CARBOHYDRATE

METABOLISM

By
Dr. Aisha Eid
METABOLISM OF FOODSTUFFS

Ptns, CHO, lipids

carbon compounds

CO2 & H2O

excretion
Dietary Carbohydrates:
 Monosaccharides:
glucose, fructose and galactose
in fruits and honey & obtained by hydrolysis of
oligo- & polysacs.
 Disaccharides:

sucrose, lactose, maltose (by hydrolysis of

starch).
 Polysaccharides:

starch (in potatoes, rice, corn and wheat)

Cellulose (in cell wall of plants)
not digested by humans due to absence of
cellulase
Digestion of Carbohydrates:
In the mouth:
Salivary amylase hydrolyzes starch into dextrin +maltose
In the stomach:
due to drop of pH salivary amylase acts for a very short time
In the small intestines:
Pancreatic and intestinal enzymes hydrolyze the oligo- and
polysaccharides as follows:
Pancreatic amylase
Starch maltose + isomaltose
Maltase
Maltose 2 glucose
Lactase
Lactose glucose + galactose

Sucrase
Sucrose glucose + fructose
Absorption of monosaccharides:
1. Simple diffusion:
Depending on the concn gradient of sugars
between intestinal lumen and mucosal cells.
e.g. Fructose and pentose
2. Facilitated transport:
It requires a transporter.
e.g. Glucose, Fructose and galactose
3. Active transport (cotransport):
It needs energy derived from the hydrolysis of
ATP.
glucose & galactose are actively transported
against
their concentration gradients by this mechanism.
Fate of absorbed
monosaccharides:
In the liver, fructose and galactose are converted
to glucose. Fate of glucose:

A. Uptake by different tissues (by facilitated diffusion)

B. Utilization by the tissues: in the form of:
1. Oxidation to produce energy:
- Major pathways (glycolysis & Krebs' cycle).
- Minor pathways (hexose monophosphate pathway & uronic acid
pathway)
2. Conversion to other substances:
Carbohydrates: ribose (RNA,DNA), galactose (in milk), fructose
(semen)
Lipids: Glycerol-3 P for formation of triacylglycerols.
Proteins: Non-essential amino acids which enter in formation of proteins.
C. Storage of excess glucose:
as glycogen in liver and muscles,
when these reserves are filled it is converted to TAG & deposited in
adipose tissue.
D. Excretion in urine
If blood glucose exceeds renal threshold (180 mg/dL), it will be excreted
in urine.
Glucose Oxidation
Extracting Energy from Glucose:
There are 3 major biochemical processes that
occur in
cells to progressively breakdown glucose with
the
release of various packets of energy:
Glycolysis (occurs in the cytoplasm and is only
moderately efficient).
Krebs' cycle (takes place in the matrix of the
mitochondria and results in a great release of
energy).
Electron transport chain.
GLUCOSE OXIDATION
 GLYCOLYSIS
Series of biochemical reactions by which
glucose is converted to:
-Pyruvate (in aerobic conditions)or
-Lactate (in anaerobic conditions).
Site: cytosol of every cell.
Physiologically it occurs in:
-muscles during exercise (lack of
oxygen)
-RBCs (no mitochondria).
Steps:

Phase one: 1 molecule of glucose (C6) is converted to 2

molecules of glyceraldehyde 3-phosphate (C3)
as follows:
ATP ATP
Glucose (C6) 2 Glyceraldehyde
3 P (C3)
Phase two: in this phase the 2 molecules of
glyceraldehyde 3-P are converted to 2 molecules of
pyruvate (aerobic)
or lactate (anaerobic):

4 ATP
2 Glyceraldehyde-3 P (C3) 2 Pyruvic Acid
(C3)

2 NADH + 2 H+

2 NAD+

2
Lactic Acid
Overall, glycolysis can thus be summarized
as follows:

Glucose 2 Pyruvic Acid + 2 net

ATP
+4 hydrogens (2 NADH2)

2 Lactic Acid + 2 net ATP

Regulation of
Glycolysis:
It can be noted that all reactions of
glycolysis
are reversible except those catalyzed by:
 Glucokinase (or hexokinase) (GK)

 Phosphofructokinase (PFK)

 Pyruvate kinase (PK)

Glycolysis is regulated by factors

which
control the activity of the key
enzymes
which catalyze the 3 irreversible
reactions.
Activity of these enzymes increase during
CHO feeding, and decreases during
starvation:

 Regulation according to
energy requirements of cell

 Regulation by hormones
Regulation according to
energy requirements of cell:

Each cell regulates glycolysis according to

the rate of utilization of ATP:
i) High levels of AMP
(indicating high ATP utilization):
+++ PFK (i.e. activates glycolysis).
ii)High levels of ATP
(indicating little utilization of ATP):
- - -PFK and PK (i.e. inhibits glycolysis).
Regulation by
hormones:
Postprandial hyperglycemia causes:
+++ of insulin
--- glucagon & adrenaline (anti-insulin
hormones)
i) Insulin:
+++ all pathways of glucose utilization.
+++ glycolysis by inducing synthesis, activation
of all the glycolytic key enzymes (GK, PFK, PK).
ii) Glucagon:
Inhibits glycolysis by acting as
repressor & inactivator of the glycolytic key
enzymes.
Importance of
Glycolysis:

1. Glycolysis provides mitochondria with pyruvic

a oxaloacetate which is the primer of the
Krebs' cycle.
2. Glycolysis provides dihydroxyacetone P
glycerol 3-P that is important for lipogenesis
(TAG synthesis)
3. Energy production:
Glycolysis liberates only a small part of energy
from glucose, however:
a. Important during severe muscular exercise,
where oxygen supply is often insufficient to
meet the demands of aerobic metabolism.
b. Provides all energy required by the R.B.Cs.
(due to lack of mitochondria).
Energy yield of
glycolysis:

In absence of oxygen:
2 ATP are consumed for conversion of
glucose to Fructose 1,6 P.
2 ATP are produced during conversion of
glyceraldehydes 3-P to pyruvate.
Since 1 glucose molecule gives 2
molecules of
G 3-P, then total number of ATP produced
is 4.
net gain of ATP in absence of oxygen
is: 4-2=2 ATP.
Energy yield of
glycolysis:

In presence of oxygen:
2 ATP are produced directly
(as in absence of oxygen),
6 ATP are produced indirectly:
from oxidation of 2 NADH2 through
ETC
net gain of ATP in presence of
oxygen is: 2+6= 8 ATP.
 Reactions
These link glycolysis to the Krebs
Cycle

Alternate Fates of Pyruvate

A. Oxidative Decarboxylation B. Carboxylation

forms Acetyl CoA forms Oxaloacetate

Oxidative decarboxylation of
pyruvate:

Puruvate dehydrodenase complex irreversibly

converts pyruvate into acetyl CoA:
Pyruvic acid (3C)+NAD++Coenzyme A
Acetyl CoA(2C)+CO2+ NADH+ H+

Acetyl CoA can also be produced by breakdown of:

 lipids or
 certain (ketogenic) amino acids.

-NAD+ is converted into NADH+H+.

Those hydrogens go through oxidative phosphorylation
and produce 3 more ATP.
 Oxidative decarboxylation of
pyruvate:

NADH+H NADH+H
2 CoA
Carboxylation of pyruvate to oxaloacetate:

Pyruvate carboxylase converts

pyruvate to oxaloacetate.

Pyruvic acid (3C) + CO2 + ATP

Oxaloacetic acid (4C) + ADP + Pi

Finally, comes the Krebs'
Cycle
Krebs' Cycle
(Citric Acid Cycle)
(Tricarboxylic Acid Cycle)
"TCA"
Site: mitochondria of every
cell
Series of biochemical reactions that
are
responsible for complete oxidation
of
CHO, fats and Ptns to form :
CO2 + H2O + Energy
Steps:

acetyl-CoA + oxaloacetate
citrate
 +H+
Acetyl CoA
×2
oxaloacetate

+H+
+H+

+H+
During this process the following is
produced:

 3x2=6 NADH+H+
 1x2=2 FADH2
 1x2=2 ATP
 2x2=4 CO2
Each glucose molecule that goes through Krebs cycle
+ the preparatory conversion to Acetyl CoA gives:

 8 NADH
 2 FADH2
 2 ATP
 6 CO2

N.B.: glycolysis produced 2 ATP + 2

NADH, so there is a net production of:
 4 ATP
 10 NADH
 Energy yield of Krebs' cycle:
Glucose 2 puruvate
2 NADH 6 ATP

2 oxaloacetate

6 ATP

6 ATP

4 ATP

6 ATP
Energy yield of Krebs'
cycle:

1 mole of acetyl CoA through Krebs' cycle produces 12

ATPs:
1 ATP (substrate level oxidative phosphorylation).
1 FADH2 → 2 ATP (respiratory chain oxidative
phosphorylation).
3 NADH+H+→9 ATP(respiratory chain oxidative
phosphorylation)
oxidative decarboxylation of pyruvate gives 1 NADH+H+
→ 3 ATP

Thus net ATP gain is: 12 + 3 = 15 ATP

Since 1 glucose molecule by undergoing glycolysis gives 2

pyruvate
Thus 1 glucose molecule yields 15 × 2 = 30 ATP.
Thus complete oxidation of
glucose (in presence of oxygen)
gives:

 Glycolysis: 8 ATP
 Total ATP yield = 30+8 = 38
ATP.
 2 Acetyl CoA

Reduced coenzymes (e-)

10 NADH + 2 FADH2

38
Regulation of Krebs'
cycle:
1. Regulation according to energy status of the cell:
+++NADH/NAD and ATP/ADP (thus no need for further
energy production) inhibit the cycle, and vice versa.

Krebs' cycle is only aerobic, since under anaerobic

conditions the respiratory chain is inhibited leading to
increased NADH/NAD ratio which inhibits the cycle.

2. Regulation according to availability of substrate:

+++ acetyl CoA and oxaloacetate +++
cycle.
+++ intermediate products of cycle (citrate & succinyl Co
A)
---feedback inhibition of the
cycle.
Importance of Krebs'
cycle:

1. Energy production: 1 acetyl CoA

yields 12 ATP.
2. It is the final common metabolic
pathway for complete oxidation of
acetyl CoA which results from the
partial oxidation of CHO, fats and
proteins (amino acids).
3. Interconversion of carbohydrates,
fats and proteins (gluconeogenesis,
lipogenesis, and formation of non-
Minor Pathways of Glucose
Oxidation:

 Hexose monophosphate pathway

(HMP shunt).

 Uronic acid pathway.

Hexose Monophosphate Pathway
(HMP shunt)
Pentose Phosphate Pathway
Pentose Shunt

Site: cytoplasm of cells e.g. liver,

adipose tissue,
adrenals, gonads, RBCs and retina.
Steps:
Glucose-6-P dehydrogenase

G-6-P R-5-
P
NADP+ CO2
NADPH+H+
 Importance of HMP shunt

R-5-P Importance
NADPH
for RBCs
Importance of HMP
shunt:

2. It is the main source of NADPH:

coenzyme for reductases, hydroxylases and NADPH
oxidase
which catalyze several important biochemical reactions,
e.g.:
i) Fatty acid synthesis lipogenesis:
HMP is active in liver, adipose tissue & lactating memory
gland.

ii) Steroid synthesis:

HMP is active in adrenal cortex, testis, ovaries and
placenta.

iii) Important for vision:

NADPH
retinal retinol (important for
3) Importance of HMP in RBCs:
-H2O2 (powerful oxidant) produces damage of:
 cellular DNA,

 Ptns

 phospholipids of cell membrane.

-RBCs are liable to oxidative damage by H2O2

due to
their role in O2 transport.
-H2O2 produces oxidative damage in the form
of:
 Oxidation of Fe2+ to Fe3+ (metHb can’t carry
O2)
 Lipid peroxidation which increases cell
membrane fragility.
HMP in RBCs produces NADPH,
which
provides reduced GSH to remove
H2O2
protects cell from oxidative
damage

GSH reductase & GSH peroxidase

remove
 glutathione peroxidase

H2O2 2
H2O

2 G-SH G-S-S-G

NADP+
NADPH, H+
glutathione reductase
Favism:

 Genetic condition due to deficiency of

(G6PD),
 There is impaired HMP in the RBCs,
and RBC capacity to protect itself from
oxidative damage is markedly
decreased (--- NADPH)
 Eating Fava beans (which contain
oxidizing agents), or administration of
certain drugs (e.g. aspirin, sulfonamides
or primaquin) which stimulate
production of H2O2, produce lysis of
the fragile red cells.
Regulation of HMP:

 NADPH produces feedback (-)

G6PD.
 Insulin produces (+) G6PD.

N.B:
Insulin produced in response to
hyperglycemia
increase glucose oxidation by HMP
( acts as inducer of synthesis of
Uronic Acid Pathway
This pathway converts glucose to glucuronic
acid.
Site: cytosol of liver cells.
Importance of Uronic Acid Pathway:
enters in different biological reactions, e.g.:
1. Synthesis of glycosaminoglycans (GAGs).
2. Conjugation with certain compounds
rendering them more water soluble, thus
helping in their excretion, e.g.:
 Steroid hormones.

 Bilirubin, which is excreted in bile in the form

of bilirubin diglucuronide.
Glycogen Metabolism

Glycogenesis
Glycogenolysis
Gluconeogenesis
Glycogen Metabolism
1. Liver glycogen:
-Forms 8-10% of the wet weight of the liver.
-Maintains blood glucose (especially between
meals).
-Liver glycogen is depleted after 12-18 hours
fasting.
2. Muscle glycogen:
-Forms 2% of the wet weight of muscle.
-Supplies glucose within muscles during
contraction.
-Muscle glycogen is only depleted after
prolonged exercise.
Glycogen metabolism includes:

 Glycogenesis: synthesis of
glycogen from glucose.
 Glycogenolysis: breakdown of
glycogen to glucose-1-phosphate.
 Gluconeogenesis: synthesis of
glucose or glycogen from non-CHO
precursors.
Glycogenesis &
Glycogenolysis
Site: cytoplasm of liver and muscles.
The key enzyme of glycogenesis is glycogen synthase.
The key enzyme of glycogenolysis is glycogen
phosphorylase.

In muscles: G-6-P is oxidized by glycolysis to provide

energy
during muscle contraction.

In liver:
G-6-Phosphatase
G-6-P Glucose + Pi Blood
G

N.B: Muscles cannot supply blood glucose due to

their lack of the enzyme G-6-phosphatase.
 hexokinase

Glycogen
Glycogenolysis Phoshorylase
Glycogenesis

Glycogen Synthase
+ Branching Enzyme
Mechanism of glycogen
synthesis (glycogenesis):
A. Synthesis of UDP-glucose.
B. Synthesis of a primer to initiate glycogen
synthesis:
A fragment of glycogen (present in cells whose glycogen
stores are not totally depleted) can serve as a primer.

C. Elongation of glycogen chains by glycogen

synthase:
-Glycogen synthase uses UDP-glucose to add glucose to
glycogen primer (1,4 link), and the process is repeated.

D. Formation of branches in glycogen:

-When the chain becomes about 6-11 glucose units long,
the branching enzyme transfers 5-8 glucosyl residues
of α-1,4-chain to a neighboring chain attaching it by α-
1,6- glucosidic linkage
Mechanism of glycogen
degradation
(glycogenolysis)
A. Shortening of chains:
Glycogen phosphorylase acts on the 1,4-glucosidic
linkage of glycogen G-1-P
residues
until each branch contains only 4 glucose units.
B. Removal of branches:
-The transferring enzyme transfers 3 glucose units from
one end
of the short branch to the end of another branch.
-The debranching enzyme cleaves 1,6-glucosidic linkage
releasing free G , and the process is repeated.
C. Conversion of G-1-P to G-6-P:
This is done by phosphoglucomutase enzyme.
Regulation of Glycogen
Synthesis vs.
Degradation
Glycogen synthase & glycogen phosphorylase: key
enzymes

Regulation of these enzymes occurs via:

 Covalent modification (phosphorylation &
dephosphn.)
 Allosterics

 Hormones

-Reciprocal control of the two pathways is

hormonally mediated through phosphorylation
and dephosphorylation of synthase and
phosphorylase.

-Phosphorylation of enzymes :
turns synthesis off (--- glycogenesis), and
turns degradation on (+++ glycogenolysis).
Covalent modification :
Phosphorylation/dephosphorylat
ion
I. Glycogen synthase is present in two forms:
a-form: it is the active form and it is dephosphorylated.
b-form: it is the inactive form and it is phosphorylated.

-Conversion of a- to b-form by protein kinase: ++ by c-

AMP
-Conversion of b- to a-form by protein phosphatase.

II. Glycogen phosphorylase is present in two forms:

a-form: it is the active form and it is phosphorylated.
b-form: it is the inactive form and it is dephosphorylated.

-Conversion of a- to b-form by the enzyme protein

phosphatase.
-Conversion of b- to a-form by phosphorylase kinase:+by
c-AMP
Allosteric regulation:

Conformational changes in the enzyme ptns affecting activity and

regulation:
 Glucose-6-phosphate
++ synthase (+) glycogenesis (excess
substrate).
- - phosphorylase (-) glycogenolysis & (+)
glycogenesis.

 ATP
+ + synthase (+) glycogenesis
- - phosphorylase (-) glycogenolysis
.

 Ca+2
++ phosphorylase kinase (+) glycogen phosphorylase
glycogenolysis
-Muscle contraction ---> Ca+2 release (+) phosphorylase
glycogenolysis
(+) glucose ATP generation for ensuing cycles of muscle
contraction. 
Hormonal regulation
Insulin:
++ phosphodiesterase - cAMP - protein
kinase
++ protein phosphatase
A. stimulates glycogenesis:
b- a-form of glycogen synthase (activation)
activation of glycogenesis in both liver and muscle.

B. inhibits glycogenolysis:
a- b-form of glycogen phosphorylase
(inactivation)
This leads to inactivation of glycogen phosphorylase
(conversion of active to the inactive form)
decrease glycogenolysis in both liver and muscle.
 Insulin

+++Glycogenesis ----Glycogenolysis
B. Glucagon (in liver) and
epinephrine (in liver and muscles):

Both hormones produce activation of adenyl cyclase

thus
increasing cAMP
This produces activation protein kinase.This
converts:
1. Active a- to inactive b-form of glycogen synthase
(phosphorylated), thus inhibiting synthase.
Accordingly glucagon & epinephrine ---
glycogenesis.

2.Inactive b- to active a-form of glycogen

phosphorylase,
thus activating glycogen phosphorylase.
Accordingly glucagon & epinephrine
+++glycogenolysis.
C. Growth hormone and
glucocorticoids:

+++ gluconeogenesis +++

G-6-P
G-6-P allosterically +glycogen
synthase-b

++glycogenesis.
Thus growth hormone &
glucocorticoids
Regulation according to
nutritional status:
A. In the well fed state:
Glycogen synthase is allosterically (+) by G6P
(which is present in high concentrations).
Glycogen phosphorylase is (-) by G6P & ATP,
i.e.
(-)glycogenolysis & (+)glycogenesis stores bl
glucose

B. During starvation:
There are decreased levels of G6P & ATP, thus
(-)glycogenesis & (+)glycogenolysis to supply
blood glucose.
Muscle glycogen and
blood glucose

Muscle glycogen can be converted

to
Bl glucose via indirect pathways:
Cori's cycle:
during muscle exercise
Glucose- alanine cycle:
during starvation
Cori's cycle:

Glycogen

gluconeogenesis glycolysis
Glucose- alanine cycle:

Glycogen

gluconeogenesis

transamination
Glycogen storage
diseases:

Inherited deficiencies of specific enzymes

of
glycogen metabolism.
Von Gierke's disease (most common)
Cause: deficiency of G-6-phosphatase.
It is characterized by:
-enlargement of liver and kidneys
-hypoglycemia
-hyperlipemia
-hypercholestorelemia.
Gluconeogenesis
Gluconeogenesis
Synthesis of glucose from non-
carbohydrate
precursors.
These precursors are metabolic
intermediates.
Importance:
Supply blood glucose in case of CHO
deficiency
>18 hrs. (fasting, starvation and low CHO
diet).
Site:
Cytosol of liver cells
Steps:
By reversal of glycolysis.
3 glycolytic key enzymes are
reversed by
4 key enzymes of gluconeogenesis
as follows:
Glucogenic Precursors:

They give directly or indirectly pyruvate,

oxaloacetate or any intermediates of
glycolysis or Krebs' cycle. They include:
1. Lactate:
It is released by R.B.Cs. and by skeletal
muscles during exercise, then
transferred to the liver to form pyruvate
then glucose.
2. Glycerol:
It is produced from digestion of fats and
from lipolysis.
3. Glucogenic amino acids:
Ptns are the main sources of blood glucose especially after
18 hrs
due to depletion of liver glycogen.
-Some amino acids by deamination directly form pyruvic
acid or oxaloacetic.
-Others may give intermediates of Krebs' cycle which go
through the cycle eventually yielding oxaloacetic acid.

4. Propionyl CoA:
Many amino acids may give propionyl CoA through their
catabolism. Also the last 3 carbons of odd chain fatty
acids form propionyl CoA and thus give glucose. This is
uncommon in humans.
Regulation of
gluconeogenesis:

Gluconeogenic regulatory key enzymes are those which

reverse the glycolytic key enzymes.
Glycolysis and gluconeogenesis are reciprocally controlled:
Insulin:
(secreted after carbohydrate meal)
--- gluconeogenic key enzymes (at the same time it acts as
inducer of glycolytic key enzymes)
decrease bl. Glucose.
Anti-insulin hormones (glucagon, epinephrine,
glucocorticoids & growth hormone):
(secreted during fasting, stress or severe muscular
exercise)
increased blood glucose.
+++ gluconeogenic key enzymes, thus increasing
gluconeogenesis
Blood Glucose
Concentration of bloog glucose:
fasting blood glucose (8-12 hrs. after the last
meal) is 70-110 mg/dL.
It increases after meals but returns to fasting
level within 2 hrs.
Sources of blood glucose:
Dietary carbohydrates.
Glycogenolysis (during fasting for less than 18
hrs.).
Gluconeogenesis (during fasting for more than
18 hrs.).
Regulation of Blood
Glucose:

Four factors are important for

regulating blood glucose level:
I. Gastrointestinal tract.
II. Liver
III. Kidney.
IV.Hormones.
I. Gastrointestinal
tract:

1. It controls the rate of glucose

absorption. The maximum rate of
glucose absorption is
1 gm/kg body weight/ hour.
An average person weighing 70 gm will
absorb 70 gm glucose/ hour.
2. Glucose given orally stimulates more
insulin than intravenous glucose. This
may be due to secretion of glucagon-
like substance by intestines. This
stimulates B-cells of pancreas to secrete
more insulin. This is called
anticipatory action.
II. Liver:
The liver is the main blood glucostat
Maintains blood glucose level within normal as follows:
A. If blood glucose level increases, the liver controls
this elevation and decreases it through:
1. Oxidation of glucose via major and minor pathways.
2. Glycogenesis.
3. Lipogenesis.
B. If blood glucose level decreases, the liver
controls this drop and increases it through:
1. Glycogenolysis.
2. Gluconeogenesis.
III. Kidney:
All glucose in blood is filtered through the
kidneys, it then completely returns to
the blood by tubular reabsorption.
If blood glucose exceeds a certain limit
(called renal threshold), it will pass in
urine causing glucosuria.
Renal threshold: it is the maximum rate
of reabsorption of glucose by the renal
tubules. Normally the renal threshold
for glucose is 180 mg/100mL.
IV. Hormones:

A. Insulin (the only hypoglycemic hormone):

Action of insulin:
Insulin decreases bl glucose level by:
1. +++ oxidation of glucose
2. +++ glycogenesis
3. --- glycogenolysis
4. --- glyconeogenesis
5. +++ lipogenesis
B. Anti-Insulin Hormones:
(hyperglycemic
hormones):
1. Growth Hormone:
It elevates the blood glucose level by stimulating
gluconeogenesis.
2. Thyroxine:
It elevates the blood glucose level by:
Increasing the rate of absorption of glucose from
intestines.
Stimulating gluconeogenesis and glycogenolysis.
Inhibiting glycogenesis.
3. Epinephrine (adrenaline):
It increases the blood glucose level by increasing
glycogenolysis in both liver and muscles.
4. Glucagon:
It increases the blood glucose level by increasing
glycogenolysis in liver only.
Mechanism of Blood
Glucose Regulation
(Glucose Homeostasis)
The blood glucose level is regulated by the balance
between the action of insulin and anti-insulin hormones
(hyperglycemic hormones).
After a carbohydrate meal:
Bl glucose increases, stimulating the secretion of insulin
which tends to decrease the blood glucose level by its
various actions.
During fasting:
Bl glucose is low; this stimulates the secretion of the anti-
insulin hormones (hyperglycemic hormones) which by
their various mechanisms lead to increasing the blood
glucose level.

The net result is a condition of glucose equilibrium,

or what we call the homeostatic mechanism.
Abnormalities of Blood
Glucose Level
These may be in the form of:
 Hyperglycemia

 Hypoglycemia

Hyperglycemia: (Diabetes
Mellitus):
It is due to:
decreased insulin secretion and/or
hypersecretion of anti-insulin
Hypoglycemia:

-It is the decrease in blood glucose level below the fasting

level.
At a level of 50mg/100 mL convulsions occur
At a level of 30 mg/100 mL coma and death result.
-Hypoglycemia is more dangerous than
hyperglycemia because glucose is the only fuel to
the brain.
Causes:
i. Excess insulin:
a) Overdose of insulin.
b) Tumor of B-cells of pancreas (insulinoma).
ii. Hyposecretion of anti-insulin hormones:
(hypo-functions of the pituitary gland, adrenals & thyroid
gland). insulin acts unopposed causing lowering of
blood glucose
iii. Liver disease:
hypoglycemia is due to decreased glycogen stores and
Glucosuria

Presence of detectable amounts of glucose in urine (>30

mg/dL).
Causes:
A. Hyperglycemic glocusuria:
Bl glucose exceeds the renal threshold (180mg/dL). It is
caused by:
1. Diabetes mellitus.
2. Emotional or stress glucosuria (epinephrine glucosuria)
3. Alimentary glucosuria;It is due to increased rate of
glucose absorption as in cases of gastrectomy or
gastrojejunostomy.
B. Normoglycemic or renal glucosuria:
1. Congenital renal glucosuria (diabetes innocens):
due to congenital defect in renal tubular reabsorption of
glucose.
2. Acquired renal disease (e.g. nephritis).