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THEME
 Metabolism

of carbohydrates
DIGESTION OF CARBOHYDRATES
Glycogen, starch and disaccharides (sucrose,
lactose and maltose) are hydrolyzed to
monosaccharide units in the gastrointestinal tract.
The process of digestion starts in the mouth by the
salivary enzyme α –amilase.
The time for digestion in mouth is limited.
Salivary α -amilase is inhibited in stomach due to the
action of hydrochloric acid.
Another α -amilase is produced in pancreas and is
available in the intestine.
α -amilase hydrolyzes the α -1-4-glycosidic
bonds randomly to produce smaller subunits like
maltose, dextrines and unbranched
oligosaccharides.

α -amilase
The intestinal juice contains enzymes hydrolyzing
disaccharides into monosaccharides (they are produced
in the intestinal wall)
Sucrase hydrolyses sucrose into glucose and
fructose

Glucose

sucrase

Fructose
Sucrose
Galactose

lactase

Glucose

Lactase hydrolyses
lactose into glucose
and galactose
Lactose

Glucose

maltase

Maltase hydrolyses
maltose into two
glucose molecules
Maltose

Glucose
ABSORPTION OF CARBOHYDRATES
Only monosaccharides are absorbed
The rate of absorption: galactose > glucose > fructose
Glucose and galactose from the intestine into endothelial
cells are absorbed by secondary active transport
Na+

Protein

Glucose

Protein
Carrier protein is specific for D-glucose or Dgalactose.
L-forms are not transported.
There are competition between glucose and
galactose for the same carrier molecule;
thus glucose can inhibit absorption of
galactose.
Fructose is absorbed from intestine into
intestinal cells by facilitated diffusion.
Absorption of glucose from intestinal cells
into bloodstream is by facilitated diffusion.
Transport of glucose from blood into cells of different
organs is mainly by facilitated diffusion.
The protein facilitating the glucose transport is called
glucose transporter (GluT).
GluT are of 5 types.
GluT1 is seen in erythrocytes and endothelial cells;
GluT2 is located mainly in hepatocytes membranes (it
transport glucose into cells when blood sugar is high);
GluT3 is located in neuronal cells (has higher affinity to
glucose);
GluT4 - in muscles and fat cells.
GluT5 – in intestine and kidneys;
The fate of glucose molecule in the cell

Glucose
Glycogenesis
(synthesis of
glycogen) is
activated in well
fed, resting state

Glucose-6phosphate

Gluconeoge
nesis
is activated
if glucose is
required

Glycogen
Glycogenolysis
(degradation of
glycogen)

Pentose phosphate
pathway supplies
the NADPH for lipid
synthesis and
pentoses for nucleic
acid synthesis

Pyruvate

Glycolysis
is activated if
energy is required

Ribose,
NADPH
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
Regulation of Glycolysis
The rate glycolysis is regulated to meet two major cellular needs:
(1) the production of ATP, and
(2) the provision of building blocks for synthetic reactions.
There are three control sites in glycolysis - the reactions catalyzed by
hexokinase,
phosphofructokinase 1, and
pyruvate kinase
These reactions are irreversible.
Their activities are regulated
by the reversible binding of allosteric effectors
by covalent modification
by the regulation of transcription (change of the enzymes amounts).
The time required for allosteric control, regulation by phosphorylation, and
transcriptional control is typically in milliseconds, seconds, and hours, respectively.
Inhibition
1) PFK-1 is
inhibited by ATP
and citrate
2) Pyruvate kinase
is inhibited by ATP
and alanine
3) Hexokinase is
inhibited by excess
glucose 6phosphate

Regulation of
Glycolysis

Stimulation
1) AMP and fructose 2,6bisphosphate (F2,6BP) relieve the
inhibition of PFK-1 by ATP
2) F1,6BP
stimulate the activity of pyruvate
kinase

Alanine
Gluconeogenesis - synthesis of "new" glucose from such
precursors as pyruvate, lactate, certain amino acids, and
intermediates of the tricarboxylic acid cycle.

Most of the reaction steps in the pathway from pyruvate to
glucose 6-phosphate are catalyzed by enzymes of the
glycolytic sequence and thus proceed by reversal of
steps employed in glycolysis. However, there are two
irreversible steps in the normal "downhill" glycolytic
pathway which cannot be utilized in the "uphill"
conversion of pyruvate to glucose 6-phosphate. In the
biosynthetic direction these steps are bypassed by
alternative reactions.
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
Reactions Unique to Gluconeogenesis
The first of these bypass steps is the phosphorylation of pyruvate to
phosphoenolpyruvate. The first step is catalyzed by pyruvate
carboxylase of mitochondria:

pyruvate + CO2 + ATP → oxaloacetate + ADP + P

The oxaloacetate formed in this mitochondrial reaction is then
reduced to malate at the expense of NADH by the mitochondrial
form of malate dehydrogenase:

oxaloacetate + NADH + H+ → malate + NAD+

The malate so formed may then leave the mitochondria and in the
cytosol the malate is then reoxidized by the cytoplasmic form of
NAD-linked malate dehydrogenase to form extramitochondrial
oxaloacetate:

malate + NAD+ → oxaloacetate + NADH + H+
In the last step of the bypass, oxaloacetate is acted upon by
phosphoenolpyruvate carboxykinase (GTP) to yield phosphoenolpyruvate
and CO2, a reaction in which GTP serves as the phosphate donor:

oxaloacetate + GTP → phosphoenolpyruvate + CO2 + GDP.
The second crucial point in gluconeogenesis in which a reaction of the
downhill glycolytic sequence is bypassed is conversion of fructose 1,6diphosphate into fructose 6-phosphate:

fructose 1,6-diphosphate + H2O → fructose 6-phosphate + P.

This reaction is catalized by the enzyme fructose diphosphatase.
In some animal tissues, particularly the liver, kidney, and
intestinal epithelium, glucose 6-phosphate may be
dephosphorylated to form free glucose; the liver is the
major site of formation of blood glucose. The hydrolytic
cleavage of glucose 6-phosphate does not occur by
reversal of the hexokinase reaction but is brought about
by glucose-6-phosphatase:
glucose 6-phosphate + H2O → glucose + P
Glucose-6-phosphatase is not present in muscles or in the
brain, which thus cannot donate free glucose to the blood.
THE PENTOSE PHOSPHATE PATHWAY
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
Diabetes mellitus


Diabetes mellitus is a disorder in which blood
sugar (glucose) levels are abnormally high because
the body does not produce enough insulin.Insulin a
hormone released from the pancreas, controls the
amount of sugar in the blood.The levels of sugar in
the blood vary normally throughout the day. They
rise after a meal and return to normal within about 2
hours after eating. Once the levels of sugar in the
blood return to normal
 Doctors

often use the full name diabetes
mellitus, rather than diabetes alone, to
distinguish this disorder from diabetes
insipidus, a relatively rare disease that does
not affect blood sugar.
Types of Diabetes mellitus
 Type

1: In type 1 diabetes ( insulindependent diabetes or juvenile-onset
diabetes), more than 90% of the insulinproducing cells of the pancreas are
permanently destroyed. The pancreas,
therefore, produces little or no insulin
Only about 10% of all people with diabetes
have type 1 disease. Most people who have
type 1 diabetes develop the disease before
age 30.
 Type

2: In type 2 diabetes ( non-insulindependent diabetes or adult-onset diabetes),
the pancreas continues to produce insulin,
sometimes even at higher-than-normal
levels. However, the body develops
resistance to the effects of insulin, so there is
not enough insulin
to meet the body's needs.


Type 2 diabetes may occur in children and
adolescents, but usually begins in people older than
30 and becomes progressively more common with
age. About 15% of people older than 70 have type 2
diabetes. Obesity is the chief risk factor for
developing type 2 diabetes, and 80 to 90% of
people with this disease are obese. Because obesity
causes insulin resistance, obese people need very
large amounts of insulin
to maintain normal blood sugar levels.



Symptoms
The two types of diabetes have very similar symptoms. The first
symptoms are related to the direct effects of high blood sugar
levels (hyperglycemia). When the blood sugar level rises above
160 to 180 mg/dL, sugar spills into the urine (glucoseuria).
When the level of sugar in the urine rises even higher, the
kidneys excrete additional water to dilute the large amount of
sugar. Because the kidneys produce excessive urine, a person
with diabetes urinates large volumes frequently (polyuria). The
excessive urination creates abnormal thirst (polydipsia).
Because excessive calories are lost in the urine, the person
loses weight. To compensate, the person often feels excessively
hungry. Other symptoms include blurred vision, drowsiness,
nausea, and decreased endurance during exercise.

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!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose

  • 2. DIGESTION OF CARBOHYDRATES Glycogen, starch and disaccharides (sucrose, lactose and maltose) are hydrolyzed to monosaccharide units in the gastrointestinal tract. The process of digestion starts in the mouth by the salivary enzyme α –amilase. The time for digestion in mouth is limited. Salivary α -amilase is inhibited in stomach due to the action of hydrochloric acid. Another α -amilase is produced in pancreas and is available in the intestine.
  • 3. α -amilase hydrolyzes the α -1-4-glycosidic bonds randomly to produce smaller subunits like maltose, dextrines and unbranched oligosaccharides. α -amilase
  • 4. The intestinal juice contains enzymes hydrolyzing disaccharides into monosaccharides (they are produced in the intestinal wall) Sucrase hydrolyses sucrose into glucose and fructose Glucose sucrase Fructose Sucrose
  • 5. Galactose lactase Glucose Lactase hydrolyses lactose into glucose and galactose Lactose Glucose maltase Maltase hydrolyses maltose into two glucose molecules Maltose Glucose
  • 6. ABSORPTION OF CARBOHYDRATES Only monosaccharides are absorbed The rate of absorption: galactose > glucose > fructose Glucose and galactose from the intestine into endothelial cells are absorbed by secondary active transport Na+ Protein Glucose Protein
  • 7. Carrier protein is specific for D-glucose or Dgalactose. L-forms are not transported. There are competition between glucose and galactose for the same carrier molecule; thus glucose can inhibit absorption of galactose. Fructose is absorbed from intestine into intestinal cells by facilitated diffusion. Absorption of glucose from intestinal cells into bloodstream is by facilitated diffusion.
  • 8. Transport of glucose from blood into cells of different organs is mainly by facilitated diffusion. The protein facilitating the glucose transport is called glucose transporter (GluT). GluT are of 5 types. GluT1 is seen in erythrocytes and endothelial cells; GluT2 is located mainly in hepatocytes membranes (it transport glucose into cells when blood sugar is high); GluT3 is located in neuronal cells (has higher affinity to glucose); GluT4 - in muscles and fat cells. GluT5 – in intestine and kidneys;
  • 9. The fate of glucose molecule in the cell Glucose Glycogenesis (synthesis of glycogen) is activated in well fed, resting state Glucose-6phosphate Gluconeoge nesis is activated if glucose is required Glycogen Glycogenolysis (degradation of glycogen) Pentose phosphate pathway supplies the NADPH for lipid synthesis and pentoses for nucleic acid synthesis Pyruvate Glycolysis is activated if energy is required Ribose, NADPH
  • 11. Regulation of Glycolysis The rate glycolysis is regulated to meet two major cellular needs: (1) the production of ATP, and (2) the provision of building blocks for synthetic reactions. There are three control sites in glycolysis - the reactions catalyzed by hexokinase, phosphofructokinase 1, and pyruvate kinase These reactions are irreversible. Their activities are regulated by the reversible binding of allosteric effectors by covalent modification by the regulation of transcription (change of the enzymes amounts). The time required for allosteric control, regulation by phosphorylation, and transcriptional control is typically in milliseconds, seconds, and hours, respectively.
  • 12. Inhibition 1) PFK-1 is inhibited by ATP and citrate 2) Pyruvate kinase is inhibited by ATP and alanine 3) Hexokinase is inhibited by excess glucose 6phosphate Regulation of Glycolysis Stimulation 1) AMP and fructose 2,6bisphosphate (F2,6BP) relieve the inhibition of PFK-1 by ATP 2) F1,6BP stimulate the activity of pyruvate kinase Alanine
  • 13. Gluconeogenesis - synthesis of "new" glucose from such precursors as pyruvate, lactate, certain amino acids, and intermediates of the tricarboxylic acid cycle. Most of the reaction steps in the pathway from pyruvate to glucose 6-phosphate are catalyzed by enzymes of the glycolytic sequence and thus proceed by reversal of steps employed in glycolysis. However, there are two irreversible steps in the normal "downhill" glycolytic pathway which cannot be utilized in the "uphill" conversion of pyruvate to glucose 6-phosphate. In the biosynthetic direction these steps are bypassed by alternative reactions.
  • 16. Reactions Unique to Gluconeogenesis
  • 17. The first of these bypass steps is the phosphorylation of pyruvate to phosphoenolpyruvate. The first step is catalyzed by pyruvate carboxylase of mitochondria: pyruvate + CO2 + ATP → oxaloacetate + ADP + P The oxaloacetate formed in this mitochondrial reaction is then reduced to malate at the expense of NADH by the mitochondrial form of malate dehydrogenase: oxaloacetate + NADH + H+ → malate + NAD+ The malate so formed may then leave the mitochondria and in the cytosol the malate is then reoxidized by the cytoplasmic form of NAD-linked malate dehydrogenase to form extramitochondrial oxaloacetate: malate + NAD+ → oxaloacetate + NADH + H+
  • 18. In the last step of the bypass, oxaloacetate is acted upon by phosphoenolpyruvate carboxykinase (GTP) to yield phosphoenolpyruvate and CO2, a reaction in which GTP serves as the phosphate donor: oxaloacetate + GTP → phosphoenolpyruvate + CO2 + GDP. The second crucial point in gluconeogenesis in which a reaction of the downhill glycolytic sequence is bypassed is conversion of fructose 1,6diphosphate into fructose 6-phosphate: fructose 1,6-diphosphate + H2O → fructose 6-phosphate + P. This reaction is catalized by the enzyme fructose diphosphatase.
  • 19. In some animal tissues, particularly the liver, kidney, and intestinal epithelium, glucose 6-phosphate may be dephosphorylated to form free glucose; the liver is the major site of formation of blood glucose. The hydrolytic cleavage of glucose 6-phosphate does not occur by reversal of the hexokinase reaction but is brought about by glucose-6-phosphatase: glucose 6-phosphate + H2O → glucose + P Glucose-6-phosphatase is not present in muscles or in the brain, which thus cannot donate free glucose to the blood.
  • 23. Diabetes mellitus  Diabetes mellitus is a disorder in which blood sugar (glucose) levels are abnormally high because the body does not produce enough insulin.Insulin a hormone released from the pancreas, controls the amount of sugar in the blood.The levels of sugar in the blood vary normally throughout the day. They rise after a meal and return to normal within about 2 hours after eating. Once the levels of sugar in the blood return to normal
  • 24.  Doctors often use the full name diabetes mellitus, rather than diabetes alone, to distinguish this disorder from diabetes insipidus, a relatively rare disease that does not affect blood sugar.
  • 25. Types of Diabetes mellitus  Type 1: In type 1 diabetes ( insulindependent diabetes or juvenile-onset diabetes), more than 90% of the insulinproducing cells of the pancreas are permanently destroyed. The pancreas, therefore, produces little or no insulin Only about 10% of all people with diabetes have type 1 disease. Most people who have type 1 diabetes develop the disease before age 30.
  • 26.  Type 2: In type 2 diabetes ( non-insulindependent diabetes or adult-onset diabetes), the pancreas continues to produce insulin, sometimes even at higher-than-normal levels. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body's needs.
  • 27.  Type 2 diabetes may occur in children and adolescents, but usually begins in people older than 30 and becomes progressively more common with age. About 15% of people older than 70 have type 2 diabetes. Obesity is the chief risk factor for developing type 2 diabetes, and 80 to 90% of people with this disease are obese. Because obesity causes insulin resistance, obese people need very large amounts of insulin to maintain normal blood sugar levels.
  • 28.   Symptoms The two types of diabetes have very similar symptoms. The first symptoms are related to the direct effects of high blood sugar levels (hyperglycemia). When the blood sugar level rises above 160 to 180 mg/dL, sugar spills into the urine (glucoseuria). When the level of sugar in the urine rises even higher, the kidneys excrete additional water to dilute the large amount of sugar. Because the kidneys produce excessive urine, a person with diabetes urinates large volumes frequently (polyuria). The excessive urination creates abnormal thirst (polydipsia). Because excessive calories are lost in the urine, the person loses weight. To compensate, the person often feels excessively hungry. Other symptoms include blurred vision, drowsiness, nausea, and decreased endurance during exercise.