There will also be an increase in the peripheral uptake of glucose,

INTRODUCTION TO GLUCOSE
such as when you have increased levels (e.g.immediately after eating),
Lecturer: Dr. Annabel Laranjo so there will be an increased peripheral uptake into the adipose tissues
and muscles to be stored as fats and as glycogen as well as in the
OUTLINE liver.
I Blood Glucose
A Functions Blood glucose can also enter in the formation of fats known as
B Metabolism lipogenesis
C Gluconeogenesis
D Pathways of Glucose It can also engage in the uronic acid pathway, hexose
II Insulin monophosphate pathways, and importantly in the glycogenesis
III Hypoglycemia wherein glucose is mainly stored as glycogen for future use.
IV Hyperglycemia
V Diabetes Mellitus Excess glucose can also be converted into other sugars such as
sucrose and lactose

BLOOD GLUCOSE Blood glucose can also be eliminated in the urine (also known as
glycosuria) whenever there is already an excess of the blood glucose
such as if you have diabetes melitus
● They start to appear in the urine as a result of the excess
glucose in the blood

GLUCOSE FUNCTIONS

1. Glucose is the primary source of energy for humans

2. The nervous system, particularly the brain, totally
depends on glucose from the surrounding extracellular
fluid (ECF) for energy
● Brain cannot store glucose
● Brain needs energy because nerve cells are
always used
DIFFERENT PROCESSES INVOLVED IN MAINTAINING YOUR BLOOD GLUCOSE
3. Nervous tissue cannot concentrate nor store
carbohydrates so they rely on glucose for energy
4. It is critical to maintain a steady supply of glucose to the
RANGE: 60-100 mg/dL nervous tissue
● The concentration of glucose in the
BLOOD GLUCOSE HOMEOSTASIS ECF (extracellular fluid) must be
maintained in a narrow range
We obtain glucose mainly from our diet in the form of starch and ● When the concentration falls below a
complex carbohydrates. certain level, the nervous tissue loses
the primary energy source and will be
WAYS TO INCREASE BLOOD GLUCOSE incapable of maintaining normal
function
1. Derive glucose from the liver through glycogenolysis or ● Therefore if you lack glucose for a
the breaking down of the glycogen, which is the stored few seconds or minutes, it would lead
form of glucose, in order to release glucose into the to an abnormality in the function of
blood when there is a decrease in blood glucose level. the brain cells

2. Derived or obtained from other carbohydrates such as GLUCOSE METABOLISM

sucrose and lactose. They can be broken down into
monosaccharides, particularly glucose to help increase
the blood glucose.
3. Use other substrates such as amino acids and ketone
bodies (or also fats) through gluconeogenesis in order
to contribute to the increase of the blood glucose during
fasting or starvation.
RIGHT SIDE OF THE PICTURE (processes involved wherein glucose
is utilized): In effect there would be a decrease in the blood glucose,
these are processes that are important also in regulating/maintaining
the normal glucose in the blood.
When you have excess glucose in the blood, glucose will be
facilitated to enter the cells of the body and they will be converted into
carbon dioxide (CO2) and water (H2O) through glycolysis through the
production of ATP.
Before carbohydrates can be absorbed and used for energy, they must
be broken down into monosaccharides
● Starch and glycogen - complex carbohydrates converted to
dextrins and disaccharides by salivary and pancreatic
amylases
● Disaccharides are hydrolyzed to monosaccharides by
maltase and lactase (enzyme from intestinal mucosa) once
starch and glycogen are broken down by the salivary and
pancreatic amylase
WHERE DO THESE OCCUR:
This occurs at the level of the small intestinal mucosa where
pancreatic amylase causes digestion of ingested starch and glycogen
to maltose
 LEC 11 - INTRODUCTION TO GLUCOSE
MALTOSE AND INGESTED LACTOSE
Maltose together with ingested lactose and sucrose is hydrolyzed by
disaccharides (sucrase and lactase) in the small intestinal mucosa to
form glucose, galactose, and fructose (main monosaccharides)
● In order to be absorbed by the body
MONOSACCHARIDES
The monosaccharides or the simple sugars are then absorbed into the
bloodstream and transported to the liver via the hepatic portal
circulation
Glucose is the only carbohydrate to be directly used for energy or
stored as glycogen
● Galactose and fructose cannot be stored as glycogen even
though they are monosaccharides
● Galactose and fructose must be converted first to glucose
before they can be used
● Remember glucose is the only carbohydrate that can be
directly used as energy
GALACTOSE AND FRUCTOSE CONVERTED BY LIVER ENZYMES
Since glucose is the only monosaccharide used by the body for energy,
the galactose and fructose are converted by liver enzymes to glucose
For glucose to be metabolized by the liver, it has to form
glucose-6-phosphate before glucose enters any of these 3 pathways
(wherein the glucose will be utilized)
● Have to phosphorylate at the 6th carbon
● You have to attach a phosphate at the 6th carbon of glucose
in order to produce glucose-6-phosphate
After the glucose enters the cell, it is quickly shunted into one of the
three pathways depending on the availability of substrates or
nutritional status of the cell
PATHWAYS OF GLUCOSE
● Hexose Monophosphate Pathway (HMP)
● Glycolytic Pathway or Embden-Meyerhof-Parnas
(GYP/EMP)
○ Energy production
● Glycogenesis Pathway (GGP)
○ Glycogen storage
The first 2 pathways are important for the generation of energy from
glucose
The last pathway, which is the conversion to glycogen pathway, is
important for the storage of glucose
The first step for all 3 pathways requires glucose to be converted to
glucose-6-phosphate using ATP (hexokinase). So when you
phosphorylate glucose to glucose-6-phosphate, it is through
hexokinase using ATP/ energy
ULTIMATE GOAL OF THE CELL
● To convert glucose to carbon dioxide and water with the
production of ATP
If the body needs energy, glucose is metabolized to carbon dioxide and
water with formation of energy via ATP production either through HMP
or GGP/EMP
Glycolysis is the conversion of glucose to pyruvate or Lactate
Embden-Mayerhof pathway
EROJA, GAYTOS, GONZALES, GUARDIARIO, HURANO, JUMAO-AS, KIERULF, LAGUNA, LEGARA, LUAGUE | 2D – GRP 2
● Glucose is broken down into 2 and 3 carbon molecules of
pyruvic acid that can enter the tricarboxylic acid (TCA)
cycle with the conversion to acetyl-coenzyme A
(acetyl-CoA)
● Requires oxygen thus is also known as the aerobic
pathway of generating energy or ATP
● Other substrate have the opportunity to enter the pathway at
several points
○ Glycerol, fatty acids, ketones and some amino
acids are converted or catabolized to acetyl-CoA,
which is part of the TCA cycle
GLUCONEOGENESIS
● Conversion of amino acids by the liver and other
specialized tissue, such as the kidney, to substrates that can
be converted to glucose
● Anaerobic glycolysis is important for tissue such as muscle,
which often have important energy requirements without an
adequate oxygen supply
○ By converting pyruvic acid into lactic acid
which diffuses from the muscle cell, enters the
systemic circulation, and is then taken up and
used by the liver
● Glycogen can also be stored in muscle, but since muscle
lacks glucose-6-phosphatase enzyme, only hepatic glycogen
can be available to blood
○ Stored glycogen in the muscles cannot be used
whenever you need glucose in the blood, therefore
when you have decreased glucose in the blood,
we usually mobilize glycogen from the liver, not
from the muscles
○ Glucose-6-phosphatase enzyme - used to
dephosphorylate glucose, which are stored as
glycogen
● If glucose is not needed by the body for immediate energy, it
is stored in the liver and muscles in the form of glycogen
● Glycogenesis is glycogen formation from glucose
○ Occurs when there is elevated blood glucose such
as after a meal
○ More than / excess than what is needed by the
blooded or cells, so the excess glucose will then
be converted to glycogen
■ After a meal
● Hepatocytes are capable of releasing glucose from
glycogen or other sources to maintain the blood glucose
concentration (glucose-6-phosphatase)
● Without this enzyme, glucose is trapped in the glycolytic
Pathway
● Muscle cells do not synthesize glucose-6-phosphatase
enzyme and, therefore, they are incapable of
dephosphorylating glucose
○ In times of crisis wherein you will have a
decreased glucose in the blood, you cannot
mobilize glycogen that are stored from the
muscles since you lack glucose-6-phosphatase
■ What we usually do is that the glucose
coming from the liver will be lysed to
form glucose
● Glucose enters a muscle cell, it remains as glycogen unless
it is catabolized
● When the blood glucose begins to drop (in cases during
fasting or starvation or nearing lunchtime or breaktime),
glucose begins to drop → glycogen is converted back to
glucose-6-phosphate for entry into the glycolytic pathway
(glycogenolysis)
○ This is the mobilization of your glycogen and the
conversion of glycogen to glucose
2
 LEC 11 - INTRODUCTION TO GLUCOSE

● The glycogenesis-glycogenolysis reactions are important because you already have glucose from the fed
mechanisms for regulating the blood glucose level state.
○ With the help of the enzyme ● Whereas conditions of starvation, gluconeogenesis is fully on
glucose-6-phosphatase and hexokinase and glycolysis is turned off
● Both the cycles are never active at the same pace at the
SUMMARY OF GLUCOSE METABOLISM: same time. They are considered to be opposite processes
● Dietary glucose and other carbohydrates such as starch, ● We do not stimulate gluconeogenesis in the presence of
either can be used by the liver and other cells for energy or excess glucose and likewise glycolysis is activated when we
can be stored as glycogen for later use have excess glucose and vice versa.
● When the supply of glucose is low, the liver will use glycogen
and other substrates to elevate the blood glucose
concentration

Ex. Glycerol from triglycerides, lactic acid from skin and muscles, and
amino acids

● If the lipolysis of triglycerides is unregulated, it results in the

formation of ketone bodies, which the brain can use as a
source of energy through the TCA cycle

GLUCONEOGENESIS (CONT.)
○ Synthesis of glucose from amino acids
○ Used in conjunction with the formation of ketone
bodies when glycogen stores are depleted
(starvation)

● The principal pathway for glucose oxidation is through

the Embden-Meyerhof pathway

PATHWAYS IN GLUCOSE METABOLISM

Glycolysis Metabolism of glucose molecule to

pyruvate or lactate for production of
energy (aerobic or anaerobic)

Gluconeogenesis Formation of glucose-6-phosphate from

noncarbohydrate sources
GLUCONEOGENESIS (CONT.)
Glycogenolysis Breakdown of glycogen to glucose for Gluconeogenesis is another important pathway in maintaining blood
use as energy glucose level especially during long term fasting

Glycogenesis Conversion of glucose to glycogen for
storage
Lipogenesis Conversion of carbohydrates to fatty
acids
Lipolysis Decomposition of fat
● The liver, pancreas, and other endocrine glands are all
involved in controlling the blood glucose concentrations
within a narrow range
● During a brief fast, glucose is supplied to the ECF
(extracellular fluid) from the liver through glycogenolysis
● When the fasting period is longer than 1 day, glucose is
synthesized from other sources through gluconeogenesis
● Control of blood glucose is under two major hormones:
○ insulin and glucagon (produced by the pancreas)
. eating
● Other hormones and neuroendocrine substances also exert
some control over blood glucose concentrations, permitting
the body to respond to increased demands for glucose or to
survive prolonged fasts/fasting
● Glycolysis and gluconeogenesis are reciprocally
regulated
● When glycolysis is on, gluconeogenesis is turned off,
especially in the fed state
○ If you’re full, you utilize glucose in order to produce
carbon dioxide and water to form energy through
glycolysis. You do not form additional glucose
● This involves formation of glucose from non carbohydrate
sources such as amino acids, lactate or glycerol portions
of lipids
○ Lactate, fatty acids and amino acids are converted
to acetyl CoA, then oxidized completely in the TCA
cycle (Kreb's cycle)
● These pathways of glycogenesis and glycogenolysis have
delicate control mechanisms such as feedback inhibition and
hormonal control that keep the blood glucose concentration
within a narrow range despite changes in feeding and fasting
○ These are important processes that will regulate or
maintain normal blood glucose, despite the
changes that will occur during feeding and fasting
INSULIN
● As the blood glucose levels tend to increase (like after
Insulin is secreted coming from the beta cells of the pancreas
Insulin would inhibit pouring of glucose into blood
Insulin also promotes utilization of glucose
Insulin is synthesized by the b-cells of islets of Langerhans in
the pancreas

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 LEC 11 - INTRODUCTION TO GLUCOSE

Insulin is considered to be the primary hormone responsible for Other hormones that affect carbohydrate metabolism
the entry of glucose into the muscle and adipose cells
As the blood glucose tends to decrease, other hormones
○ We need insulin in order for the glucose to be can also elevate the blood glucose
taken up in the periphery by the muscle and
adipose cells
1 Epinephrine
○ When you lack insulin (such as in Diabetes
● Produced by the adrenal medulla
mellitus), there will be an excess glucose in the
● Increases plasma glucose by inhibiting insulin
blood, because they cannot enter into the
secretion
muscles and adipose cells due to the lack of
● Increasing glycogenolysis with the production of
insulin
glucose
■ Known as Insulin Resistance, which
● Promoting lipolysis
is present in Diabetes mellitus
● Released during times of stress

By nonspecific receptors 2 Glucocorticoids, primarily cortisol

● Thereby increasing glycogenesis, lipogenesis, and glycolysis ● Released from the adrenal cortex on stimulation
and inhibiting glycogenolysis by adrenocorticotropic hormone (ACTH)
○ All of these processes are activated by insulin ● Increases plasma glucose by decreasing intestinal
● Insulin is the only hormone that decreases glucose levels entry into the cell
and can be referred to as a hypoglycemic agent ● Increasing gluconeogenesis, liver glycogen, and
lipolysis
● As the blood glucose tend to decrease as a result of the
insulin production, the blood glucose now will decrease to Growth hormone and ACTH – promote increased plasma
normal glucose by:
○ Decreasing the entry of glucose into the
Decrease insulin secretion is brought about: cells
○ Increasing glycolysis
○ Release of GH is stimulated by
Hormones like glucagon, catecholamines, growth hormone, decreased glucose levels and inhibited
glucocorticoids, thyroid hormones, ACTH by increased glucose
- These hormones are the reverse of insulin and are thus ● Decreased levels of cortisol stimulate the anterior
called counter regulatory hormones pituitary to release ACTH
3 ● ACTH, in turn, stimulates the adrenal cortex to
release cortisol and increase plasma glucose
levels by converting liver glycogen to glucose and
GLUCAGON promoting gluconeogenesis.

Glucagon is the primary hormone responsible for increasing Whenever you have decreased blood glucose level
glucose levels synthesized by the a-cells of islets of Langerhans in the following hormone is elevated
the pancreas ➔ Growth hormone
○ released during stress and fasting states ➔ ACTH
○ acts by increasing plasma glucose levels by ➔ Cortisol
■ Promoting glycogenolysis in the liver ➔ Glucagon
■ increase in gluconeogenesis ➔ Epinephrine

○ referred to as the main or primary Thyroxine increased plasma glucose levels by

hyperglycemic agent 4 ● Increasing glycogenolysis, gluconeogenesis, and
intestinal absorption of glucose

Somatostatin
IN CASES OF HYPOGLYCEMIA ● Produced by the d-cells of the islets of
Langerhans of the pancreas
1 1st line of defense: Inhibition of insulin 5 ● Increased plasma glucose levels by the inhibition
of insulin, glucagon, growth hormone, and other
endocrine hormones.
2 2nd line of defense: Increase release of glucagon - which
is the major hormone that would stimulate increase in
glucose
THE ACTION OF HORMONES
3 3rd line of defense: Release of catecholamines, anterior
pituitary hormones (i.e., growth hormone), ACTH ACTION OF INSULIN

4 Thyroid hormones and growth hormones are not Increases glycogenesis and glycolysis:
essential for maintenance of blood glucose concentration glucose→glycogen→pyruvate→acetyl CoA
but have impact on carbohydrate metabolism
Increased lipogenesis

Decreases glycogenolysis

EROJA, GAYTOS, GONZALES, GUARDIARIO, HURANO, JUMAO-AS, KIERULF, LAGUNA, LEGARA, LUAGUE | 2D – GRP 2 4
 LEC 11 - INTRODUCTION TO GLUCOSE

ACTION OF GLYCOGEN

Increased glycogenolysis: glycogen → glucose

Increases gluconeogenesis: fatty acids → acetyl CoA →ketone,

proteins → amino acid

● Hypoglycemia can be due to insufficient food, excess

exercise, or excess insulin. All of these can cause or lead
to hypoglycemia.

● The onset can be rapid in 1-3 hours and the presentation

will be anxious, sweaty. Patient is hungry, confused, there
can be blurring of vision or double vision as a result of
decreased glucose in the brain, shaky, irritable, and the
This table shows the summary of the hormonal control in blood
patient has cool, clammy skin. All of these symptoms
glucose. Take note of this
would mean presence of hypoglycemia.
[Take note of the symptoms]

HYPOGLYCEMIA

2 TYPES OF HYPOGLYCEMIA

Postabsorptive of Fasting This occurs before eating.

hypoglycemia

Reactive or Postprandial Usually seen 2 hours after

hypoglycemia (PPH) eating.

These are the variations in blood glucose.
The normal blood glucose is said to be at 60-100 or 60-110 mg/dL.
That’s considered to be the normal concentration of blood glucose.
Whenever your blood glucose is less than 60 mg/dL, this is already
known as hypoglycemia, and if it is above 110 mg/dL, it is called
hyperglycemia.
HYPOGLYCEMIA
● Low blood glucose
● CNS symptoms
● Improvement of symptoms upon glucose administration
● All of these three together is known as: Whipple’s triad
So, whenever a person experiences low blood glucose plus the
presence of CNS symptoms and the improvement of such
symptoms upon glucose administration, all of these three are known
as your Whipple’s triad. This is a triad that could diagnose
hypoglycemia. The three criteria should be present in order for you
to say that you have Whipple’s triad.
● Current approaches to hypoglycemia suggest classification
based on clinical characteristics
● Separates patients into those who appear healthy and those
who are sick
● Among healthy-appearing patients are those with and
without a compensated coexistent disease
● Includes individuals in whom medications may be the cause
of hypoglycemia through accidental ingestion or by
dispensing error
● Sick person may have an illness that predisposes to
hypoglycemia (Ex. Insulinoma: you have excessive
production of insulin as a result of a tumor) or may
experience drug and illness interaction leading to
hypoglycemia
● Hypoglycemia in hospitalized patients can often be ascribed
to iatrogenic factors.
SYMPTOMS OF HYPOGLYCEMIA
1. Increased hunger

2. Hunger

3. Nausea and Vomiting

4. Dizziness

5. Nervousness and Shaking

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 LEC 11 - INTRODUCTION TO GLUCOSE

6. Blurring of Speech and Sight DIAGNOSTIC CRITERIA FOR INSULINOMA INCLUDE:

7. Mental Confusion ● Change in glucose level > 25 mg/dL (1.4mmol/L)

● Insulin level > 6uU/mL (41.7pmol/L)
● Hypoglycemia can lead to release of epinephrine into the ● C-peptide levels > 0.2 nmol/L
systemic circulation and of norepinephrine at nerve endings ● Proinsulin levels > 5 pmol/L and/ or
of specific neurons, they act in unison with glucagon to ● b-hydroxybutyrate levels < 2.7 mmol/L
increase plasma glucose
● Glucagon is released from the islet cells of the pancreas and
inhibits insulin production ● Reactive hypoglycemia PPH
● Epinephrine is released from the adrenal gland and (Post-Prandial Hypoglycemia) – occurs within 2 hours of
increases glucose metabolism and inhibits insulin food intake, due to sudden release of insulin
● Cortisol and growth hormone are released and increase
● Leucine induced hypoglycemia in certain individuals a
glucose metabolism
● Decreased plasma glucose levels protein rich diet containing leucine may cause sudden
release of insulin causing hypoglycemia
● Hypoglycemia has many causes – some are transient and ● Observed in chronic alcoholics
relatively insignificant, but others can be life threatening who are also malnourished
● Glucagon and other glycemic factors are released is for
● Also precipitated by simultaneous administration of insulin
plasma glucose between 65 and 70 mg/dL (3.6 to 3.9
mmol/L, transient hypoglycemia) and about 50 to 55 mg/dL ● So patients with type 1 diabetes are given a warning not to
(2.8 to 3.1 mmol/L, life-threatening) consume alcohol because this can also facilitate
● Observable symptoms of hypoglycemia appear (mentioned hypoglycemia
previously)
● Due to hepatic glycogen depletion
● Warning signs and symptoms of hypoglycemia are all related
to the central nervous system (CNS) combined with alcohol-mediated inhibition of
gluconeogenesis (lead to alcohol-related hypoglycemia)
● It is most common in malnourished alcohol abusers
● The implications of alcohol abuse are due to altered
+
NAD /NADH ratio.

Figure. Pathway where alcohol is metabolized

● This is the pathway where alcohol-related hypoglycemia or
If there is no coexisting disease, patients would appear healthy where the alcohol is metabolized
However, hypoglycemia most likely can be due to drugs, tumor in the ● There is the production of lactate and glucose from pyruvate
pancreas aka insulinoma, islet hyperplasia/nesidioblastosis, and also the production of NAD from NADH in the presence
factitial hypoglycemia from excess insulin or sulfonylurea (which of alcohol dehydrogenase and aldehyde dehydrogenase.
is an antidiabetic drug), severe exercise, as well as ketotic ● In metabolizing alcohol, alcohol in the presence of alcohol
hypoglycemia. dehydrogenase in the liver cells with the help of NAD, NAD
is reduced to NADH
INSULIN INDUCED ● Alcohol or ethanol (CH3CO2OH) is converted to
Another Form of Hypoglycemia, most common is Insulin induced acetaldehyde (CH3CHO)
● Then Acetaldehyde in the presence of aldehyde
➢ Observed in Type 1 diabetic patient on insulin therapy dehydrogenase with the presence of NAD is converted to
(they lack insulin, there is absolute deficiency of insulin
therefore they require insulin) acetate or acetic acid (CH3COOH) with the production of
pyruvate and NAD.
○ Overdose of insulin can produce hypoglycemia
● So there will be accumulation
➢ Observed in insulinoma and other tumor which cause of acetic acid and acetaldehyde
increase abnormal secretion of insulin ● These pathways or the accumulation of acetaldehyde will
now promote the destruction of the liver cells.

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 LEC 11 - INTRODUCTION TO GLUCOSE
● In the process of producing pyruvate, pyruvate can be
converted to glucose or lactate
● So when you have chronic alcoholism, the formation of
lactate from pyruvate is favored, and there will be depletion
of glucose and ATP or energy due to the change in the
NAD/NADH ratio as a consequence of inhibition of
gluconeogenesis and accumulation of acetaldehyde or
alcohol adducts and acetic acid
Resulting to/ in effect…
● There will be excessive NADH production
● This would inhibit fatty acid oxidation that will provide
ATP
○ With the accumulation of fatty acids because of
the inhibition, the fats will now accumulate in the
liver
● Pyruvate to lactate reaction is favored depleting supply of
pyruvate for gluconeogenesis
Figure: Alcohol Metabolism in Liver Cells
● Once the alcohol enters the cell, in the presence of NAD
and alcohol dehydrogenase, it is converted to
acetaldehyde
● Acetaldehyde, on the other hand, with the help of aldehyde
dehydrogenase, is converted to acetate
● Acetate will now be converted to acetyl coenzyme A
which is an important substrate for the tricarboxylic acid
cycle for the production of ATP and also in the beta
oxidation of your free fatty acids which are all sources of
ATP.
● But because you have accumulation of acetate or acetyl
coenzyme A, there will be inhibition of the beta-oxidation
of free fatty acids and also TCA cycle in the process, so in
effect, you will have accumulation of ketone bodies
which are byproducts of fat metabolism
● There will be enhanced production of ketone bodies or
ketogenesis with accumulation of free fatty acids since
they are not converted to ATP; instead, they are converted
to fats, so that they would be enhanced lipogenesis in the
presence of chronic alcoholism
● Aside from that, there will be reduction of ATP
production as a result of inhibition on your TCA cycle
because of the shunted pathway due to the increase acetyl
coenzyme A
● (Left side of Figure) In the process, glycolysis inside the
liver cells will facilitate the formation of pyruvate; with the
presence of excessive amount of NADH, pyruvate is
converted to lactate (this is the anaerobic form of
glycolysis)
EROJA, GAYTOS, GONZALES, GUARDIARIO, HURANO, JUMAO-AS, KIERULF, LAGUNA, LEGARA, LUAGUE | 2D – GRP 2
● Lactate is converted to lactic acid, thus it would explain
the metabolic acidosis found in patients with chronic
alcoholism.
● Then pyruvate formation to oxaloacetate which is an
important byproduct or important substrate for TCA cycle
and gluconeogenesis will be shunted
● There will be decreased production of glucose from
other sources, so inhibition of the gluconeogenesis,
thus, there will be, in effect:
● Decrease in the glucose
● Reduced ATP
● Accumulation of fats
● Increased ketone bodies and lactic acid
(in patients who are alcoholics)
● Hypoglycemia
Figure. Summary
● In summary, there is a shifting of the ratio, so there will be
more of the NADH/NAD+ Ratio
● This will facilitate a decrease in gluconeogenesis with a
subsequent increase in glycolysis which would lead to
Severe Hypoglycemia (Loss of Consciousness)
● There is also favored production or formation of Lactate
from Pyruvate which would also lead to Lactic Acidosis
● There is also a decreased Fat Breakdown with increased
Fat Synthesis leading to Fatty Change of the Liver
(Steatosis)
● All of these mechanisms can lead to alcohol-induced
Hypoglycemia
HYPOGLYCEMIA IN BABIES OF DIABETIC MOTHERS
● The growing fetus of a diabetic mother is exposed to
maternal hyperglycemia which leads to hyperplasia of
pancreatic islet cells (the baby’s pancreas will undergo
hyperplasia)
● After delivery, the baby fails to suppress the excessive
insulin secretions and develops hypoglycemia
HYPOGLYCEMIA IN PREMATURE AND LOW BIRTH WEIGHT
INFANTS
● Premature and low birth weight babies are more
susceptible to hypoglycemia since they have little
adipose tissue to provide alternative fats such as free
fatty acids, acetone bodies during the transition from fetal
dependency to the free-living state
● The enzyme of gluconeogenesis may not be completely
functional at this time
● Little glycerol, which could normally be released if
adipose tissue is available for gluconeogenesis, but that
is not sufficient to fulfill the energy needs
● All of these mechanisms can lead to hypoglycemia in
premature and low birth weight infants
7
 LEC 11 - INTRODUCTION TO GLUCOSE

HYPOGLYCEMIA IN SMALL FOR DATE BABIES

● Small for date babies have inadequate glycogen stores

as well, so at the time of need there is diminished
outpouring of glucose
● The situation worsens further due to prematurity since the
glycogen stores are laid in the last months of pregnancy
○ Therefore, there is not enough glycogen stores
in these premature and low birth weight infants
● Hence, a premature baby has diminished stores and ● Shaking
frequently undergoes hypoglycemia ● Sweating
● ● Anxious
● Dizziness
ENDOCRINE DISORDERS THAT CAN LEAD TO HYPOGLYCEMIA ● Hunger
● Hypothyroidism ● Fast Heartbeat
● Hypopituitarism ● Impaired Vision
● Hypocorticism ● Weakness Fatigue
● Liver disorders
● Headache
● Glycogen storage diseases
● Irritable
● Heavy exercise

CLINICAL MANIFESTATIONS FOR HYPOGLYCEMIA TREATMENT FOR HYPOGLYCEMIA

● If person is alert: Oral glucose administration
NEUROGLYCOPENIC ● In unconscious and/or bedridden patients: Intravenous
● Confusion, headache, convulsions, syncopal attacks, coma, glucose administration
and death (untreated) ○ This will facilitate a faster increase in the blood
● Due to deprivation of glucose to blood cells glucose as compared to oral blood glucose
○ This will also prevent the aspiration of glucose into
the lungs in an unconscious patient
ADRENERGIC ● Definite cure/treatment: Treat primary cause
● Palpitations, tremors, excessive sweating ○ Know what is the cause of the hypoglycemia
● Due to release of catecholamines (e.g., epinephrine and
norepinephrine) especially
HYPERGLYCEMIA
LABORATORY FINDINGS ● Characterized by high blood glucose
● Decreased plasma glucose ● Most common cause is diabetes mellitus
● Extremely elevated insulin levels in patients with pancreatic ● Up to 500mg% of glucose or even more
b-cell tumors (insulinoma)

MEN VS WOMEN IN PROLONGED FASTS
Men and women have different metabolic patterns in prolonged fasts
● Healthy male will maintain plasma glucose of 55 to 60
mg/dL (3.1 to 3.3 mmol/L) for several days
● Healthy females will produce ketones more readily and
permit glucose to decrease to 40 mg/dL (2.2 mmol/L) or
lower
WHIPPLE’S TRIAD
● Diagnosis of hypoglycemia is known as the Whipple’s triad
characterized by a:
○ Low plasma blood glucose
○ High plasma insulin
○ Reversion of the symptoms upon giving of glucose
● Once we have detected a low blood glucose and a high
plasma insulin in a patient, we suspect endocrine and liver
disorder
○ Blood glucose is low
○ Plasma insulin high
○ Endocrine and liver disorder suspected
LOW BLOOD SUGAR SYMPTOMS
PATIENTS WITH HYPERGLYCEMIA WILL PRESENT THE
FOLLOWING SYMPTOMS:
● Very thirsty
● Needing to pass urine more often than usual (polyuria)
● Dry skin
● Very hungry/ increased appetite
● Sleepiness
● Blurry vision
● Infection or injuries heal more slowly than usual
These symptoms and signs are possible pointing out to
hyperglycemia which is manifested by diabetes mellitus
● An increase in plasma glucose levels
○ Once detected, there is a release of insulin
● Insulin is secreted by the b-cells of the pancreatic islets of
Langerhans
● Insulin enhances membrane permeability of cells in the liver,
muscle, and adipose tissue to glucose from the blood.
○ This is to facilitate the uptake of glucose by the
mentioned tissues
● It also alters the glucose metabolic pathways
● Hyperglycemia, or increased plasma glucose levels, is
caused by an imbalance of hormones that would regulate the
level of your blood glucose

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 LEC 11 - INTRODUCTION TO GLUCOSE
ENDOCRINE- CAUSED HYPERGLYCEMIA
Diabetes mellitus
Hyperthyroidism ● Increase in thyroid
hormones
● Also has an effect on the
carbohydrate metabolism
Hyperpituitarism ● Increase in pituitary
hormones
Hypercorticism ● Increase in cortisol
● Can increase the blood
glucose
Hyperadrenalism
These diseases/ endocrine disorders can contribute to
hyperglycemia in a patient
Patient with hyperthyroidism (above) and below Patient with
Hypercorticism (below) with the presence of abdominal girth and
abdominal straya with a puffy face
NON-ENDOCRINE
Diabetes mellitus ● Characterized by deficiency
of insulin secretion or
action resulting in
hyperglycemia and the
probable development of
complications over time
● Deficiency of insulin may be
absolute, relative or
associated with certain other
conditions or syndromes
● Therefore the presence of
insulin deficiency is usually
present in patients with
diabetes mellitus. However
there is also a condition
where there is presence of
insulin but there is a
limitation to the entry of
insulin into the cells so
glucose can be inhibited in
entering the peripheral cells
(such as your muscles, liver,
and adipose tissue) known
as “insulin resistance”
○ Which is a common
mechanism that
would result to
EROJA, GAYTOS, GONZALES, GUARDIARIO, HURANO, JUMAO-AS, KIERULF, LAGUNA, LEGARA, LUAGUE | 2D – GRP 2
hyperglycemia among
diabetic patients
TYPES OF DIABETES MELLITUS
TYPE 1 - DIABETES MELLITUS
● Constitutes only 10% to 20%
● Commonly occurs in childhood and adolescence
● Usually initiated by an environmental factor or infection
(usually a virus) in individuals with a genetic predisposition
○ Patients already have the genetic predisposition
plus they suffered from infection, usually a viral
infection + environmental factor that would lead to
the development of Diabetes Mellitus
● Causes the immune destruction of the b-cells of the
pancreas and a decreased production of insulin
○ There is a production of antibodies as a result of
previous infection that would destroy the beta cells
of the pancreas leading to decreased production of
insulin resulting to hyperglycemia
● Abrupt onset, insulin dependence, and ketosis tendency
(production of ketones)
● Genetically-related
● One or more of the following markers are found in 85% to
90% of individuals with fasting hyperglycemia. Among
these patients, you will see islet cell autoantibodies (since
this is immune-mediated), insulin autoantibodies, glutamic
acid decarboxylase autoantibodies, and tyrosine
phosphatase IA-2 and IA-2B autoantibodies
● Signs and Symptoms Include:
○ Polydipsia (increased thirst)
○ Polyphagia (increased food intake)
○ Polyuria (excessive urine production)
○ Rapid weight loss
○ Hyperventilation
○ Mental confusion, and
○ Possible loss of consciousness (due to increased
glucose to brain)
● 3Ps in Diabetes Mellitus: Polydipsia, polyphagia, polyuria
● Hypoglycemia could also lead to coma, so the signs and
symptoms of hypo- and hyperglycemia are more or less the
same. You will know the differences between the two just by
getting the plasma or the blood glucose
● Complications Include:
○ Microvascular problems
■ e.g. Nephropathy- problems in the
kidney
■ Neuropathy- affect the small blood
vessels of the brain
■ Retinopathy- affect the blood vessels in
the eye
○ Cardiovascular/Heart disease
● Idiopathic Type 1 Diabetes
○ No known etiology, is strongly inherited, and does
not have b-cell autoimmunity (so there’s no
visible presence of autoantibodies)
○ Episodic requirements for insulin replacement
■ They don’t rely on insulin unlike the type
1 diabetes mellitus
TYPE 2 - DIABETES MELLITUS
● Result of an individual's resistance to insulin with an insulin
secretory defect
● Results in a relative, not an absolute, insulin deficiency
○ There is no absolute absence of insulin
● Constitutes the majority of the diabetes cases
● Most patients are obese
● Often goes undiagnosed for many years (10 - 20 years
before they are diagnosed)
● Associated with a strong genetic predisposition (runs in
the family)
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 LEC 11 - INTRODUCTION TO GLUCOSE

● Increased risk with an increase in age, obesity (BMI is more

than 25), and lack of physical exercise endocrine also regulate glucose
● Type 2: Adult onset of the disease (usually around 20 yrs. levels.
old and above) and milder symptoms
○ WHEREAS Type 1 occurs more among the
adolescents and children Drug or chemical-included -
● Ketoacidosis is seldom-occurring insulin receptor abnormalities
○ Compared to type 1 which is seen in children with
severe symptoms and usually they present with Certain genetic syndromes -
ketoacidosis
● However, these patients are more likely to go into a
hyperosmolar coma and are at an increased risk of ● The characteristics and prognosis of this form of diabetes
developing macrovascular and microvascular depend on the primary disorder
complications. ● Maturity-onset diabetes of youth (MODY) is a rare form of
○ Meaning the complications are much higher in diabetes that is inherited in an autosomal dominant
type 2 diabetes mellitus involving now the bigger fashion
blood vessels, not only the blood vessels in the
kidney, brain and eyes
○ Affects also the bigger blood vessels such as the DRUGS THAT CAN CAUSE DIABETES MELLITUS
blood vessels supplying the legs and arms. That’s
why if you see patients with type 2 diabetes they Corticosteroids (cortisol) Increase blood glucose
usually present with problems in the legs
(non-healing wound). They eventually end up
being amputated for the recurrent wound or Thiazide diuretics For hypertension; known to
cool-wound healing as a complication of absorb glucose and at the same
poorly-controlled diabetes mellitus time, decrease sodium and
other electrolytes from the body.
PANCREATIC DISORDER
● Pancreatectomy - removal of pancreas due to a certain
tumor or inflammatory lesion at the head of the pancreas
which affects insulin production High dose of niacin -
● Pancreatitis - inflammation of the pancreas
○ Somehow you will have hyperglycemia due to the Phenytoin Anti-seizure drug which can also
failure of the production of insulin or there is a predispose you to diabetes
diminished function of the pancreas leading to mellitus
decreased insulin and thus an increase of blood
glucose
● Other Causes
○ Rubella
■ agent for measles
■ Viral infection
○ Intracranial infections
○ Sepsis
○ Exposure to anesthesia
■ Prolonged exposure to anesthesia can
lead to diabetes mellitus
○ Intracranial tumors

GESTATIONAL DIABETES MELLITUS

● Infants born to mothers with diabetes are at increased risk
for respiratory distress syndrome, hypocalcemia, and
hyperbilirubinemia
● Fetal insulin secretion is stimulated in the neonate of a
mother with diabetes
● When you undergo pancreatectomy (removal of pancreas) ○ If ang mama diabetic na daan, so increased ang
because of a certain tumor/ inflammatory lesion at the head iyang blood glucose in the blood, this will stimulate
of the pancreas, as shown in the pic, this can also affect the fetal insulin production as a result of pancreatic
insulin production. hyperplasia (increased production of insulin)
● However, when the infant is born and the umbilical cord is
severed, the infant’s oversupply of glucoses is abruptly
OTHER SPECIFIC TYPES OF DIABETES ARE ASSOCIATED terminated, causing severe hypoglycemia
WITH CERTAIN CONDITIONS (aka secondary diabetes mellitus) ○ Wala nay daghang glucose coming from the
mother who is a known diabetic, so the baby will
now have a severe hypoglycemia due to the
Genetic defects of b-cell Hyperglycemia increased insulin production as a response to the
function or insulin action pancreatic hyperglycemia because of the diabetes
in the mother
● Defined as any degree of glucose intolerance with onset or
Pancreatic disease Pancreatitis or pancreatic tumor first recognition during pregnancy
(e.g. insulinoma) ● Identified through oral glucose tolerance
● Causes include metabolic and hormonal changes
● Frequently return to normal postpartum
● Associated with increased perinatal complications and an
Diseases of endocrine origin Because hormones in the increased risk for the development of diabetes in later years

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 LEC 11 - INTRODUCTION TO GLUCOSE
PATHOPHYSIOLOGY OF DIABETES MELITUS
● Hyperglycemia - both type I and type II diabetes
● Glucosuria (presence of glucose in urine) can also occur
after the renal tubular transporter system for glucose
becomes saturated
○ When the glucose concentration of plasma
exceeds roughly 180 mg/dL in an individual with
normal renal function and urine output
● As hepatic glucose overproduction continues, the plasma
glucose concentration reaches a plateau around 300 to
500 mg/dL (17 to 28 mmol/L)
○ Provided urine output is maintained, glucose
excretion will match the overproduction
● Type I diabetes has a higher tendency to produce
ketones
● Patients with type II diabetes seldom generate ketones but
instead have a greater tendency to develop hyperosmolar
nonketotic states.
○ Meaning, patients with type 2 diabetes have
higher sugar levels but lesser ketone production
● The difference in glucagon and insulin concentrations in
these two groups appears to be responsible for the
generation of ketones through increased b-oxidation
● In type 1, there is an absence of insulin with an excess
of glucagon which permits gluconeogenesis and lipolysis to
occur
○ Remember, glucagon will facilitate
gluconeogenesis, wherein you will also make use
of other sources (like ketones) and glycolysis,
when you lyse fats, you will divide ketone bodies.
Therefore, they are at risk for ketosis
● In type 2, insulin is not absent (but is deficient) and
may, in fact, present as hyperinsulinemia at times
therefore, glucagon is attenuated (or inhibited)
○ Diba dili sila pwede mag dungan
○ Insulin is deficient but not absent.
○ So that your gluconeogenesis will be inhibited
because of the inhibition of glucagon due to
the presence of insulin
● Fatty acid oxidation is inhibited in type 2 (as
compared to type 1) which causes fatty acids to be
incorporated into triglycerides (there will be lipogenesis)
for release as very low-density lipoproteins (VLDL)
which is a bad cholesterol
● The laboratory findings of a patient with diabetes with
ketoacidosis tend to reflect dehydration, electrolyte
disturbances, and acidosis
● (Ketone bodies) Acetoacetate, b-hydroxybutyrate, and
acetone are produced from the oxidation of fatty acids
○ Remember: Fatty acid oxidation is facilitated
with Type 1 Diabetes Mellitus,therefore, you
will have more of ketones (ketosis) in Type 1
● Two former ketone bodies contribute to the acidosis -
Acetoacetate, b-hydroxybutyrate
○ So they contribute to the acidosis
of px with diabetes mellitus
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● Bicarbonate and total carbon dioxide are usually
decreased due to Kussmaul Kien respiration (deep
respirations)
○ Bicarbonate and total carbon dioxide are
usually decreased in px with diabetes
mellitus because there is more acidosis kay
daghan na kaayog lactic acids,etc. So there
will be increased respiration known as
Kussmaul Kien respiration – rapid deep
respirations which are characteristic of
acidotic px. This is also due to Bicarbonate
and total carbon dioxide.
● Compensatory mechanism to blow off carbon dioxide
and remove hydrogen ions in the process
○ So mu paspas ka og ginhawa para ma blow
off nimo ang carbon dioxide which is also
acid
● Anion gap in this acidosis can exceed 16 mmol/L
● Serum osmolality is high as a result of hyperglycemia
● Sodium concentration tends to be lower due in part
to losses(polyuria) (magsige og pangihe) and in part to
a shift of water from cells because of the
hyperglycemia.
○ Sodium is low however the potassium is high.
Sodium and Potassium are always the
opposites.
● Hyperkalemia is due to displacement of
potassium from inside the cells in acidosis
○ Remember if acidotic gani ka sa sulod sa cell
it can facilitate the exit of potassium into the
blood and the entry of the sodium, and the
exclusion of the sodium in the urine , so
therefore you will have hyperkalemia in
acidosis.
NONKETOTIC HYPEROSMOLAR STATE-UNTREATED DIABETES
MELLITUS TYPE 2
● Overproduction of glucose
● Precipitated by heart disease, stroke, or pancreatitis
● Glucose concentration exceed 300 to 500 mg/dl (17 to
28 mmol/L)
● Severe dehydration is present which contributes to the
inability to excrete glucose in the urine
● Mortality is high with this condition
● Ketones are not observed because the severe
hyperosmolar state inhibits the ability of glucagon to
stimulate lipolysis
LABORATORY FINDINGS
In patient with
With nonketotic hyperosmolar coma (Type II diabetes)
Plasma glucose Values Exceeding 1,000
mg/dL (55 mmol/L)
Plasma Na and K Normal or elevated
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 LEC 11 - INTRODUCTION TO GLUCOSE
Bicarbonate Slightly decreased
Blood Urea nitrogen Elevated (Because
(BUN) and Creatinine of the dehydration)
Osmolality >320 mOsm/dL
mOsm/dL: Millimoles
per deciliter
All of these findings will be diagnostic for the nonketotic
hyperosmolar state
● Gross elevation in glucose and osmolality, the
elevation on BUN, and the absence of ketones
distinguish this condition from diabetic ketoacidosis
Diabetic ketoacidosis: more common in Type I
● Other forms of impaired glucose metabolism that do
not meet the criteria for diabetes mellitus would be
impaired fasting glucose and impaired glucose
tolerance.
○ Meaning your sugar level is
still high but it does not meet the criteria
for diabetes mellitus
CRITERIA FOR TESTING FOR DIABETES AND PREDIABETES
ACCORDING TO THE AMERICAN DIABETES ASSOCIATION
These are the recommendations from American Diabetes
Association
When do you test or screen for diabetes and prediabetic state?
● Recommended that all adult beginning at the age of
45 years should be tested for diabetes every 3
years using either the hemoglobin A1c (HbA1c:
glycosylated hemoglobin), fasting plasma glucose,
or a 2-hour 75g oral glucose tolerance test (OGTT)
unless the individual has otherwise been diagnosed
with diabetes
TESTING SHOULD BE CARRIED OUT AN EARLIER AGE OR
MORE FREQUENTLY IN:
● Individuals who display overweight tendencies, i.e.,
BMI ≥ 25 kg/m^2 (at-risk BMI may be lower in some
ethnic groups)
● Habitually physically active
● Strong family history of diabetes in a first degree
relative
○ Warrant earlier screening or testing for
diabetes mellitus
● When you have the symptoms, do not wait until
you are 45 years old in order to avoid
complications
● In a high-risk minority population
■ African American,
■ Latino, Native American,
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■ Asian American, and
■ Pacific Islander
History of gestational diabetes (GDM) or delivering a baby
weighing more than 9 lb (4.1 kg)
● Is possible due to pregnancy
Hypertension (blood pressure > 140.90 mm Hg)
Low high-density lipoprotein (HDL) cholesterol
concentrations (250 mg/dL (2.82 mmol/L)
● HDL is a good cholesterol, low values mean you
are at risk for possible diabetes
History of impaired fasting glucose/impaired glucose
tolerance
Women with polycystic ovarian syndrome (PCOS)
Other clinical conditions associated with insulin resistance
(e.g., severe obesity and acanthosis nigricans)
History of cardiovascular disease
All of these mentioned conditions and risk factors will
be considered for earlier testing/screening for
diabetes/prediabetes. If you fulfill one of the mentioned
population or risk factors, then you should be tested.
● In the absence of the above criteria, testing for
prediabetes and diabetes should begin at age
45 years or more
● If results are normal, testing should be repeated
at least at 3-year intervals, with consideration
of more frequent testing depending on initial
results and risk status (Layo na kaayo ang 3
years. Ideally if you can afford, test every year.)
● As the incidence of adolescent type 2 diabetes
has risen dramatically in the past few years,
criteria for the testing for type 2 diabetes in
asymptomatic children have been developed
○ Initiation of testing at the age 10 years
○ At the onset of puberty
○ If puberty occurs at a younger age
■ this is most likely because of
endocrine problem that can
predispose to diabetes
mellitus
○ with follow up testing every 2 years
NOTE: Adolescence can be diabetic therefore you have to
consider many factors specially genetic predisposition.
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 LEC 11 - INTRODUCTION TO GLUCOSE

CATEGORIES FOR THE RISK OF DEVELOPING DIABETES

CHARACTERISTICS
(Testing should be carried out on children who display the Individuals who did not meet the criteria of diabetes mellitus but who
have glucose levels above normal be placed into three categories for
following characteristics
the risk of developing diabetes:

Overweight
(BMI >85th percentile for Impaired fasting individuals with fasting glucose levels
age and sex, weight for glucose ≥ 100 mg/dL but <126 mg/dL
height more than 85th
percentile or weight more
than 120% of ideal for Impaired glucose individuals who have 2-hour OGTT levels
height) tolerance ≥ 140 mg/dL but <200 mg/dL

Family history of type 2 first - or second degree Third, at risk individuals with a HbA1c (glycosylated
diabetes relative category Hgb) of 5.7% to 6.4%

Race/ethnicity Native American, African Are referred to as having “prediabetes” indicating the relatively high
risk for the development of diabetes in these patients.
American, Latino. Asian
American, and Pacific
Islander This is a table (below) showing you the diagnostic criteria for DM. We
have already mentioned that (in Diagnosis).

Signs of insulin resistance Acanthosis nigricans,

or conditions associated hypertension, dyslipidemia,
with insulin resistance and PCOS TABLE 14-5. DIAGNOSTIC CRITERIA FOR DIABETES
MELLITUS

Maternal history of 1 HbA1c ≥ 6.5% using a method that is NGSP certified and
diabetes or GDM standardized to the DCCT assay
(gestational diabetes
mellitus)
2 Fasting plasma glucose ≥ 126 mg/dL (≥ 7.0 mmol/L)

3 Two-hour plasma glucose ≥ 200 mg/dL (≥ 11.1 mmol/L)

DIAGNOSIS during an OGTT
(four methods diagnosis of DM)

4 Random plasma glucose ≥ 200 mg/dL (≥ 11.1 mmol/L) plus

symptoms of diabetes
1 HbA1c (glycosylated hemoglobin) ≥ 6.5% using a National
Glycohemoglobin Standardization Program (NGSP) -
certified method
HbA1c, hemoglobin A1c; NGSP, National Glycohemoglobin
Standardization Program; OGTT, oral glucose tolerance test;
DCCT, Diabetes Control and Complications Trial
2 A fasting plasma glucose ≥ 126 mg/dL
In the absence of unequivocal hyperglycemia, these criteria
should be confirmed by repeat testing on a different day. The fourth
measure (OGTT) is not recommended for routine clinical use.
3 An OGTT with a 2-hour postload (75g glucose load) level ≥
200 mg/dL

Please take note of these criteria for the diagnosis of Diabetes

Mellitus.
4 Symptoms of diabetes plus a random plasma glucose level ≥
200 mg/dL

TABLE 14-6. CATEGORIES OF FASTING

● Each of which should be confirmed on a subsequent day PLASMA GLUCOSE
by any one of the first three methods
● Any of the first three methods are considered appropriate
for the diagnosis of diabetes Normal fasting FPG 70 - 99 mg/dL
glucose (3.9 - 5.5 mmol/L)
● The decision on which method to use is the decision of the
healthcare provider depending on various patient factors
Impaired fasting FPG 100 - 125 mg/dL
glucose (5.6 - 6.9 mmol/L)

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Provisional FPG ≥ 126 mg/dL One-Hour plasma ≥ 180 mg/ dL (10 mmol/L)
diabetes diagnosis (≥ 7.0 mmol/L) a glucose

FPG, fasting plasma glucose Two-hour plasma ≥ 153 mg/dL (8.5 mmol/L)
glucose
a
must be confirmed

Your fasting plasma glucose should be confirmed with the other Note: One-hour plasma glucose (after one hour of taking the oral
diagnostic criteria for DM glucose load); Two-hour plasma glucose (after two hours of taking the
oral glucose load). If you have these values, then you most likely have
DIAGNOSTIC CRITERIA FOR GESTATIONAL DIABETES Gestational Diabetes Mellitus.

● The diagnostic criteria for gestational diabetes were revised
by the International Association of the Diabetes and
Pregnancy study groups
● Recommend that all nondiabetic pregnant women should be
screened for GDM at 24 - 28 weeks of gestation
○ Screening and diagnosis is the performanceof a
2-hour OGTT using a 75 g glucose load
● Glucose measurement should be taken at:
○ fasting
○ 1 hour
○ 2 hours
(after taking the glucose load)
● Diagnostic of GDM if any of the three criteria are met:
○ Fasting plasma glucose value ≥ 92 mg/dL
(5.1mmol /L)
○ 1-hour value ≥ 180 mg/dL (10 mmol/L), or
○ 2-hour glucose value ≥ 153 mg/dL
(8.5 mmol/L)
● This test should be performed in the morning after an
overnight fast of at least 8 hours.
TREATMENT FOR DIABETES MELLITUS
● Based on treating primary cause
● Lowering of the blood glucose by either insulin
supplementation or oral hypoglycemic drugs can be done in
Type 1 and Type 2 Diabetes Mellitus.
● However, if the cause would be secondary to genetic
problems or other secondary causes (e.g., pancreatic
diseases, endocrine disorders), then you correct the primary
cause in order to correct the secondary Diabetes Mellitus.
GENETIC DEFECTS THAT CAN PRESENT WITH DIABETES MELLITUS
GLYCOGEN STORAGE DISEASES
● Result of the deficiency of a specific enzyme that causes an
alternation of glycogen metabolism
GLUCOSE-6-PHOSPHATASE DEFICIENCY TYPE 1

● Most common congenital form of glycogen storage

TABLE 14-7 CATEGORIES OF ORAL diseases
GLUCOSE TOLERANCE ○ aka Von Gierke disease
● Autosomal recessive disease
● Characterized by severe hypoglycemia that coincides with
metabolic acidosis, ketonemia, and elevated lactate and
alanine
Normal fasting Two- hour PG ≤ 140 mg/dL
● Hypoglycemia occurs because glycogen cannot be
glucose (≤7.8 mmol/L)
converted back to glucose by way of hepatic glycogenolysis
(because of the deficiency of G6P enzyme)
● Glycogen accumulation is irreversible
Impaired fasting Two-hour PG 140-199 mg/dL (7.8-11.1 ● Disease can be kept under control by avoiding the
glucose mmol/L) development of hypoglycemia
● Liver transplantation corrects the hypoglycemic condition
● Glycogen buildup is found in the liver, causing
hepatomegaly
Provisional Two-hour PG ≥ 200 mg/dL ● Patients usually have severe: (HHUG)
diabetes diagnosis (≥ 11.1 mmol/L) aq ○ Hypoglycemia
○ Hyperlipidemia
○ Increased uric acid or uricemia, and
PG, plasma glucose ○ Growth retardation
● Liver biopsy will show a positive glycogen stain
a
must be confirmed ○ Due to the accumulation of glycogen because
of a deficiency of the G6P enzyme that is
supposed to convert the glycogen back to
This should be confirmed with the other tests for Diabetes Mellitus. glucose via gluconeogenesis

OTHER ENZYME DEFECTS OR DEFICIENCIES THAT CAUSE

HYPOGLYCEMIA
TABLE 14-8 DIAGNOSTIC CRITERIA FOR
GESTATIONAL DIABETES
● Glycogen synthase
● Fructose-1,6-bisphosphatase
● Phosphoenolpyruvate carboxykinase, and
Fasting ≥ 92 mg/dL (5.1mmol/L) ● Pyruvate carboxylase
plasma glucose

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GLYCOGEN DEBRANCHER ENZYME DEFICIENCY For questions & suggestions,

you can message any of the batch reps on messenger:
● Does not cause hypoglycemia but does cause
hepatomegaly Khrysthl Khyll Loquere
Sevilla Luis
GALACTOSEMIA Mikaela Singco
● Cause of failure to thrive syndrome in infants
✧ HAPPY STUDYING, BATCH DAMIANOS! ✧
● Congenital deficiency of one of three enzymes involved in
galactose metabolism, resulting in increased levels of LABAN 2ND YEARS
galactose in plasma ♡

GALACTOSE-1-PHOSPHATE URIDYLTRANSFERASE
DEFICIENCY

● most common enzyme deficiency (cause of galactosemia)

● Because of inhibition of glycogenolysis
● Accompanied by diarrhea and vomiting
● Galactose - must be removed from diet to prevent the
development of irreversible complications
● If left untreated, the patient will develop mental retardation
and cataracts
● The disorder can be identified by measuring erythrocyte
galactose-1-phosphate uridyltransferase activity
● Laboratory findings include:
○ Hypoglycemia
○ Hyperbilirubinemia, and
○ Galactose accumulation in the blood, tissue,
and urine following milk ingestion

FRUCTOSE-1-PHOSPHATE ALDOLASE DEFICIENCY

● Causes nausea
● Caused by an increase in the release of insulin in response
to rapid absorption of nutrients after a meal or the rapid
secretion of insulin-releasing gastric factors

IDIOPATHIC POSTPRANDIAL HYPOGLYCEMIA

● Idiopathic postprandial hyperglycemia is a controversial
diagnosis that may be overused by hypoglycemia after
fructose ingestion
● Specific inborn errors of amino acid metabolism and
long-chain fatty acid oxidation are also responsible for
hypoglycemia
● There are also alimentary and Idiopathic hypoglycemia

Favorite Quote from the bible:

I can do all things through Christ who strengthens me.

- Philippians 4:13

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