1. Carbohydrates are digested into monosaccharides like glucose in the small intestine through the actions of digestive enzymes. 2. Monosaccharides are absorbed into the bloodstream and transported to tissues where they undergo further metabolism. Glucose is the primary fuel for tissues like the brain. 3. Glycolysis is the first step of glucose metabolism, occurring in the cytosol of cells. It breaks down glucose into pyruvate while generating a small amount of ATP.

1. Carbohydrate metabolism
CHO Digestion
• Carbohydrate: polyhydroxy aldehyde or
ketone
• Carbohydrate classification
– Monosaccharide (glucose, fructose, galactose
mannose)
– Di saccharides (maltose, lactose, sucrose,
isomaltose)
– Polysaccharides (cellulose, starch, glycogen)
Introduction

2. DIETARY CARBOHYDRATES
• Normal diet contains 200-300 g
(50% of caloric intake)
• Serves an energy and carbon source
• Digestion includes a luminal phase and
a brush border phase
• Only monosaccharaides are appreciably
absorbed
Introduction

3. Starch= Amylose & Amylopectin

4. • alpha-Amylase (pH optima 7)
cleaves interior α1-4 linkages
but not α1-6
• End product is a mixture of maltose,
maltotriose and limit dextrin
• Acarbose (anti diabetic drug) –
Amylase inhibitor
Introduction

5. Introduction
Intestinal brush border hydrolysis
Products
site of
hydrolysis
Substrates
Enzyme
Glucose
α- 1,4 linkage
Maltose ,
maltotriose
Maltase
Glucose
fructose
α- 1,2 linkage
Sucrose
Sucrase
Glucose,
galactose
β- 1,4 linkage
But not of
cellulose
Lactose
Lactase
Glucose,
maltose,
oligosaccharides
α- 1,6 linkage
α- limit
dextrins
α- dextrinase
(Isomaltase)

6. Maltose

10. SGLT1 Na+ - glucose symporter
Absorption of carbohydrate Introduction

11. • The glucose and galactose is taken up by a
Na+-monosaccharide co-transporter,.
• Na+ will be pumped out by Na+ K+–ATP-ase.
• Fructose is taken up by Na+ -independent
facilitated-diffusion, mediated by GLUT5.
• The monosaccharides could leave enterocytes
into interstitial through GLUT2.
Absorption of carbohydrate Introduction

12. Lactase Deficiency
Lactose accumulation
In bowel lumen
Increased luminal osmolality
Watery diarrhea
Lactic acid
Production
By bacteria
Net water accumulation in lumen
Luminal distention
Enhanced peristalsis
Introduction

13. Lactase is present in infancy and
disappears to a variable extent during
childhood in most humans.
Exception is Northern Europeans and
European Americans-commonly retain
lactase into adulthood.
Introduction

14. Sucrase Deficiency
Sucrase accumulation
In bowel lumen
Increased luminal osmolality
Watery diarrhea
Lactic acid
Production
By bacteria
Net water accumulation in lumen
Luminal distention
Enhanced peristalsis
Introduction

15. • Blood Transport: (portal vein to liver):
• 1. Release monosaccharides into
bloodstream
• 2. Deliver sugars for storage as
glycogen (liver, muscle tissue ) or fat
(adipose tissue)
Blood transport Introduction

16. • GLUT proteins
Na+ -independent monosaccharide transporters
are responsible for the thermodynamically
downhill movement of glucose across the plasma
membrane of animal cells.
– GLUT 1: red blood cells, brain, adipose tissue
– GLUT 2: liver, pancreatic β cells, kidney
– GLUT 3: brain
– GLUT 4: muscle, adipose tissue (insulin
dependent)
– GLUT 5: fructose transporter
Introduction

17. This experiment was
performed in the
culture of adipocytes
by attaching green
fluorescent protein to
GLUT4
Change of the
localization of
GLUT4 glucose
transporter protein
treated with insulin
Introduction

18. PET scans can image biological processes within the body.
Glucose metabolism significance

19. Glucose metabolism significance
Positron emission tomography (PET)
:Injection with 18fluorodeoxyglucose
(short-lived radioactive element: fluorine-18
and glucose) to track
glucose metabolism
and therefore brain
activity – glucose is virtually the only energy
source in the brain in normal.
Introduction

20. Glucose metabolism significance
Diabetes
• related to blood glucose concentration
• altered ability to regulate glucose metabolism
• normally: when [glucose] high, insulin is released
• T1DM lack the ability to secrete insulin
•T2DM insulin resistance and decrease to secrete
insulin
Cancer
• glucose uptake/glycolysis ~ 10x faster
in cancer cells
• some glycolytic enzymes are
overproduced
Introduction

21. CT scan
PET

22. glucose Sources:
1.Endogenous
2.Exogenous
• The daily requirement of glucose for the
human body is about 160 g, from which 120 g
is utilized by the brain.
Carbohydrate metabolism

23. Carbohydrate metabolism
Glycolysis & the Oxidation of Pyruvate
1. Glycolysis
2. Gluconeogenesis
3. Glycogenolysis
4. Glycogenesis

24. Summary of
glycolysis.
− , blocked by
anaerobic conditions
or by absence of
mitochondria
containing key
respiratory enzymes,
eg, as in erythrocytes

25. Glycolysis

26. Glycolysis cont.

27. Glycolysis
Occur in
cytosol

28. Characteristic
features of
glycolysis
 Localized in the
cytosol
 An ancient
metabolic
pathway
• Could produce
ATP without
using molecular
oxygen

29. Glycolysis is a preparatory pathway
for aerobic metabolism of glucose
TCA

30. The Oxidation of Pyruvate to form Acetyl CoA for Entry
Into the Krebs Cycle
Pyruvate dehydrogenase (complex enzyme) convert pyruvate
into acetyl CoA
•2 NADH's and 2 CO2 are generated (1 per pyruvate)

31. .Three possible
catabolic fates
of the pyruvate
formed in
glycolysis.
Pyruvate also
serves as a
precursor in
many anabolic
reactions, not
shown here

32. Generation of high-energy phosphate in the
catabolism of glucose.

33. CLINICAL ASPECTS
• Inhibition of Pyruvate Metabolism Leads
to Lactic Acidosis
• 1- Arsenite and mercuric ions inhibit
pyruvate dehydrogenase
• 2- Dietary deficiency of thiamin (cofactor of
pyruvate dehydrogenase,), allowing pyruvate
to accumulate.

34. • 3- Inherited pyruvate dehydrogenase
deficiency - causes lactic acidosis, particularly
after a glucose load.
– neurologic disturbances because Brain is
dependences on glucose as a fuel
CLINICAL ASPECTS

35. • Inherited aldolase A deficiency and
pyruvate kinase deficiency in
erythrocytes cause hemolytic anemia.
CLINICAL ASPECTS
Pphosphofructokinase deficiency
The exercise capacity of muscle is low,
particularly on high carbohydrate diets.
The capacity is improved By providing lipid
fuel, eg, during starvation, when blood free
fatty acids and ketone bodies are increased.