FACULTY OF NURSING AND ALLIED HEALTH SCIENCE

NBHS1212

BIOCHEMISTRY

BIOCHEMISTRY

Name: P.M.N. HARSHANI

Rg NO: OUM30068

Email: harshinimali1984@gmail.com

0772458580

Tutor’s name: Dr Rakitha Rathnaweera

Learning Centre: IIHS, walisara, Sri Lanka

May 2021

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 TABLE OF CONTENT

Introduction…………………………………………………………………….03

Question 01

1:1 Type 1 Diabetes……………………………………………………………05

1:2 long term treatment for diabetes type 1………………...………………….08

1:3 Effects of treatment for long term treatment………………………………10

Question 02

2:1 Hyperglycemia…………………………………………………………….11

2:2 Causes of hyperglycemia………………………………………………….11

2:3 Complications of hyperglycemia………………………………………….12

2:4 Relationship between hyperinsulinemia condition and hyperglycemia…...12

Question 03

3:1 What is glucosuria…………………………………………………………13

3:2 Causes for glucosuria………………………………………………………13

3:3 Signs and symptoms……………………………………………………….14

3:4 Explanation of patient’s dehydration situation related to glucosuria

condition……………………………………………………………………….14

Question 04

4:1 What is Kussmaul respiration……………………………………………...16

4:2 Metabolic acidosis…………………………………………………………17

4:3 Ketoacidosis with the relationship at an elevated glucose level…………..18

4:4 Effect of ketoacidosis on kidney…………………………………………..20

Question 05

5:1 what are ketone bodies……………………………………………………21

5:2 What is fatty acid oxidation……………………………………………….22

5:3 What is physiological stress………………………………………………23

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 INTRODUCTION

This assignment is a case study with a diabetic type 1 patient with complex medical conditions.
According to the scenario, I analyzed information 40 years old women with metabolic acidosis.
This assignment, mainly discussed Diabetes type 1, how to maintain long-term treatment,
metabolic acidosis, and related other medical conditions.

The objective of this assignment is to apply biochemistry knowledge to patient care. I believed
problem-solving skills, decision-making skills, and analysis skills are improved from doing
this assignment.

Scenario:

A 40 years old woman was brought to the hospital in a confused and disorientated state. She
has had type 1 diabetes for the last 24 years. The patient displayed signs of dehydration and
acidosis such as deep and rapid breathing (Kussmaul respiration). Her body temperature was
normal. Blood and urine test results show that she is positive for glucose and acetoacetate.

Negative for protein.

Readings Patient Reference Range

Glucose 414 mg/dl (23 mmol/l) (H) 70-99 (3.9 – 5.5)

Blood urea nitrogen (BUN) 8 mmol/l (H) 2.5 – 6.4

3-Hydroxybutyrate 350 mg/dl (H) 0-3

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HCO3- 12 mmol/I (L) 22 - 28

Na+ 136 mmol/l 138 - 150

K+ 5.3 mmol/l 3.5 – 5.0

Cl- 102 mmol/l 95 - 105

pH 7.1 (L) 7.35 – 7.45

H = High L = Low

A microscopic examination of the patient’s urine revealed a urinary tract infection (UTI).

Diagnosis: The patient is in a ketoacidosis condition that was caused by a urinary tract
infection (UTI).
Immediate treatment: The patient was rehydrated with normal saline given intravenously
(IV). She also was given insulin intravenously (IV). Blood glucose, ketone bodies, and
electrolytes were measured periodically. The patient was started on an antibiotic for her
urinary tract infection (UTI).

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Question 01

1:1 Diabetes type 1

The energy needed by our body is provided via carbohydrates, proteins, and fats which are the
main nutrients in our food. The most important of these nutrients, which are divided into the
smallest parts to be absorbed; is a simple sugar called glucose. Glucose is an important energy
source for all organs of the body, especially the brain. Cells use the glucose needed by the
hormone secreted by the pancreas gland behind the stomach. If this hormone, which is known
as insulin, cannot be made in the body, the foods taken cannot be used as energy. Diabetes
caused by an absolute deficiency of insulin hormone is called Type 1 diabetes. As can be seen
at any age, it often begins in childhood and youth. It is therefore also called juvenile diabetes.

The cause of type 1 diabetes is unknown, but it is believed to involve a combination of genetic
and environmental factors. The underlying mechanism involves an autoimmune destruction of
the insulin-producing beta cells in the pancreas. Recent studies suggest this autoimmune islet
destruction may be triggered by persistent enteroviral infections. Diabetes is diagnosed by
testing the level of sugar or glycated hemoglobin (HbA1C) in the blood. Type 1 diabetes can
be distinguished from type 2 by testing for the presence of autoantibodies.

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Causes of Type 1 diabetes

Type 1 diabetes is caused by the destruction of β-cells – the only cells in the body that produce
insulin – and the consequent progressive insulin deficiency. Without insulin, the body is unable
to respond effectively to increases in blood sugar and diabetics have persistent hyperglycemia.
In 70–90% of cases, β-cells are destroyed by someone's immune system, for reasons that are
not entirely clear. The best-studied components of this autoimmune response are β-cell-
targeted antibodies that begin to develop in the months or years before symptoms arise.
Typically someone will first develop antibodies against insulin or the protein GAD65, followed
eventually by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with more of
these antibodies, and who develop them earlier in life, are at higher risk for developing
symptomatic type 1 diabetes.

Various environmental risks have been studied in an attempt to understand what triggers β-
cell autoimmunity. Many aspects of environment and life history are associated with slight
increases in type 1 diabetes risk, however, the connection between each risk and diabetes often
remains unclear. Type 1 diabetes risk is slightly higher for children whose mothers are obese
or older than 35, or for children born by cesarean section. Similarly, a child's weight gain in
the first year of life, total weight, and BMI are associated with slightly increased type 1 diabetes
risk.[25] Some dietary habits have also been associated with type 1 diabetes risk, namely the
consumption of cow's milk and dietary sugar intake. Animal studies and some large human
studies have found small associations between type 1 diabetes risk and intake of gluten or fibre;
however, other large human studies have found no such association. Many potential
environmental triggers have been investigated in large human studies and found to be
unassociated with type 1 diabetes risk including duration of breastfeeding, time of introduction
of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and
maternal intake of omega-3 fatty acids.

Type 1 diabetes is partially caused by genetics, and family members of type 1 diabetics have a
higher risk of developing the disease themselves.

Some medicines can reduce insulin production or damage β cells, resulting in a disease that
resembles type 1 diabetes. The antiviral drug diagnosing triggers pancreas inflammation in 5
to 10% of those who take it, sometimes causing lasting β-cell damage.

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Signs and symptoms

• Polyuria
• Polydipsia
• Polypepsia
• Increased appetite
• Blurred vision
• Persistent fatigue
• Dry or flushed skin
• Loss of consciousness
• Coma

Diagnosis

Glycated hemoglobin (A1C) test. This blood test indicates your average blood sugar level for
the past two to three months. It measures the percentage of blood sugar attached to the oxygen-
carrying protein in red blood cells (hemoglobin). The higher your blood sugar levels, the more
hemoglobin you'll have with sugar attached. An A1C level of 6.5 percent or higher on two
separate tests indicates diabetes.

Random blood sugar test. A blood sample will be taken at a random time and may be
confirmed by repeat testing. Blood sugar values are expressed in milligrams per deciliter
(mg/dL) or millimoles per litre (mmol/L). Regardless of when you last ate, a random blood

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sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, especially when coupled
with any of the signs and symptoms of diabetes, such as frequent urination and extreme thirst.

Fasting blood sugar test. A blood sample will be taken after an overnight fast. A normal
fasting blood sugar level of less than 100 mg/dL (5.6 mmol/L). Prediabetes is considered a
fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L). If it's 126 mg/dL (7
mmol/L) or higher on two separate tests, you have diabetes.

1:2 long term treatment for diabetes type1

Treatment for type 1 diabetes includes:

Taking insulin
Carbohydrate, fat, and protein counting
Frequent blood sugar monitoring
Eating healthy foods
Exercising regularly and maintaining a healthy weight

The goal is to keep blood sugar levels as close to normal as possible to delay or prevent
complications. Generally, the goal is to keep daytime blood sugar levels before meals
between 80 and 130 mg/dL (4.44 to 7.2 mmol/L) and your after-meal numbers no higher
than 180 mg/dL (10 mmol/L) two hours after eating.

1) Insulin
Anyone who has type 1 diabetes needs lifelong insulin therapy.
Types of insulin are many and include:
Short-acting (regular) insulin
Rapid-acting insulin
Intermediate-acting (NPH) insulin
Long-acting insulin

Examples of short-acting (regular) insulin include Humulin R and Novolin R. Rapid-acting

insulin examples are insulin glulisine (Apidra), insulin lispro (Humalog), and Insulin

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 Aspart (Novolog). Long acting insulins include insulin glargine (Lantus, Toujeo Solostar),
insulin detemir (Levemir) and insulin degludec (Tresiba). Intermediate-acting insulins
include insulin NPH (Novolin N, Humulin N).

2) Other medications

Additional medications also may be prescribed for people with type 1 diabetes, such as:
High blood pressure medications. - Your doctor may prescribe angiotensin-converting
enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) to help keep your kidneys
healthy.
These medications are recommended for people with diabetes who have blood pressures above
140/90 millimetres of mercury (mm Hg).
Aspirin. -Your doctor may recommend you take a baby or regular aspirin daily to protect
your heart if your doctor feels you have an increased risk for a cardiovascular event, after
discussing with you the potential risk of bleeding.
Cholesterol-lowering drugs. - Cholesterol guidelines tend to be more aggressive for people
with diabetes because of the elevated risk of heart disease.

3)Blood sugar monitoring

Depending on what type of insulin therapy, one needs to check and record blood sugar levels
at least four times a day.
testing blood sugar levels before meals and snacks, before bed, before exercising or driving,
and if you suspect you have low blood sugar. Careful monitoring is the only way to make sure
that your blood sugar level remains within your target range — and more frequent monitoring
can lower A1C levels.
Even if you take insulin and eat on a rigid schedule, blood sugar levels can change
unpredictably. You'll learn how your blood sugar level changes in response to food, activity,
illness, medications, stress, hormonal changes, and alcohol.
Continuous glucose monitoring (CGM) is the newest way to monitor blood sugar levels and
may be especially helpful for preventing hypoglycemia. The devices have been shown to lower
A1C.

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 Continuous glucose monitors attach to the body using a fine needle just under the skin that
checks blood glucose levels every few minutes. CGM isn't yet considered as accurate as
standard blood sugar monitoring, so at this time it's still important to check your blood sugar
levels manually.

1) Healthy eating and monitoring carbohydrates

There's no such thing as a diabetes diet. However, it's important to centre your diet on
nutritious, low-fat, high-fibre foods such as:

• fruits
• Vegetables
• Grains

2) Physical activity
Everyone needs regular aerobic exercise, and people who have type 1 diabetes are no
exception. First, get your doctor's OK to exercise.

3) Artificial pancreas
In September 2016, the Food and Drug Administration approved the first artificial pancreas
for people with type 1 diabetes who are aged 14 and older. A second artificial pancreas was
approved in December 2019.

1:3 Effects of treatment for long term treatment

Hypoglycemia is the most common and most serious complication of insulin therapy. If a
patient has too much insulin, blood glucose can fall low enough to cause hypoglycemia.

Insulin resistance is frequently associated with increased lipid content in muscle and liver.
Insulin excess stimulates tissue lipid accumulation. To examine the effects of insulin and
improved glycemia on insulin sensitivity and intracellular lipids.

Fat necrosis may develop in people who regularly inject insulin. This condition causes a painful
lump to grow in the subcutaneous tissue, which is just below the skin’s surface.

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Insulin therapy had an increased risk of several complications. Such as;

heart attack, stroke, eye complications, and kidney problems.

Question 02

2:1 Definition of hyperglycemia

The term "hyperglycemia" is derived from the Greek hyper (high) + glykys (sweet/sugar) +
haima (blood). Hyperglycemia is blood glucose greater than 125 mg/dL while fasting and
greater than 180 mg/dL 2 hours postprandial. A patient has impaired glucose tolerance, or
pre-diabetes, with a fasting plasma glucose of 100 mg/dL to 125 mg/dL. A patient is termed
diabetic with a fasting blood glucose of greater than 125 mg/dL.

When hyperglycemia is left untreated, it can lead to many serious life-threatening

complications that include damage to the eye, kidneys, nerves, heart, and peripheral vascular
system. Thus, it is vital to manage hyperglycemia effectively and efficiently to prevent
complications of the disease and improve patient outcomes.

2:2 Cause of hyperglycemia

Factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose

utilization, and increased glucose production. Glucose homeostasis is a balance between
hepatic glucose production and peripheral glucose uptake and utilization. Insulin is the most
important regulator of glucose homeostasis.

The secondary causes of hyperglycemia include the following:

Destruction of the pancreas from chronic pancreatitis, hemochromatosis, pancreatic cancer,

and cystic fibrosis.

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Endocrine disorders that cause peripheral insulin resistance like Cushing syndrome,
acromegaly, and pheochromocytoma.

Use of medications like glucocorticoids, phenytoin, and estrogens.

Gestational diabetes is known to occur in 4% of all pregnancies and is primarily due to

decreased insulin sensitivity.

Total parental nutrition and dextrose infusion.

Reactive as seen postoperatively or in critically ill patients.

2:3 Complications of hyperglycemia

Emergency complication

• Diabetic ketoacidosis.

Long term complications

• Cardiovascular disease
• Nerve damage (Neuropathy)
• Kidney damage (Nephropathy)
• Damage to the blood vessel of the Retina (Retinopathy), leads to blindness, Cataract.
• Severe skin, teeth, and gum infections.
• Bone and joint problems.

2:4 Relationship between Hypoinsulinimic condition and Hyperglycemia.

According to the scenario A 40yrs old woman had type 1 diabetes and on admission her Blood
Glucose level was high. (414 mg/dl). Type 1 diabetes is a multisystem disease with both
biochemical and anatomic consequences. It is a chronic disease of carbohydrate, fat, and
protein metabolism caused by the lack of insulin, which results from the marked and
progressive inability the destruction of the beta cells in the pancreas. That results in a low level
in the bloodstream. It is called Hyperinsulinemia. Insulin is a hormone that helps control blood

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sugar levels. When high levels of blood glucose levels, insulin affects the blood glucose and
insulin helps move glucose into the cell.

Type 1 diabetes is characterized by absolute insulin deficiency. So, blood glucose levels
increased related to hyperinsulinemia. When a patent has hyperinsulinemia, blood glucose
cannot move into the cell and excess glucose in the blood. That is called hyperglycemia.

Question 03

3:1 What is Glucosuria?

Glucosuria is defined as Glucose passing from the urine. When there is too much glucose in
the blood, the kidneys may not be able to reabsorb it all. when this occurs, the body excretes
the glucose from the body through urine. It can identify from a blood urine test, result up to
250mg/dl.

3:2 Causes for glucosuria

• High sugar diet

• Diabetes mellitus; - The lack of insulin in the blood elevates the glucose level. The
excess blood glucose levels make it difficult for the kidneys to properly reabsorb the
glucose back into the bloodstream, leading to some excretion in the urine.
• Hyperthyroidism; -Overproduction of thyroid hormone can cause decreased absorption
of glucose that is leaked from the filtration and passed into the urine.
• Liver cirrhosis
• Pregnancy
• Raised intracranial pressure
• Emotions
• Wilson’s disease, heavy metal poisoning

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3:3 signs and symptoms

• Excessive hunger
• Excessive thirst
• Fatigue
• Unexplained weight loss
• High blood sugar level
• Renal pain and abdominal pain
• Difficulty in passing urine
• Frequent urination
• Infection and fever
• Slower healing of the wound

3:4 Explanation of patient’s dehydration situation related to glucosuria condition

Under normal circumstances, all of the glucose filtered by the kidneys is reabsorbed. When
Glucose levels reach 180mg/dl, the proximal tubular transport of glucose from the tubular
lumen into the renal interstitium becomes saturated, and further glucose reabsorption is no
longer possible. The glucose that remains in the renal tubules continues to travel, passing into
the distal nephron and, eventually, the urine, carrying water and electrolyte with it. Osmotic
diuresis results, causing a decrease in the body water. Due to the body’s loss of body water
volume, the patient was going dehydration situation.

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Question 04

4:1 what is Kussmaul respiration?

Kussmaul respiration is fast, deep breaths that occur in response to metabolic acidosis. When
the patient breathed in that condition, was fruity acid smell can present.

K- ketones

U- Uremia

S- Sepsis

S- Salicylates

A-Aldehydes

(U)

L- Lactic acidosis

what’s the mechanism behind Kussmaul respiration?

One of the most common causes of Kussmaul breathing is Diabetic Ketoacidosis. When the
body fails to produce enough insulin, is non-processing enough glucose into the cell, and
becomes extremely dehydrated, it begins to enter into survival mode, relying on fats rather than
carbohydrates for energy.

When fats are broken down, they release Ketones that accumulate in the blood and arise blood
acidity. There called Ketoacidosis and it is a serious condition. Blood gasses of the patient
show a low partial pressure of CO2 and in conjunction with low Bicarbonate, because of a

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forced increase in respiration rate. (blowing off the CO2) Base excess is servilely negative. The
patient feels an urge to breathe deeply, an “air hunger” and it appears almost involuntary.

Causes of Kussmaul respiration

• Diabetic Ketoacidosis
• Renal tubular acidosis
• Organ Failure (eg: Heart, Kidney, Liver)
• Cancer
• Toxins in the body
• Alcohol abuse
• Sepsis

Diagnosis

• Medical history
• Physical exam- Nausea and vomiting, Fruity smelling breath, extreme thirst
• Blood test- Arterial Blood Gas, Serum Electrolytes, Blood Glucose and Ketone, Blood
urea nitrogen, and creatinine
• Chest X-ray, CT scan in kidney

Treatment for the Kussmaul respiration

• IV insulin
• IV bicarbonate
• Diuretics
• Maintain fluid balance chart.
• Check Arterial blood gases

4:2 Metabolic acidosis

Metabolic acidosis is a condition in which there is too much acid in the body fluids. It can also
occur when the kidneys cannot remove enough acid from the body. There are several causes
of metabolic acidosis.

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 • Diabetic acidosis (diabetic ketoacidosis)
• Hyperchloremic acidosis- caused by the loss of too much NaHCO3 from the body,
which can happen with several diarrhea.
• Lactic acidosis
• Kidney disease
• Poisoning by Aspirin, Methanol
• Severe dehydration

Signs and symptoms

• Rapid breathing
• Very tried
• Confused
• Shock
• Death

4:3 Ketoacidosis with the relationship at an elevated glucose level

When the patient had type 1 diabetes, is a loss of insulin activity causes intracellular glucose
transfer to fail, leading to cellular starvation. This can occur with absolute or relative lack of
insulin production by pancreatic beta cells, loss or inactivity of insulin receptors at the cellular
level. Insulin promotes cellular uptake of glucose for energy by most cells in the body,
especially muscles, adipose tissues and the liver. In the absence of insulin, cells are not able to
take up and use glucose for energy. So, most cells in the body can use free fatty acids (FFAs)
as an energy source in the absence of glucose. Circulating FFAs are taken up by the liver for
triglyceride (TG) production as well as for the manufacture of Ketone bodies. When continued
that process, Ketone bodies are excess body fluids. It is called Ketoacidosis.

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 ADIPOCYTE

Triglycerides
FREE

CIRCULATION
Free fatty acids

–
Insulin
Free fatty
Ketoacids acids

Glucose

Glycogen
+

+
LIVER
Glucagon

Malonyl
coenzyme A

Acetoacetic acid

β-Hydroxybutyric acid

MITOCHONDRION

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(–) = inhibits (+) = favors

4:4 effect of ketoacidosis on kidney

A relative or absolute deficiency of insulin results in hyperglycemia. High serum glucose level
results in increased serum osmolality, resulting in a shift of water from the intracellular
compartment to the extracellular compartment. Increased osmolality also results in increased
thirst, and hence increased water intake. High glucose levels act as osmotic diuretic agents,
leading to extracellular volume depletion. The overall volume effect of hyperglycemia is
intracellular, interstitial, and intravascular dehydration.

Normally, insulin pushes glucose and potassium from the extracellular compartment to the
intracellular compartment. Lack of insulin, therefore, results in hyperglycemia and
hyperkalemia. An additional, minor role is played by the intracellular generation of ketoacids
and the resultant shift of potassium from the intracellular to the extracellular compartment.12
Some of this excess extracellular potassium is excreted through the urine along with the
osmotic diuresis. Insulin de iciency thus results in intracellular potassium deficit with higher
serum potassium levels. The net result is hyperkalemia with lower than normal total body
potassium.

Intracellular energy pathway shifts from carbohydrate-based to lipid-based metabolism. The

end-products of carbohydrate-based metabolism are carbon dioxide and water, which are easily
excreted by the lungs and kidneys. The end-products of lipid metabolism are keto-acids. Of
these ketoacids, acetone being highly volatile is excreted by the lungs. Non-volatile ketoacids
are dependent on effective kidney function for clearance. Generation of these ketoacids out-
paces the excretion, and thus results in accumulation, leading to ketoacidosis.

In summary, insulin deficiency among patients with normal kidney function results in
hyperglycemia, hyperkalemia with total body potassium deficit, ketoacidosis, and dehydration
at the cellular, interstitial and intravascular levels.

DKA is associated with hyperglycemic crisis and featured by metabolic acidosis, the
production of ketoacidosis, volume depletion and electrolyte imbalance. Due to glucose-
induced osmatic polyuria and even emesis, volume depletion is a major cause of acute kidney
injury in DKA patients.

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Question 5

5:1 What are Ketone Bodies?

Ketone bodies are produced by the liver and uses peripherally as an energy source when
glucose is not readily available. The two main Ketone bodies are Acetoacetate (AcAc) and 2
Beta-hydroxybutyrate, while acetone is the third and least abundant, ketone body.

Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty
acids by the liver. They are readily transported into tissues outside the liver when they are
converted into Acetyl CoA which then enters the citric acid cycle and is oxidized for energy.

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5:2 What is fatty acid oxidation

Fatty acid oxidation is the mitochondrial aerobic process of breaking down a fatty acid into
Acetyl-CoA units. Fatty acid moves in this pathway as CoA derivatives utilizing NAD and
FAD. Fatty acids are activated before oxidation, utilizing ATP in the presence of CoA-SH and
Acetyl-CoA synthesis. They are several types of fatty acid oxidations.

1. Beta oxidation of fatty acid

2. Alpha oxidation of fatty acid
3. Gamma oxidation of fatty acid

Beta oxidation of fatty acid is the major pathway of oxidation of fatty acid. It is the process in
which there is successive removal of two carbon fragments from the carboxyl end of fatty acid
and involves its Beta carbon. The process of Beta oxidation occurs in mitochondrial in most
organs in the body.

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What is the relationship with ketone bodies?

Ketone bodies are produced using acetyl-CoA derived from fatty acid Beta oxidation in the
lever under specific metabolic conditions. Fatty acids in the blood are converted to ketone
bodies when insulin is low, and the fatty acid concentration is high. Fatty acetyl-CoA is
transported into the liver mitochondria by the carnitine shuttle system.

What happens when the fatty acid oxidation is impaired?

Fatty acid oxidation is an important source of energy in periods of catabolic stress (fasting or
illness) Their oxidation produces acetyl-CoA, which supplies energy to other tissues when
glycogen stores are depleted. When impaired fatty acid oxidation can cause low blood sugar
and harmful substances to build up in the blood. Hypoglycemia as one major clinical sings in
all fatty acid oxidation defects occurs due to a reduced hepatic glucose output.

5:3 what is physiological stress?

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Physiological stress can be defined as any external or internal condition that challenges the
homeostasis of a cell or an organism. It can divide into three different aspects. There are:

1) Environmental stress
2) Intrinsic developmental stress
3) Aging

Ex: Starvation, noise, cold compressor, hemorrhage

What happens to ketone bodies and glucose during physiological stress

Ketone bodies are affected by physiological stress and increased concentrations of serum beta-
hydroxybutyrate. The increase in ketone bodies during stress in normal-weight subjects was
associated with an increase in ACTH, norepinephrine and epinephrine concentration.

When a person has physiological stress, hormones are released that increase blood sugar levels.
Cortisol and adrenaline are other primary hormones involved in it.

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