Correlation between Fasting

Blood Sugar Level and HbA1C

Levels in Type 2 Diabetes
Mellitus Patients”
 CERTIFICATE

This is to certify that BHUBANYU BASU, has worked

satisfactorily and completed the summer project entitled ,
“Correlation between Fasting Blood Sugar Level and
HbA1C Levels in Type 2 Diabetes Mellitus Patients” ,
at Bharat Sevasram Sangha Kakdwip during April 2015
to October 2015.

Guide Swami Adhyatmananda

BSS Secretary , Kakdwip

West Bengal.
 ACKNOWLEDGEMENTS
Dedicated to the holy feet of Guru Maharaj

I express my deep sense of gratitude to

Swami Adhyatmananda secretary of
Bharat Sevasram Sangha , for his entire efforts in
helping me at every stage of this project and his
constant encouragement was a major contribution
towards the completion of this research work .

I wish to extend my sincere thanks to all the staff

members of Bharat Sevasram Sangha Kakdwip for
their cooperation.

Last but not the least I am highly grateful to my

parents and my friends for their sustained support,
which was more arduous than anticipated throughout
the duration of the work.

BHUBANYU BASU
 CONTENTS

1. ABSTRACT
2. INTRODUCTION
3. SYMPTOMS AND SIGNS
4. MTERIALS AND METHODS
5. RESULTS
6. DISCUSSION
7. CONCLUSION
Correlation between Fasting Blood Sugar Level and
HbA1C Levels in Type 2 Diabetes Mellitus Patients

ABSTRACT

Introduction: Diabetes Mellitus is one of the most

common endocrinal diseases in the world. Incidences of
this disease are increasing worldwide and this disease is
called disease of this millennium. This study was
undertaken to correlate fasting blood sugar level and
Glycosylated haemoglobin (HbA1C) level in patients with
diabetes mellitus.
Material and Methods: This study was a cross sectional
study conducted on 100 patients of diabetes mellitus in
Kakdwip area, under Bharat Sevasram Sangha. The
fasting blood sugar (FBS) levels and HbA1C levels were
performed and then correlated fasting blood sugar level .
There was a significant positive correlation between FBS
and HbA1C.
Results: This study demonstrated that HbA1C level was
increased in diabetics and it showed correlation with the
status of control of diabetes.
Conclusion: HbA1C showed stronger correlation with
FBS.
Keywords: Diabetes Mellitus (DM), Fasting Blood
Sugar (FBS), Glycosylated Haemoglobin (HbA1C).
INTRODUCTION

Diabetes Mellitus (DM) refers to a group of common

metabolic disorder that share the phenotype of
hyperglycaemia caused due to either deficiency of insulin
secretion or insulin resistance.1 Diabetes Mellitus is one
of the most common endocrinal Diseases in the world.
Incidences of this disease are increasing worldwide and
this disease is called disease of this millennium. The
worldwide prevalence of this disease has risen
dramatically over the past two decades, from an estimated
30 million in 1985 to 85 million in 2010 and 415 million
in 2017. India is thought to be capital for DM, the
incidences of this disease is 73 million in 2015.1
Diabetes mellitus is commonly associated with
abnormalities of carbohydrate metabolism, lipid
metabolism, insulin resistance etc.

A good control of DM is believed in diabetic individuals

when he can obtain levels of fasting and postprandial
blood glucose values as much close to those of the non-
diabetic as possible. This concept may be philosophically
correct but in actual practice difficult to obtain, and even
with quite good control of diabetes, fluctuations in blood
glucose level may be marked, not only from day to day
but even from hour to hour. As our aim of treatment is not
simply the control of blood glucose levels but to kept the
total metabolic state to as much normal as possible, the
study of hyperglycaemia has distinct limitations as a
marker for proper diabetic control.
Therefore, many investigations have been suggested to
look out for some other marker which could give us better
idea for proper metabolic control. The study of
Glycosylated haemoglobin (HbA1C) during last few years
has been found to be very helpful in this respect.

Diabetes mellitus (DM) is impaired insulin secretion and

variable degrees of peripheral insulin resistance leading
to hyperglycemia. Early symptoms are related to
hyperglycemia and include polydipsia, polyphagia,
polyuria, and blurred vision. Later complications include
vascular disease, peripheral neuropathy, nephropathy,
and predisposition to infection. Diagnosis is by
measuring plasma glucose. Treatment is diet, exercise,
and drugs that reduce glucose levels, including insulin
and oral antihyperglycemic drugs. Complications can be
delayed or prevented with adequate glycemic control;
heart disease remains the leading cause of mortality in
DM.

There are 2 main categories of diabetes mellitus—

type 1 and type 2, which can be distinguished by a
combination of features . Terms that describe the age
of onset (juvenile or adult) or type of treatment are no
longer accurate because of overlap in age groups and
treatments between disease types.

Type 2 diabetes

 Resistance to insulin

In type 2 diabetes mellitus (previously called adult-onset

or non– insulin-dependent), insulin secretion is
inadequate because patients have developed resistance
to insulin. Hepatic insulin resistance leads to an inability
to suppress hepatic glucose production, and
peripheral insulin resistance impairs peripheral glucose
uptake. This combination gives rise to fasting and
postprandial hyperglycemia. Often insulin levels are very
high, especially early in the disease. Later in the course
of the disease, insulin production may fall, further
exacerbating hyperglycemia.
The disease generally develops in adults and becomes
more common with increasing age; up to one third of
adults > age 65 have impaired glucose tolerance. In older
adults, plasma glucose levels reach higher levels after
eating than in younger adults, especially after meals with
high carbohydrate loads. Glucose levels also take longer
to return to normal, in part because of increased
accumulation of visceral and abdominal fat and
decreased muscle mass.
Type 2 DM is becoming increasingly common among
children as childhood obesity has become epidemic. Over
90% of adults with DM have type 2 disease. There are
clear genetic determinants, as evidenced by the high
prevalence of the disease within ethnic groups (especially
American Indians, Hispanics, and Asians) and in
relatives of people with the disease. Although several
genetic polymorphisms have been identified over the past
several years, no single gene responsible for the most
common forms of type 2 DM has been identified.
Pathogenesis is complex and incompletely understood.
Hyperglycemia develops when insulin secretion can no
longer compensate for insulin resistance.
Although insulin resistance is characteristic in people
with type 2 DM and those at risk of it, evidence also
exists for beta-cell dysfunction and
impaired insulin secretion, including impaired first-
phase insulin secretion in response to IV glucose
infusion, a loss of normally pulsatile insulin secretion, an
increase in proinsulin secretion signaling
impaired insulin processing, and an accumulation of islet
amyloid polypeptide (a protein normally secreted
with insulin). Hyperglycemia itself may
impair insulin secretion, because high glucose levels
desensitize beta cells, cause beta-cell dysfunction
(glucose toxicity), or both. These changes typically take
years to develop in the presence of insulin resistance.
Obesity and weight gain are important determinants
of insulin resistance in type 2 DM. They have some
genetic determinants but also reflect diet, exercise, and
lifestyle. An inability to suppress lipolysis in adipose
tissue increases plasma levels of free fatty acids that may
impair insulin-stimulated glucose transport and muscle
glycogen synthase activity. Adipose tissue also appears
to function as an endocrine organ, releasing multiple
factors (adipocytokines) that favorably (adiponectin) and
adversely (tumor necrosis factor-alpha, IL-6, leptin,
resistin) influence glucose metabolism. Intrauterine
growth restriction and low birth weight have also been
associated with insulin resistance in later life and may
reflect adverse prenatal environmental influences on
glucose metabolism.

Impaired glucose regulation (impaired glucose

tolerance, or impaired fasting glucose—see
table Diagnostic Criteria for Diabetes Mellitus and
Impaired Glucose Regulation ) is an intermediate,
possibly transitional, state between normal glucose
metabolism and diabetes mellitus that becomes more
common with aging. It is a significant risk factor for DM
and may be present for many years before onset of DM.
It is associated with an increased risk of cardiovascular
disease, but typical diabetic microvascular
complications are not very common (albuminuria and/or
retinopathy develop in 6 to 10%).

This study was undertaken to correlate between fasting

blood sugar level, HbA1C level and serum lipid levels in
type 2 diabetes mellitus.
Symptoms and Signs

The most common symptoms of diabetes mellitus are

those of hyperglycemia. The mild hyperglycemia of early
DM is often asymptomatic; therefore, diagnosis may be
delayed for many years. More significant hyperglycemia
causes glycosuria and thus an osmotic diuresis, leading to
urinary frequency, polyuria, and polydipsia that may
progress to orthostatic hypotension and dehydration.
Severe dehydration causes weakness, fatigue, and mental
status changes. Symptoms may come and go as plasma
glucose levels fluctuate. Polyphagia may accompany
symptoms of hyperglycemia but is not typically a
primary patient concern. Hyperglycemia can also cause
weight loss, nausea and vomiting, and blurred vision, and
it may predispose to bacterial or fungal infections.

Patients with type 2 DM may present with symptomatic

hyperglycemia but are often asymptomatic, and their
condition is detected only during routine testing.
In some patients, initial symptoms are those of diabetic
complications, suggesting that the disease has been
present for some time. In some patients, hyperosmolar
hyperglycemic state occurs initially, especially during a
period of stress or when glucose metabolism is further
impaired by drugs, such as corticosteroids.
Diagnosis

 Fasting plasma glucose (FPG) levels

 Glycosylated Hb (HbA1C)
 Sometimes oral glucose tolerance testing
Diabetes mellitus is indicated by typical symptoms and
signs and confirmed by measurement of plasma glucose
(1). Measurement after an 8- to 12-h fast (FPG) or 2 h
after ingestion of a concentrated glucose solution (oral
glucose tolerance testing [OGTT]) is best (see
table Diagnostic Criteria for Diabetes Mellitus and
Impaired Glucose Regulation ). OGTT is more sensitive
for diagnosing DM and impaired glucose tolerance but is
less convenient and reproducible than FPG. It is therefore
rarely used routinely, except for diagnosing gestational
diabetes and for research purposes.
In practice, diabetes mellitus or impaired fasting glucose
regulation is often diagnosed using random measures of
plasma glucose or of HbA1C. A random glucose
value > 200 mg/dL (> 11.1 mmol/L) may be diagnostic,
but values can be affected by recent meals and must be
confirmed by repeat testing; testing twice may not be
necessary in the presence of symptoms of diabetes.
HbA1C measurements reflect glucose levels over the
preceding 3 mo. HbA1C measurements are now included
in the diagnostic criteria for DM:
 HbA1C ≥ 6.5% = DM
 HbA1C 5.7 to 6.4% = prediabetes or at risk of DM

However, HbA1C values may be falsely high or low and

tests must be done in a certified clinical laboratory with
an assay that is certified and standardized to a reference
assay. Point-of-care HbA1C measurements should not be
used for diagnostic purposes, although they can be used
for monitoring DM control.
Urine glucose measurement, once commonly used, is no
longer used for diagnosis or monitoring because it is
neither sensitive nor specific.

Risk factors for type 2 diabetes include

 Age ≥ 45
 Overweight or obesity
 Sedentary lifestyle
 Family history of diabetes mellitus
  History of impaired glucose regulation
 Gestational diabetes mellitus or delivery of a baby >
4.1 kg
 History of hypertension
 Dyslipidemia (HDL cholesterol < 35 mg/dL [0.9
mmol/L] or triglyceride level > 250 mg/dL [2.8
mmol/L])
 History of cardiovascular disease
 Polycystic ovary syndrome
 Black, Hispanic, Asian American, or American
Indian ethnicity
People ≥ age 45 and all adults with additional risk factors
described above should be screened for DM with an FPG
level, HbA1C, or a 2-h value on a 75-g OGTT at least
once every 3 yr as long as plasma glucose measurements
are normal and at least annually if results reveal impaired
fasting glucose levels

TREATMENT
For type 2 DM, oral antihyperglycemics,
injectable glucagon-like peptide-1 (GLP-1) receptor
agonists, insulin, or a combination
MATERIAL AND METHODS

It was a cross sectional study conducted on 100 patients

of type 2 diabetes mellitus. Approval was taken by the
Ethical committee. Written informed consent was taken in
all patients. Detailed history and examination was done in
all patients who were having typical history suggestive of
diabetes and satisfied the inclusion criteria. Following
criteria were used for diagnosis of Diabetes (inclusion
criteria) and following were exclusion criteria:
1. Diagnostic criteria for diabetes mellitus:

FBS after at least 8 hours of fasting ≥ 126 mg/dl or

2 hours after meal plasma glucose level ≥ 200 mg/ dl
or
Glycosylated haemoglobin ≥ 6.5 % or
Symptoms of diabetes plus random blood glucose
concentration ≥ 200 mg/dl.

2. Exclusion criteria includes:

Patients with evidence of primary
hyperlipoproteinemia
Patients with secondary hyperproteinemia due to
endocrine diseases such as acromegaly, hypothyroidism,
cushing syndrome

Patients with nephrotic syndrome

Patients with liver diseases
Pregnancy
Patients of chronic kidney disease and on dialysis
Decompensated heart failure.
 RESULTS

GOD/POD methods were used for blood sugar

estimation. Method of used for estimation of glycosylated
haemoglobin (HbA1C) was High Performance Liquid
Chromatography (HPLC).
Age No. of %
group patients
(years)
40-49 25 25.0
50-59 18 18.0
60-69 31 31.0
70-79 21 21.0
≥ 80 5 5.0
Table-1: Age wise
distribution

Sex No. of %
patients
Male 47 47.0
Female 53 53.0
Table-2:Sex wise
distribution
Degree of Goo Fair Poo
control d r
No. of 27 30 53
cases
FBS Mea 104. 161. 202.
(mg n 09 0 50
/dl) S 11.9 22.9 43.7
. 6 7 2
D
.
S 0.36 0.81 0.95
.
E
.
Hb Mea 6.82 8.99 11.7
A1 n 4
C S 0.92 1.61 1.99
(%) .
D
.
S 0.02 0.05 0.04
.
E
.
Table-3: Showing levels of
FBS and HbA1C level in
 different groups according
to control of diabetes

DISCUSSION

In our study FBS level varies 86 mg/ dl to 310 mg/dl

with a mean level of 167.63 ± 54.53 mg/dl. Values of
HbA1C level was in range of 5.42% - 14.78% with a
mean level of 9.86±2.56. This increase in HbA1C level in
these patients was significant (P < 0.001).
Paulsen et al. (1976)8, Javid et al. (1978) studied
demonstrated similar type of results in their studies. Mean
fasting blood sugar level in diabetic patients with good
control was 104.09 mg/dl and level of HbA1C was
6.82%, while in fairly control, the FBS level was 161
mg/dl and level of HbA1C was 8.99% and in those with
poor control, the FBS was 202.50 mg/dl and level of
HbA1C was 11.74%. The P value (0.001) for FBS and
HbA1C between those three groups of diabetic patients
was highly significant. This shows that the level of
HbA1C in diabetic patients is linearly correlated with the
abnormal blood glucose level.
Same has been reported by various workers including
Gabbay et al. (1976)9 and Elkeles et al. (1978).10
Kennedy et al. (1979)11 found correlation between FBS
and HbA1C levels were satisfactory while Nabarro et al.
(1979)12 found correlation between HbA1C and FBS
were not satisfactory. However, in some individual cases,
there was no correlation between HbA1C and FBS.
Compagnucci et al. (1981)13 observed that during periods
of wide fluctuations in blood sugar, HbA1C level remains
nearly constant and in these patients measurement of
HbA1C is much more valuable in providing the
assessment of diabetic control not available from random
blood sugar measurements.
However, these levels were elevated in diabetics who
were in poor control as compared to well controlled
diabetics and also in obese male diabetics, although they
were in good control.
In our studied there was statistically significant direct
correlation between FBS level and Glycosylated
Hemoglobin level.
On comparison we found that HbA1C was definitely a
better marker of diabetic control as compared to FBS.
While correlation of HbA1C to serum cholesterol was
significant (r= 0.39, P < 0.02).
CONCLUSION

100 patients of diabetes mellitus were studied to

determine correlation between FBS level, HbA1C level
and serum lipid levels. In this study we observed that
mean value for FBS in diabetics was 167.63 mg/dl and
mean value of HbA1C were found to be raised in diabetic
patients and in this study it was 9.86%. In good control
group, FBS was 104.09 mg/dl and HbA1C level was
6.82%. In fairly controlled group, FBS was 161.0 mg/dl
and HbA1C level was 8.99%. In poorly controlled group,
FBS was 202.5 mg/dl and HbA1C level was 11.74%.
Analysis of some individual cases revealed discrepancy
between FBS and HbA1C level. However HbA1C
showed better correlation to status of diabetic control than
fasting blood sugar level. Both HbA1C and FBS showed
direct positive correlation .
Hence we conclude that HbA1C level was increased in
diabetics and it shows correlation with the status of
control of diabetes. HbA1C showed stronger correlation
with FBS.
REFERENCES

1. Harrison’s principles of internal medicine 20th edition:

page no. 2850-2851
2. Reimer F et al: Incidence of hyperlipoproteinemia in
patients with chemical and clinical diabetes. Klin
Wochenshr 1973; 51:973.
3. Ricketts HT. Derangement vascular disease in diabetes
Am J Med 1955;29:933.
4. Sharma D, Bansal BC nad Prakash C. Serum lipid
studies in insulin dependent diabetes below the age of
30 years. JIMA 1970;54:416.
5. Sosenko JM, Breslow JL and Miettinen OS.
Hyperglycemia and plasma lipid levels. A prospective
study of insulin dependent diabetic patients. New Eng J
Med 1980; 302:650.
6. Pietri A, Dunn FL and Raskin P. The effect of
improved diabetic control on plasma lipid and
lipoprotein level: a comparison of conventional therapy
and continuous subcutaneous insulin infusion. Diabetes
1980; 29:1001- 5.
7. Somogyi M. and Nelson. Determination of blood sugar.
J. Biochem. 19: 160, 1945.
8. Paulsen E.P.: Glycosylated haemoglobin in childhood
diabetes. Metabolism 1973;22: 269.
9. Gabbay K.H. Glycosylated haemoglobin and diabetic
control.(editorial) New.Engl.J.Med. 1976;295: 443.
10. Elkeles R.S., Wu J. and Hambley J. Glycosylated
haemoglobin, blood glucose and HDL-cholesterol in
insulin requiring diabetics. Lancet 1978;2: 547.
11. Kennedy L., Kandell T.W. and Merimee T.J. Serum
protein bound hexose in diabetes. The effect of
glycemic control. Diabetes 1979;28:1006.

1. Kennedy L., Kandell T.W. and Merimee T.J. Serum

protein bound hexose in diabetes. The effect of
glycemic control. Diabetes 1979;28:1006.
2. Nabarro J.D.N., Mustaffa B.E., Morris D. et al. Insulin
deficient diabetes. Diabetologia 1979;16:5.
3. Compagnucci P., Cartechni M.G., Bolli G. et al. The
importance of determining irreversible glycosylated
haemoglobin in diabetes. Diabetes 1981;30:607.
4. Dinesh kumar and Gupta N.N: Serum cholesterol,
phospholipids and betalipoproteins in untreated
diabetics. J.A.P.I. 1967;15:357.
5. Maleva I.J. A study of protein fractions and blood
lipoproteins in diabetes. Abs. W. Med. 1961;30:229.

1. Akeel bai-Yaqobi, Adnan al-Khafaji, Dheaa K. Alomar.

Thi-qui medic singh G and Kumar A al
journal(T.Q.M.J.) 2011;52:39-44.
2. Piia P., Simonen, Helena K. Gylling and Tatu A.,
Miettinen. Serum cholesterol level in diabetics. A.D.A.
2011.
3. Lopes-Virella M.F., Wohltmann H.J., Loadholt C.B.,
and Buse M.G. plasma lipids and lipoproteins in young
insulin dependent diabetic patients. Diabetologia
1981;21:216-23.
4. Peterson C.M., Koenig R.J., Jones R.L., Saudek C.D.
and Cerami A. Correlation of serum triglycerides levels
and glycosylated haemoglobin concentration in diabetes
mellitus. Diabetes 1977;26:507-509.
5. Gonen B. and Rubenstein A.H., Rochman H., Tancga
S.P. and Horwitz D.L. Glycosylated haemoglobin: an
indicator of the metabolic control of diabetic patients.
Lancet 1977;2:734-70.
6. Gabbay K.H., Hasty K., Breslow J.L., Ellison R.C.,
Bunn H.F. and Gallop P.M. Glycosylated haemoglobin
and long term blood glucose control in diabetes
mellitus.J.Clin.endocr.meta 1977;44:859.
7. Falko J.M., O Dorisio T.M. and Cataland S. Long term
improvement of HDL-cholesterol and cholesterol/HDL-
CH ratio in ambulatory type2 diabetics, treated using
subcutaneous insulin pump. Diabetes. 1981;30:280.
8. Samatha P, Venketeswarum and Siva Praboh. Journal
of clinical and diagnostic research 2012;4302:0012.