Carbohydrates (CHO)

JEANNIE LIMAYO, RMT MPH DTA

BCM 314

Carbohydrates
Are hydrates of aldehyde or ketone derivatives
based on the location of the CO functional grp.
Monosaccharide, disaccharides,
oligosaccharides, polysaccharides- CHOs.
Glycol aldehyde-is the simpliest CHO
Glucose, maltose, fructose, lactose and
galactose- reducing substances/sugars.

 The presence of a double bond and a negative

charge in the enol anion makes glucose an active
reducing substance.
Sucrose- most common non-reducing sugar
Non-reducing sugar do not contain an active
ketone or aldehyde group.
Glucose is the only CHO to be directly used for
energy or stored as glycogen.

Pathways in Glucose
Metabolism
Glycolysis metabolism of glucose
molecule to pyruvate or lactate for
production of energy

Pathways in Glucose
Metabolism
Gluconeogenesis- formation of
glucose 6-phosphate from
noncarboydrate sources

Pathways in Glucose
Metabolism
Glycogenolysis breakdown of
glycogen to glucose for use of energy

Pathways in Glucose
Metabolism
Glycogenesis conversion of glucose
to glycogen for storage

Pathways in Glucose
Metabolism
Lipogenesis conversion of
carbohydrates to fatty acids

Pathways in Glucose
Metabolism
Lipolysis decomposition of fat

Carbohydrates Classification
CLASSIFICATION is based on 4 different
properties

Size of the base carbon chain

Location of the CO function group
Number of sugar units
Stereochemistry of the compound

CLASSIFICATIONS OF
CARBOHYDRATES:
Based on the number of carbons in the molecule
(Generic classifications)
3 carbons compound (Trioses) e.g. glyceraldehyde
4 carbons compound (Tetroses)
5 carbons compound (Pentoses)* (Note: *most
important)
6 carbons compound (Hexoses)*

CLASSIFICATIONS OF
CARBOHYDRATES:
Based on the location of CO functional group
Hydrates of aldehyde or ketone
Aldose functional group: aldehyde
Ketose functional group: ketone

anomeric carbon carbon in the functional group

MODELS TO REPRESENT
CARBOHYDRATES

FISHER PROJECTION

Has the aldehyde or ketone at the top of the

drawing
Carbons are numbered starting at the aldehyde or
ketone end
Straight chain or cyclic (linked in hemiacetal form)

MODELS TO REPRESENT
CARBOHYDRATES

HAWORTH PROJECTION

Cyclic form
More representative of the actual structure
Formed when the functional group (ketone or
aldehyde) reacts with an alcohol group on the same
sugar to form a ring (hemiacetal ring)

Pancreas
Functions: an endocrine and exocrine organ in
the control of the CHO metabolism
As an exocrine gland, it produces and secretes
an amylase responsible for the breakdown of
ingested complex CHO.
As an endocrine gland, it secrets the hormones;
insulin, glucagon and somatostatin from different
cells residing in the islets of langerhans in the
pancreas.

INSULIN
The primary hormone responsible for the entry of
glucose into the cell.
Synthesized by the beta cells of the islets of
langerhans in the pancreas
It is normally released when glucose levels are high.
It is the only hormone that decreases glucose levels
hyploglycemic agent
Stored from sources such as liver, fat and muscles.
Has a reciprocal relationship with glucagon.
Promotes glycogenesis, lipogenesis and glycolysis;
decreases glycogenolysis.

GLUCAGON
The primary hormone responsible for increasing
glucose hyperglycemic agent
Synthesized by the alpha cells of the islets of
langerhans in the pancreas
It is released during stress and fasting states.
It enhances catabolic functions during fasting
periods; promotes glycogenolysis and
gluconeogenesis

Other hormones that tend to increase

glucose concentration
1. Cortisol and corticosteroids (Glucocorticoids)
. Secreted by the cells of the zona fasciculata and
zona reticularis of the adrenal cortex
. Decreases intestinal entry of glucose into the cell
. It promotes gluconeogenesis and lipolysis
2. Cathecolamines
. It is released from the chromaffin cells of the
adrenal medulla
. Inhibits insulin secretions and promotes
glycogenolysis and lipolysis.

3. Growth hormones(Somatotrophic)
Secreted by the anterior pituitary gland
Decreases entry of glucose into the cell
It promotes glycogenolysis and glycolysis.
4. Thyroid hormones
Secreted by the thyroid gland.
Promotes glycogenolysis, gluconeogenesis and
intestinal absorption of glucose.
5. Adrenocorticotropic hormones (ACTH)
It stimulates release of cortisol from the adrenal
cortex
It promotes glycogenolysis and gluconeogenesis.

6. Somatostatin
Produced by the delta cells of the islets of
langerhans of the pancreas
It is primarily inhibits the action of insulin and
glucagon.

Clinical conditions of carbohydrate

metabolism
1. Hyperglycemia
. Increase in blood glucose levels
. Causes: stress, severe infection, dehydration or
pregnancy, pancreatectomy, hemochromatosis,
insulin deficiency, abnormal insulin receptor.
. FBS level= 126 mg/dL
. All adults older than 45 yrs.old should have a
measurement of FBS every 3 years unless the
individual is diabetic.

Lab. findings in Hyperlgycemia

1.
2.
3.
4.

Increase glucose in plasma and urine

Increase urine specific gravity
Ketones in serum and urine
Decrease blood and urine
pH(acidosis)
5. Electrolyte imbalance

2. Hypoglycemia
Involves decreased glucose levels and can have many
causes.
Warning signs and symptoms of hypoglycemia are all
related to CNS.
80 mg/dl to 5mg/dl (2.8-3.0 mmol/L) observable
symptoms of hypoglycemia occur.
CLASSIFICATION:
1. Drug administration- insulin alcohol, salicylates,
sulfonamides, pentamidine. Etc.
2. Critical illnesses- hepatic failure, sepsis, renal failure,
cardiac failure, malnutrition
3. Hormonal deficiency- epinephrine, glucagons, cortisol,
growth hormone

4. Endogenous hyperinsulinism- pancreatic beta cell

disorder
5. Autoimmune hypoglycemia- insulin antibodies
6. Non beta cell tumors- leukemia, hepatoma,
pheochromocytoma, lymphoma etc.
7. Hypoglycemia if infancy and childhood- galactosemia,
GSD, Reyes syndrome
8. Alimentary (reactive) hypoglycemia- post-gastric surgery
9. Idiopathic (functional) postprandial hypoglycemia
A diagnosis of hypoglycemia should not be mad unless a
patients meets the criteria WHIPPLES TRIAD low
blood glucose concentration with typical symptoms
alleviated by glucose administration.

Diabetes Mellitus(DM)
A group of metabolic disorders characterized by
hyperglycemia resulting from defects in insulin
secretion, insulin or both.
Fasting plasma glucose concentrations > 26
mg/dL on more than one testing are diagnostic
DM.
Glucosuria occurs when the plasma glucose
levels exceeds 180 mg/dL (9.99mmol/L) with
normal renal function
In severe DM, the ratio of beta-hydroxybutyrate
to acetoacetate is 6:1

Classification of DM:

A. Type 1 DM
Formerly known as:
Insulin Dependent Diabetes Mellitus (IDDM)
Juvenile Onset Diabetes Mellitus
Brittle Diabetes
Ketosis-Prone Diabetes
. Is a result of cellular-mediated autoimmune destruction of the
beta cells of the pancreas.
. Diabetic individuals have insulinopenia (absolute insulin
deficiency) because of loss of pancreatic beta-cells and
depend on insulin to sustain life and prevent ketosis.
. 80-90% reduction in the vol. of the beta cell is required to
induce symptomatic type 1 DM

 Signs and symptoms: polyuria, polydipsia,

polyphagia, rapid wt. loss, hyperventilation, mental
confusion and possible loss of consciousness.
Complications: nephropathy, neuropathy, and
retinopathy microvascular disorders.
Microalbumin of 50-200 mg/24hrs. diabetic
nephropathy
Urine albumin excretion rate of 200 g/minute
overt diabetic nephropathy.
Idiopathic Type 1 DM is a form of type DM that has no
known etiology, is strongly inherited, does not have
beta-cell auto antibodies and have episodic
requirements for insulin replacement.

 Type 2 DM
Formerly known as: Non-insulin Dependent Diabetes Mellitus
Adult Type/maturity Onset Diabetes Mellitus
Stable Diabetes
Ketosis- Resistant Diabetes
Receptor-Deficient Diabetes Mellitus
Characterized by hyperglycemia du to an individuals
resistance to insulin; there is relative insulin deficiency.
Associated with strong genetic predisposition and not
related to an autoimmune disease.
It has been described as a geneticists nightmare.
Has a milder symptoms as compared to type 1, however,
untreated type 2 DM will result to nonketotic hyperosmolar
coma- overproduction of glucose (>500mg/dL), sever
dehydration, electrolyte imbalance, and increased BUN
and creatinine.

Risk factors
Risk factors:
obesity, family history, advanced age,
hypertension, lack of exercise,
impaired glucose metabolism.

C. Other specific types of diabetes

1. Pancreatic disroders
2. Endocrine disorders Cushings syndrome,
pheochromocytoma, accromegaly and thyrotxicosis
3. Drugs or chemical inducers of beta cells dysfunction
(dilantin and pentamidine)and impair insulin action
(thiazides,glucocorticoids)
4. Genetic syndromes- down syndrome, klinefelters
syndrome, leprechaunism etc.
D. Gestational DM(GDM)\
. Characterized by impaired ability to metabolized CHO
usually caused by a deficiency of insulin,metabolic or
abnormal changes occuring in pregnancy and
disappearing after delivery but in some cases returning
yrs. later

 Glucose intolerance with onset or first recognition

during pregnancy
Screening should be performed between 24 and
23 wks. Of gestation
A plasma glucose concentration of 140 mg/dL or
greater requires a full diagnostic glucose
tolerance test (3hr GTT with 100g glucose)

GDM results:
FBS = >105 mg/dL
1 hr. = < 190 mg/dL
2 hrs. = 165 mg/dL
3 hrs. = 145 mg/dL

 GDM is diagnosed when any two of the above

mentioned four values are met or exceeded.
After giving birth, woman with GDM should be
evaluated 6-12 wks. Postpartum
Infants born to diabetic mothers are at increased
risk for respiratory distress syndrome,
hypocalcemia and hyperbilirubinemia.
4. Impaired Fasting Glucose
Characterized by fasting blood glucose
concentrations between normal and diabetic
values.

5. Impaired Glucose tolerance

Characterized by fasting blood glucose
concentration less than those required for the
diagnosis of DM, but the OGTT is between
normal and diabetic values.

Diabetes Insipidus
Deficiency of anti diuretic hormone released by
the posterior gland.
Clinical picture include:
1. Normoglycemia
2. Polyuria with low specific gravity
3. Polydipsia
4. Polyphagia - ocassional

Glucose Methodologies
Fasting glucose in whole blood is 15% lower
than in serum or plasma.
Serum or plasma must be separated from the
cells within one hour to prevent losses of
glucose.
At rm. Temp. (20-25C), glycolysis decreases
glucose by 5-7%/hour (5-10mg/dL) in normal
uncentrifuged coagulated blood.
At refrigerated temp. (4 C) glucose is
metabolized at the rate of about 1-2 mg/dL/hr.

 WBC and RBC metabolize glucose resulting to

decrease value in clotted, uncentrifuge blood.
CSF glucose concentration should be
approximately 60% (40-60 mg/dL) of the plasma
concentrations.
Plasma glucose levels increase with age
fasting 2 mg/dL/decade; postprandial,
4mg/dL/decade; glucose challenge, 8-13
mg/dL/decade.

I.
A.
1.
.
a.
b.
c.
d.

e.

CHEMICAL METHODS
Oxidation Reduction Methods
Alkaline Copper Reduction Methods
Reduction of cupric ions to cuprous oxide in
hot alkaline solution by glucose.
Folin Wu Method
Nelson Somogyi Method
Neocuproine method
Benedicts method- used for detection and
quantitation of reducing substances in body
fluids like blood and urine.
Citrate or tartrate as stabilizing agent

2. Alkaline Ferric Reduction Method (Hagedorn

Jensen)
Reduction of a yellow ferricyanide to a colorless
ferrocyanide by glucose (inverse colorimetry)
3. Condensation Method
II. Enzymatic Method
Acts on glucose but not on other sugars and not
on other reducing substances.
1. Glucose oxidase method
> Measures the beta-D glucose

a. Colorimetric Glucose Oxidase Method (saifer

Gernstenfield Method)
b. Polarographic Glucose oxidase
. The enzymatic conversion of glucose is
quantitated by the consumption of oxygen
. Measure rate of oxygen consumption.
2. Hexokinase Method
. Most specific glucose method ; reference
method

NOTES TO REMEMBER
Elevated amounts of bilirubin, uric acid and
ascorbate false decreased values of
glucose(glucose oxidase method)
Hemolysis affects hexokinase method false
low glucose value
The enzymatic conversion of glucose to product
is quantitated by a color change reaction at the
last of a series of coupled chemical reactions
(kinetic analysis)

3. Dextrostics
Important in establishing correct insulin amount
for next dose
Effective in reducing the rate of development of
diabetic complications

Samples for Glucose Measurement

1. RBS random Blood Sugar
- requested during insulin shock,
hyperglycemic ketonic coma
2. FBS Fasting Blood Sugar
- NPO (Non-Per Orem) 6-8hrs.
3. 2-HR PPBS 2 hour Post Prandial Blood
Sugar
- below 110 mg/dL at 2 hours
4. GTT Glucose Tolerance Test

Requirements:

CHO depletion and inactivity or bed rest impair

glucose tolerance
GTT is unnecessary to do for women under 25
yrs. Old who have normal body wt. no family
history of diabetes and are not member of an
ethnic group with high prevalence of diabetes.
1. Patient should be ambulatory
- CHO depletion and inactivity or bed rest
impair glucose tolerance
2. Fasting of 8-16 hrs.

3. Unrestricted diet of 150 gms. CHO/day for 3

days prior to testing.
4. The patient should not smoke and drink alcohol.
5. Glucose Load
- 75 gms (standard glucose load)
-100 gms
-1.75g of glucose/kg body wt. (children)

Procedure for GTT

The patient should avoid exercise, eating and
drinking (except water) and smoking during
testing
For nonpregnant women and adults, only the
fasting and the 2 hour sample may be measured
or accrdg. To the physicians request
1. Collect the fasting blood sample
2. Instruct the patient to drink the glucose load
within 5 mins.
3. Collect blood sample after 30 mins., 1 hour, 2
hours, 3 hours respectively.

Kinds of Glucose Tolerance Test

a. Oral Glucose Tolerance Test
> Janney-Isaacson Method (single dose method)
>Exton Rose Method (divided oral dose or
double method)
b. Intravenous GTT
> used for DM patients with GI disorders.
>determine glucose by getting blood samples
every 10mins.for one hour
>0.5 g of glucose/kg body wt. (given within
3mins.) administered intravenously
>fasting sample is also required.

Indications

a. Those who are unable to tolerate a large CHO

load.
b. Those with altered gastric physiology
c. Those who had undergone previous operation
or surgery in the intestine.
d. Those with chronic malabsorption syndrome.

Criteria of Fasting Plasma Glucose (FPG)

1. Non-diabetic = <110mg/dl
2. Impaired PG = 110g/dl but <126mg/dl
3. DM = 126mg/dl
Categories of Oral Glucose Test
1. Normal GTT = 2hr PG <140mg/dl
2. Impaired GTT = 2hr PG 140mg/dl but < 200
mg/dl
3. DM = 2hr PG 200mg/dl

Diagnostic criteria for DM

1. RBS = 200 mg/dl (w/ symptoms of DM)
2. FBS = 126 mg/dl
3. 2-hr post glucose = 200 mg/dl

5. Glycosytated/glycated hemoglobin
Also called glycated hemoglobin
Largest subfraction of normal hemoglobin in both
diabetic and non-diabetic individuals.
A glucose molecule attached to one or both N-terminus
valines of the beta-polyp chains of normal adult
hemoglobin
A reliable method in the monitoring of long term
glucose control
It reflects the average blood glucose level over the
previous 2-3mos.
3-6% of Hgb is glycosylated; 18-20% is prolonged
hyperglycemia.
For every 1% change in the HbA value, 35mg/dL is
added to plasma glucose.

 Older RBCs have higher HbA, iron deficiency

anemia high levels
Not suitable for patients with shortened RBC
lifespan disorders.
Specimen for testing, EDTA whole blood
Preferred method, affinity chromatography

6. Fructosamine
Also called glycosylated or glycated
albumin/plasma protein ketoamine.
A reflection of short term glucose control (2-3wks)

 May be useful for monitoring diabetes

individuals w/ chronic hemolytic anemias and
hemoglobin variants.
It should not be measured in cases of low
plasma albumin.

Other clinical Disorders of Carbohydrate

Metabolism
1.Galactosemia
> A congenital deficiency; one of three enzymes
involved in galactose metabolism

 Cause of failure to thrive syndrome in infants

3deficient enzymes: galactose 1-phophate uridyl
transferase galactokinase and uridine
diphosphate galastose 4-epimerase
Cllinical features: jauncide, hepatomegally, easy
bruisability,sepsis, cataract, hypotonia and
sensory neural deafness.
Diagnostic test: erythrocyte galactose- 1-PO4
uridyl transferase activity.

2. Essential fructosuria
An autosomal recessive disorder characterized by
fructokinase deficiency
Diagnostic indicator: (+) fructose in urine
3. Hereditary fructose intolerance
A defect of fructose 1-6-b phosphate aldolase B
activity in the liver, kidney and intestine.
Inability to convert fructose-1-phosphate and
fructose-1,6-phosphate into dihyroxyacetone
phosphate,glyceraldehyde-3-phosphate and
glyceraldehydes.
Clinical features: irritability, seizures, and
hepatomegaly

4. fructose-1,6-biphosphate deficiency
A defect in fructose-1,6-biphosphate results in
failure of hepatic glucose generation by
glucoriogenic precursors such as lactate and
glycerol.
Clinical features: hypoglycemia, lactic acidosis
convulsion and coma.
5. Glycogen Storage Disease (GSD)
Deficiency of a specific enzyme involved in the
metabolism of glycogen
Inherited as autosomal recessive trait

 Blood specimen are collected for 2hrs at 15

mins. Interval
Von Gierke disease most common GS

Notes to Remember
1. CSF glucose
. It is abt. 60-70% of the blood plasma glucose
level
. Any changes in blood sugar are reflected in the
CSF approximately one hour later because of
the lag in CSF equilibrium time.
. A blood glucose specimen should be collected
at least 60 mins. Before the lumbar puncture.
. Increased levels: diabetes
. Decreased levels: bacterial meningitis, TB,
fungal and amebic meningitis.

 Reference value:40-70 mg/dL (adult)

60-80 mg/dL (child)
Normal CSF to glucose ratio: <0.5
2. C-Peptide test
Formed during the conversion of pro-insulin to
insulin.
The amount of circulating C-peptides provides
reliable indicators for pancreatic and insulin
secretionS (beta cells functions)

 Used to monitor individual responses to pancreatic

surgery.
To evaluate hypoglycemia
Specimen: fasting blood
Test for ketone bodies:
1. Gerhards ferric chloride test- reacts only w/
acetoacetate
2. Nitroprusside test- 10x more sensitive to
acetoacetate than to acetone
3. Acetest tablets- detects acetoacetate and acetone

4. ketosux- detects acetoacetate better

than acetone
5. Ketosite assay- detects beta
hydroxybutyrate; not widely used.

Thank You for Listening