CARBOHYDRATE METABOLISM

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
1- Inherited lactase deficiency (Lactose Intolerance)
It starts early with lactation. The infant complains of abdominal distension
and colics. This is due to the gases produced from fermentation of
unabsorbed sugars by intestinal bacteria.
2- Inherited sucrase deficiency
It is similar to lactase deficiency, as it produces abdominal distension
and colic. It starts later after addition of cane sugar (sucrose) to the
infant's diet.

Absorption of monosaccharides:
1. Facilitated transport:
It requires a transporter.
e.g. Glucose, Fructose and galactose
2. Active transport (cotransport):
It needs energy derived from the hydrolysis of ATP.
glucose & galactose are actively transported against
their concentration gradients by this mechanism.

Glucose Uptake by Tissues (Glucose

Transporters):
GLUT-2 in liver, kidney and B-cells of pancreatic islets:
GLUT-2 is for rapid uptake and release of glucose, which makes
intracellular glucose concentration reflects the blood glucose level.
 This is important for regulation of blood glucose as liver and
kidneys are the main glucose homeostatic organs.
Also, pancreatic β-cells are responsible for secretion of insulin, which is
responsible for lowering blood glucose in cases of hyperglycemia.
GLUT-4 in heart, skeletal muscles and adipose tissue
In these tissues insulin produces translocation of the glucose transporters
to the outer cell membrane surface, therefore increases the number
of transporters and stimulates glucose uptake by these tissues when
the blood glucose is increased. In absence of insulin, the transporters
are endocytosed to form intracellular pool and glucose uptake is
reduced.
This mechanism prevents these organs from consuming a large
amount of
glucose (when blood glucose is normal or lowered), which prevents
the drop of its level, and keep it for the brain.

Fate of absorbed monosaccharides:

A. Uptake by different tissues (by facilitated diffusion)
B. Utilization by the tissues: in the form of:
A. Oxidation :
- Major pathway (glycolysis) mainly for energy
production
-Minor pathways (hexose monophosphate pathway &
uronic acid pathway)
B. 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.

GLYCOLYSIS:
Series of biochemical reactions by which
glucose is converted to:
-2 molecules of Pyruvate (in aerobic conditions)or
-2 molecules of 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

Regulation of Glycolysis:
It can be noted that all reactions of glycolysis
are reversible except those catalyzed by:
◼ Glucokinase (or hexokinase) (GK)
◼ Phosphofructokinase-1 (PFK-1)
◼ 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):
(i.e. activates glycolysis).
ii)High levels of ATP
(indicating little utilization of ATP):
(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
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 alone 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 [Link]. (due to lack of
mitochondria).

Oxidative decarboxylation of
pyruvate:
Under aerobic conditions :
Puruvate dehydrodenase
irreversibly converts 2 pyruvate into 2 acetyl CoA ( in the mitochondria) + 2 NADH
.
×2
Thus complete oxidation of glucose (in
presence of oxygen) gives:
1- Under aerobic condition
◼ Glycolysis alone under aerobic conditions = 7 ATP
Complete oxidation ATP yield = 25+7 = 32 ATP.
2- Under anaerobic condition
◼ This occurs in muscles during severe exercise and in red cells
(due to absence of mitochondria).
◼ Under anaerobic condition NADH is not oxidized by the
ETC.
The net gain of ATP under anaerobic condition is 2 ATP only

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

Importance
R-5-P NADPH
for RBCs

Importance of HMP shunt:

1- It provides ribose 5-phosphate
which is required for synthesis of nucleotides and nucleic acids.
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 mamary gland.
ii) Steroid synthesis:
HMP is active in adrenal cortex, testis, ovaries and placenta.
iii) Important for vision:
NADPH
retinal retinol (important for vision)
Thus HMP is active in the eye.
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:
2+ 3+
◼ Oxidation of Fe to Fe (metHb can’t carry O2)
◼ Lipid peroxidation which increases cell membrane
fragility.
RBC lysis + anemia & jaundice

HMP in RBCs produces NADPH, which

provides reduced GSH to remove H2O2
protects cell from oxidative damage
GSH reductase & GSH peroxidase remove
H O produced by biochemical reactions:
2 2

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 G6PD).

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

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-6-
phosphate
Glycogenolysis is responsible for maintainance of blood
glucose during fastig for less rhan 18 hrs.

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

Muscles cannot supply blood glucose due to their lack of

the enzyme G-6-phosphatase.

A-Insulin:
A. stimulates glycogenesis:
activation of glycogen synthase
activation of glycogenesis in both liver and muscle.
B. inhibits glycogenolysis:
inactivation of glycogen phosphorylase

decrease glycogenolysis in both liver and muscle.

B. Glucagon (in liver) and

epinephrine (in liver and muscles):
glucagon & epinephrine --- glycogenesis.

glucagon & epinephrine +++glycogenolysis.

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:
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
and to a lesser extent in kidneys.

Steps:
By reversal of glycolysis.

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 [Link]. 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.

Regulation of gluconeogenesis:
Gluconeogenic regulatory key enzymes are those which
reverse the glycolytic key enzymes They are :
1. Pyrunate carboxylase (PC)
2. Phopsphoenol pyruvate carboxy kinase (PEPCK)
3. Fructose 1,6 bisphosphatase
4. Glucose -6-phosphatase
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)
+++ gluconeogenic key enzymes, thus increasing
gluconeogenesis increased blood glucose.

Blood Glucose:
Concentration of bloog glucose:
fasting blood glucose (8-12 hrs. after the last meal) is 70- less
than 100 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.
[Link].
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 Kg 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. Increase uptake into skeletal ms. and adipose tissues (GLUT-4)
2. +++ oxidation of glucose
3. +++ glycogenesis
4. +++ lipogenesis
5. --- glycogenolysis
6. --- gluconeogenesis

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 hormones.

DIABETES MELLITUS (DM)

Is a disease characterized by high blood glucose level
(hyperglycemia) and
decreased glucose tolerance.
The main symptoms are:
◼ polyphagia, polyuria, polydepsia and rapid loss of
weight.
◼ Hyperglycemia may be accompanied with glucosuria (if
blood glucose exceeds 180 mg/dL).
Diabetes mellitus is due to:
◼ decreased insulin secretion or action (primary types)
or increased secretion of anti-insulin hormones (secondary
types)
◼ e.g. increased secretion of epinephrine, thyroid
hormones, corticoids and growth hormone
Type I (autoimmune destruction of b cells)
Type II ( usually due to insulin resistance)
◼ Changes occur due to DM are mainly due to:
decreased insulin action (defects in insulin
secretion or receptors or hypersecretion of anti-
insulin hormones).
 ◼ Therefore there is a decrease in the insulin / anti-
insulin ratio, which produces the following changes
(reversal of insulin action).
I- Changes in carbohydrate metabolism
II- Changes in lipid metabolism
III- Changes in protein metabolism
IV- Other changes
V- Vascular complication
VI- Diabetic cataract
VII- Diabetic retinopathy, nephropathy and neuropathy

I- Changes in carbohydrate metabolism

◼ Decreased glucose uptake and oxidation by tissues,

which produce decrease in ATP production especially in
muscles leading to muscle weakness.
◼ Decreased glucose utilization (glycogenesis and
lipogenesis).

◼ Increased glucose formation :

◼ (glycogenolysis+
gluconeogenesis)

The net result is hyperglycemia.

-Glucosuria occurs when blood glucose level exceeds 180
mg/dL (renal threshold).

II- Changes in lipid metabolism

 ◼ - Decreased lipogenesis and increased lipolysis in
adipose tissues produce loss of weight and increase
the release of FFA.
◼ - Fatty liver due to over mobilization of depot fat.
◼ - Hypercholesterolemia and
hypertriacylglycerolemia (hyperlipidemia)
◼ - Increased oxidation of FFA increases ketogenesis in
liver which may lead to ketosis (ketonemia and
ketonuria) in sever cases of DM (diabetic ketosis )
and acidosis which may be fatal.

III- Changes in protein metabolism

◼ Increased protein catabolism and decreased protein

synthesis (negative nitrogen balance)
◼ Decreased protein synthesis leads to increased
sensitivity to infection and delayed healing of
wounds .

IV- Other changes

◼ Glucosuria produces polyurea, dehydration and
polydepsia (excessive water drinking).
◼ Polyphagia due to decreased glucose utilization by
brain centers.
◼ Polyurea leads to loss of electrolytes (sodium and
potassium).
◼ Proteinuria in case of kidney damage and
Microalbuminuria
V- Vascular complication

◼ These include : atherosclerosis, hypertension, kidney

failure, myocardial infarction, blindness and neuropathy.
◼ Most of these complications are due to:
◼ damage of the vascular system.
◼ most of this damage is initiated by hyperglycemia.
◼ High blood glucose levels promote
glycosylation of protein molecules.
Glycosylated proteins produce complex
aggregates (Advanced glycation end
products) (AGE) with cross linkages that cause
extensive damage to the cardiovascular system and
promote atherosclerosis, which decrease the
efficiency of vascular system.
◼ Hypercholesterolemia and

hyperlipoproteinemia add another risk

factor for the development of atherosclerosis
in diabetic subjects.

VI- Diabetic cataract:

◼ It is due to accumulation of sorbitol, which produces

osmotic damage for the lens.
VII- Diabetic retinopathy, nephropathy and neuropathy:
◼ These complications are due to both :
 ◼ vascular damage and sorbitol accumulation.

Tests For Diabetes

◼ I- Measurement of blood glucose (plasma glucose)
◼ II- Measurement of glycated – Hb (HbA1c)

I- Measurement of blood glucose

(plasma glucose):
This is usually done to diagnose DM and to
assess treatment efficiency.

◼ 1- Fasting and two hours

postprandial (2PP) plasma glucose
levels (two hours after meal or oral
glucose).
◼ Normal fasting level is 70 - 100 mg/dL

(diabetics  126 mg/dL).

◼ Normal 2h PP level is 70 – 120 mg/dL

(diabetics  200 mg/dL)

II- Oral Glucose Tolerance Test

(OGTT).
 ◼ OGTT is done to :measure the ability of the
body to utilize glucose.
◼ How to perform the test
◼ After 8 - 12 hours fasting (usually overnight
fasting),the subject is given 75 g glucose
dissolved in 250 mL of water orally.
◼ Blood samples and urine samples are taken
from patient at fast and every half-hour after
the glucose meal for 2 to 3 hours.
◼ Blood samples are analysed for plasma
glucose levels.
◼ Urine samples are examined for the presence
of glucose and ketone bodies (acetone).

Normal OGTT:
◼ Fasting plasma glucose level ranges form 70–100
mg/dL
◼ it reaches a maximum of 120–170 mg/dL at one
hour,
◼ then declines to 70 – 120 mg/dL at two hours.
◼ All urine samples are free from glucose and acetone
.
Analysis of normal curve :
❑ The rise of blood glucose during OGTT is due to

absorption of glucose, which exceeds the rate of glucose

utilization stimulated by insulin.
❑ As the blood glucose level rises, the insulin level in
plasma increases, which stimulates more and more of
 glucose utilization, till the blood glucose returns to the
fasting level again.
❑ Sometimes, slight drop in blood glucose (insulin notch
or reactive hypoglycemia) occurs after return to
fasting. This transient drop is due to over production of
insulin and it is corrected by anti-insulin.

Diabetic OGTT:
◼ In case of diabetics, the fasting plasma glucose and peak
levels are higher than normal, the return to fasting
level takes longer time.
◼ The patient is considered diabetic if he has a
◼ fasting level  126 mg/dL or two levels  200
mg/dL during the tolerance test.
Glucose is present in urine when it exceeds 180 mg/dL and
acetone is detected in urine in severe cases (diabetic ketosis).

Impaired Glucose Tolerance:

◼ In this case the blood glucose levels are higher than
normal but less than DM.
 ◼ Subjects having impaired OGTT are liable to develop
DM later on and considered as pre- diabetics.

II- Measurement of glycated – Hb

(HbA1c):
◼ The hemoglobin A1c test, also called HbA1c, glycated
hemoglobin test, or glycohemoglobin,
importance
◼ shows how well diabetes is being controlled
◼ Hemoglobin A1c provides an average of the blood
sugar control over the past 2 to 3 months .
◼ When diabetes is not controlled (meaning that blood
sugar is too high), sugar builds up in the blood and
combines with hemoglobin, becoming "glycated." If
 glucose levels have been high over recent weeks, Hb A1c
test will be higher.
range
◼ The normal range for the Hb A1c is between 4% and
5.6%.
◼ Hemoglobin A1c levels between 5.7% and 6.4%
indicate increased risk of diabetes, and
◼ levels of 6.5% or higher indicate diabetes.
goal
◼ the goal for people with diabetes is: a hemoglobin
A1c less than 7%. The higher the hemoglobin A1c, the
higher the risks of developing complications related to
diabetes.

Diabetic Coma:
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- Fasting Hypoglycemia
1- Excess insulin:
a) Overdose of insulin.
b) Tumor of B-cells of pancreas (insulinoma).
2 Hyposecretion of anti-insulin hormones:
(hypo-functions of the pituitary gland, adrenals & thyroid gland).
insulin acts unopposed causing lowering of blood glucose
3-Liver disease:
hypoglycemia is due to decreased glycogen stores and
impaired gluconeogenesis.
4- Chronic renal diseases
In this case, hypoglycemia is due to impaired gluconeogenesis.
5- Hereditary metabolic disorders
Von Gierk’s disease due to deficiency of glucose 6-phosphatase
II- Postprandial Hypoglycemia
It is the temporary drop of blood glucose that occurs about 2-5
hours after a carbohydrate meal. Its causes include the
following:
1- Alimentary postprandial hypoglycemia
This occurs in cases of gastrectomy due to rapid absorption of
glucose
produces rapid rise of blood glucose and excessive secretion of
insulin, which is followed by hypoglycemia.
2- Reactive hypoglycemia
Normally, the rise of blood glucose after a carbohydrate meal
produces stimulation of insulin secretion. The latter produces
drop in blood glucose to the fasting [Link], the
blood glucose drops below the fasting level, which is known
as
reactive hypoglycemia. This reactive hypoglycemia usually takes a
short time, if prolonged it indicates either exaggerated insulin
response or decreased activity of antiinsulin hormones.

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).
3. Pregnancy glucosuria:
It appears during pregnancy and disappears later on after labour.