsy.  A fructose tolerance test, fructose is injected introvenously under controlled condition where acute glucose, fructose & phosphate levels are monitered.
  • 21.  And hydrogen breathe test it is a method currently used to diagnosis following ingestion of fructose, the hydrogen concentration of the patients breathe is measured at various time intervals.
  • 22. Treatment  Avoiding fructose, sucrose or sorbitol from diet to avoid foods like honey, palm or coconut sugar, high fructose corn syrup etc.  Treatment with dietary supplements of xylose isomerase may reduce the sympotoms of FI  Xylose isomerase acts to convert fructose sugar to glucose.