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Available online at ajdhs.com 

Asian Journal of Dental and Health 
Sciences 

Open Access to Dental and Medical Research 

Copyright  © 2023 The  Author(s): This is an open-access article distributed under the terms of the 
CC BY-NC 4.0 which permits unrestricted use, distribution, and reproduction in any medium for 

non-commercial use provided the original author and source are credited 
 

 

 

Evaluation of Biochemical Parameters of Patients with Type 2 Diabetes 
Mellitus Based on Age and Gender in Umuahia 

Godfrey Ogochukwu Ezema1, Ndukaku Yusuf Omeh1, Simeon Egbachukwu1, Ejiofor C. Agbo2, Adachukwu 
Pauline Ikeyi3 and Emmanuel Ifeanyi Obeagu4*  

1 Department of Biochemistry, Michael Okpara University of Agriculture, Umudike, Abia State, Nigeria. 
2 Department of Medical Laboratory Services, Federal Medical Centre, Umuahia, Abia State, Nigeria. 
3 Department of Science Technology, Institute of Management and Technology, Enugu, Nigeria. 
4 Department of Medical Laboratory Science, Kampala International University, Uganda. 

Article Info: 
_______________________________________________ 
Article History: 
Received 07 April 2022      
Reviewed  11 May 2023 
Accepted 27 May 2023 
Published 15 June 2023 

________________________________________________ 
Cite this article as:  

Ezema GO, Omeh NY, Egbachukwu S, Agbo EC, Ikeyi AP, 
Obeagu EI, Evaluation of Biochemical Parameters of 
Patients with Type 2 Diabetes Mellitus Based on Age 
and Gender in Umuahia, Asian Journal of Dental and 
Health Sciences. 2023; 3(2):32-36 

DOI: http://dx.doi.org/10.22270/ajdhs.v3i2.43         

____________________________________________
*Address for Correspondence:   

Emmanuel Ifeanyi Obeagu, Department of Medical 
Laboratory Science, Kampala International University, 
Uganda Email: emmanuelobeagu@yahoo.com   

Abstract 
________________________________________________________________________________________________________________ 

Diabetes mellitus is a major public health issue. The study was done to determine the changes in 
some biochemical parameters between type 2 diabetes mellitus patients and apparently healthy 
adults in Umuahia. The fasting blood glucose was significantly higher in females than in males in 
the diabetic   population. The table   revealed a significantly (P<0.05) higher levels of serum total 
cholesterol, trialytglycerol, LDL-cholesterol, in females than males, except low HDL cholesterol 
(P<0.05) compared to male matched patients. Glycated haemoglobin was significantly (P<0.05) 
higher in female than male. Creatinine was significantly (P<0.05) higher in male. Urea was also 
significantly (P<0.05) higher in female. Potassium was significantly (P<0.05) higher in females. 
Bicarbonate was significantly (P<0.05) lower in female.The study showed a significantly (P<0.05) 
higher levels of total cholesterol, trialyglycerol, LDL- cholesterol in patient’s aged between 57-
74years, except low HDL-cholesterol (P<0.05) compared to those aged between 40-56years.   
Fasting blood glucose and HbAIC were significantly (P<0.05) higher in age limit 57-74years than 
40-56years. Urea and creatinine were significantly (P<0.05) low in patients aged 57-74years 
when compared to age 40-56years.  However, HDL concentration was significantly (P<0.05) high 
in the 40-56years when compared to 57-74years.Elevated levels of triglyceride (TG), total 
cholesterol (TC), and glycated haemoglobin (Glyc.Hb) and reduced levels of HD.   

Keywords: Type 2 diabetes mellitus, lipid profile, kidney function, liver function, glycated 
haemoglobin, fasting blood sugar. 

 

INTRODUCTION 

Diabetes mellitus (DM) is a group of metabolic diseases 
characterized by high blood glucose. It is a carbohydrate 
metabolic disorder characterized by elevated blood glucose 1-4. 
Frequently it is a consequence of deficient insulin secretion, 
insensitivity or both 5. In 2013, the global estimate of diabetics 
was about 382 million, amounting to a prevalence of 8.3%. 
North America and the Caribbeans had the higher prevalence 
of 11% or 37 million people with diabetes, followed by the 
Middle East and North Africa with a prevalence of 9.2% or 35 
million diabetics 6. The incidence of known cases as reported 
is essentially the same for men and women except among the 
elderly and generally increases with age. The prevalence of 
diabetes rises from about 6% in people aged 45-64years to 
12% in those aged 65years and above 7. In the older group, 
more women than men are diagnosed with disease each year, 
with relatively higher risk in non-whites 8. Three million two 
hundred thousand diabetes related deaths are reported 
annually, 8,700 deaths per day or 6 deaths each minute 8.   

In the African continent, prevalence was estimated to be 3 
million in 1994 and 7.1 million in 2000. This figure is expected 
to rise by 2030 to 18.6 million 6. The prevalence of 23.4% was 
reported among oil workers in Port Harcourt Nigeria 9.  

Diabetes as one of the five leading causes of death in most 
countries poses financial implication on the sector and 
patients. World Health Organization (WHO) estimated that as 
at 2007 diabetes alone accounted for $215-375 billion on cost 
7.  

Diabetes mellitus can be classified into 3 broad groups namely; 
Type 1 diabetes mellitus (formally called insulin dependent 
diabetes mellitus, IDDM) characterized by lack of insulin 
production due to autoimmune destruction of pancreatic beta 
cells and constitute 5-10% of cases. Type 2 (formally called 
non-insulin dependent diabetes mellitus, NIDDM) is 
characterized by impaired insulin action which accounts for 
90-95% of diabetes mellitus 10. The third category gestational 
diabetes is a form of glucose intolerance during pregnancy 
which resolves after the mother has given birth 11. Diabetes 
can be associated with many complications. Nephropathy, 
neuropathy, retinopathy and cardiovascular diseases which 
are the most commonly encountered episodes 12. Type 2 
diabetes, the most common type is characterized by disorder 
of insulin resistance and insulin secretion, either of which may 
be the predominant feature. The important point is that 
insulin secretion does not cease when the disease develops 
but may be inadequate for the purpose for which it is secreted. 
There is usually too much glucose to be metabolized for the 
amount of insulin present.   

                       Open Access                                                                                                                                                                                                         Research Article                                          

http://jddtonline.info/
http://dx.doi.org/10.22270/ajdhs.v3i2.43
mailto:emmanuelobeagu@yahoo.com
https://crossmark.crossref.org/dialog/?doi=10.22270/ajdhs.v3i2.43&amp;domain=pdf
https://orcid.org/0000-0002-4538-0161


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 MATERIALS AND METHODS  

SAMPLE COLLECTION AND PROCESSING  

The blood samples were collected in the morning from 
subjects after overnight fasting from the left or right 
superficial vein of median cubital vein at cubital fossa by vein 
puncture. A tourniquet was applied at mid upper arm. The 
area of the suitable vein was cleansed with cotton wool soaked 
in 70% alcohol.   

 A ten-milliliter syringe with needle was used. Nine milliliters 
of blood samples were collected from both the diabetic 
patients and control subjects and dispensed into the separate 
test tubes. An aliquot (2ml) of each sample was taken into a 
fluoride oxalate test tube for fasting blood glucose. A volume 
(7ml) of each sample was taken into a plain test tube for 
electrolytes, urea and creatinine(S/E/U/Cr) and lipid profiles 
estimations. Each sample bottle was labeled with the 
subject’s/patient’s name, date and serial number, placed 
mouth up in a rack and stored in freezer until used.  

The blood samples for S/E/U/Cr and lipid profiles were 
allowed to clot at room temperature and centrifuged at 1,500 
revolutions per minute (rpm) for 5 minutes to separate the 
serum from whole blood.  

ESTIMATION OF PLASMA GLUCOSE   

Plasma glucose was estimated by the glucose oxidaze method 
described by Trinder (1969). The reagent kit used was 
manufactured by Randox Laboratories Limited Ardmore, 
Diamond Road, United Kingdom.  

PROCEDURE   

Test tubes were placed in a rack and labelled blank, standard, 
test and control respectively. One milliliter of glucose reagent 
was dispensed into each tube. Ten microliters each of distilled 
water, standard, plasma and control were dispensed into the 
respective tubes. The contents   of each tube were properly 
mixed and incubated for 10 minutes at room temperature. The 
absorbances of the standard, test and control were read on a 
spectrophotometer against a reagent blank at 540 nm within 
30 minutes.  

ESTIMATION OF GLYCATED HAEMOGLOBIN   

Glycated hemoglobin was measured using 
NyocardHbAlcboronate affinity assay method described by 
Jeppson et al. (2002). 

PROCEDURE   

 The reagent I (RI) was equilibrated at room temperature 
before use. Five micro liters (5ul) of whole blood was added to 
the test tube with 20ul RI/reagent. It was well- mixed and then 
incubated for 2 minutes. It was then mixed to obtain a 
homogenous suspension twenty-five micro liters (25ul) of the 
reaction mixture was applied to a test device (TD) by holding 
the pipette approximately 0.5cm above the test well. The 
content of the pipette was then emptied quickly into the 
middle of the test well. The reaction mixture was allowed to 
soak completely into the membrane. Twenty-five (25ul) 
microliters of the washing solution/reagent 2 mixture were 
applied to the test device (TD). The washing solution was also 
allowed to soak completely into the membrane by allowing it 
to stand for ten minutes. The test result was read within five 
minutes using the Nycocard Reader II.  

ESTIMATION OF SERUM SODIUM   

Serum sodium was estimated by colorimetric method of Henry 
et al. (1974). The reagent kit was manufactured by Obour 
Industrial Company, Cairo, Egypt.  

PROCEDURE   

Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter of 
sodium reagent was dispensed into each tube. Ten microliters 
(10ul) each of standard, serum and control was dispensed into 
the respective tubes. The contents of each tube were 
thoroughly mixed and incubated at room temperature for 5 
minutes and the absorbance of the Standard, test and control 
samples read against reagent blank on a spectrophotometer at 
630nm.    

 ESTIMATION OF SERUM POTASSIUM  

Serum potassium was estimated by the turbidimetrictetra 
pheylborate (TPB) method Hillman (1967). The reagent kit 
was manufactured by Obour industrial company, Cairo, Egypt.   

PROCEDURE    

 Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter of 
potassium reagent was dispensed into each tube. Twenty 
microlitres (20ul) of standard, sample and control were 
dispensed into the respective reaction tubes. The contents of 
each tube were thoroughly mixed and incubated at 370C for 
3minutes and their absorbances read against reagent blank at 
578nm.  

ESTIMATION OF SERUM CHLORIDE  

Serum chloride was estimated by the mercuric chloride 
method of Schonfeld [13].  The reagent kit was manufactured 
by Agape Diagnostics, Switzerland.   

PROCEDURE   

Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter of 
chloride reagent was dispensed into each tube. Tenmicrolitres 
(10ul) of standard, sample and control were dispensed into 
the respective reaction tubes. The contents of each were 
thoroughly mixed and incubated at 37 C for a minute and their 
absorbances read against reagent blank at 505nm.  

ESTIMATION OF SERUM BICARBONATE   

Serum bicarbonate was estimated by spectrophotometric 
method of Norris [14]. The reagent kit was manufactured by 
Chema Diagnostica Monsano-Italy.  

PROCEDURE  

Clean test tubes were placed in a rack and labeled blank, 
standard, test and control respectively. One milliliter of 
bicarbonate reagent was dispensed into each tube. Ten 
microlitres (10ul) each of water, standard, serum and control 
were dispensed into the respective reaction tubes. The 
contents of each tube were thoroughly mixed and incubated at 
37 C for 2 minutes.  

ESTIMATION OF SERUM CREATININE   

Serum creatinine was estimated by the buffered kinetic Jaffe 
reaction without deproteinization method of Bowers and 
Wong 15. The reagent kit was manufactured by  

Obour industrial company Cairo, Egypt.  

CREATININE   

Clean tubes were placed in a rack and labelled standard, test 
and control respectively. One milliliter of creatinine reagent 
was dispensed into each tube. One hundred microlitres  

(100uL) each of standard, test and control reagents were 
dispensed into the respective tubes. The contents of each tube 
were properly mixed. After 30 seconds, the respective 



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[34]                                                                                                                                                                                                   AJDHS.COM 

absorbances (AI) of the standard, test and control tubes were 
read. Exactly 2 minutes later, the absorbances (A2) of the 
standard, test and control tubes respectively were read again.   

A2-A1=A specimen or A standard  

ESTIMATION OF SERUM UREA  

 Serum urea was estimated by the urease method of 
Wheatherburn 16. The reagent kit was manufactured by Chema 
Diagnostica, Italy.  

PROCEDURE  

 Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter of urea 
reagent A was dispensed into each test tube. Ten microlitres  

(10uL) each of distilled water, standard, test control was 
dispensed into the respective tubes.  

The contents of each tube were thoroughly mixed and 
incubated at 370C for 5 minutes.   

Next, one milliliter of urea reagent B was dispensed into the 
each of the tubes.   

The contents were mixed and incubated at 370C for 5 minutes. 
The absorbances of the standard (AC), test(AX) and 
control(AV) were read against a reagent blank at 600nm.  

ESTIMATION OF SERUM CHOLESTEROL   

Serum cholesterol was estimated by the cholesterol oxidase 
peroxidase method of Arntz 17. The reagent kit was 
manufactured by Agape Diagnostics, Switzerland.  

PROCEDURE    

Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter (1ml) of 
cholesterol working reagent was dispensed into each tube. 
Ten microlitres (10ul) each of standard, test and control 
reagent was dispensed into the respective tubes.   

The contents were mixed and incubated for 5minutes at 37˚C. 
The absorbance of each tube was read at 540nm against a 
reagent blank.  

Cholesterol cone (mg/dl)= Absorbance of test or control   ×200    
Absorbance of standard                     

ESTIMATION OF SERUM TRIACYLGLYCEROL   

Serum triacylglycerol was estimated by the glycerol -3- 
phosphate oxidase-TOPS method of Schettler and 
Nussel(1975). The reagent kit was made by Agape Diagnostics, 
Switzerland.  

PROCEDURE    

Clean test tubes were placed in a rack and labelled blank, 
standard, test and control respectively. One milliliter (1ml) of 
triacylglycerol reagent was dispensed into each tube. Ten 
microliters(10ul) of standard, test and control reagents were 
dispensed into each tube mixed and incubated for 5 minutes at 
370C. Change in absorbance was measured at 546nm against a 
reagent blank for each sample.  

ESTIMATION OF HDL-CHOLESTEROL   

Serum HDL –Cholesterol was estimated by the precipitation. 
The reagent kit was made by Agape Diagnostics, Switzerland 

PROCEDURE    

1. Precipitation   

Clean test tube was placed in a rack and 30uL of HDL reagent 
and 30uL of test sample added to the tube. The content was 

mixed, well, allowed to stand for 10 minutes at room 
temperature, mixed again and centrifuged for 10 minutes at 
4000 rpm. After centrifugation, the clear supernatant was 
separated from the precipitate within one hour using a 
Pasteur pipette. HDL cholesterol concentration was 
determined using  

cholesterol reagent.   

2. HDL cholesterol determination  

Three clean test tubes were placed in a rack and labelled 
blank, standard, test and control respectively. One thousand 
microliters (1000uL) of cholesterol reagent were dispensed 
into each tube. Fifty mircoliters (50uL) of HDL standard and 
the HDL supernatant were dispensed into standard and test 
tubes respectively. The contents were mixed incubated for 5 
minutes at 37C. The absorbances of the standard and test 
samples were measured at 630nm against a reagent blank.   

STATISTICAL ANALYSIS   

The data generated were analyzed using statistical software 
SPSS version 16.0. Students t- test was used for analysis of 
difference between means for two groups at P<0.05 level of 
significance. Pearson correlations were conducted to 
determine associations among different variables.    

RESULT  

BIOCHEMICAL PARAMETERS BETWEEN MALES AND 
FEMALES 

In table 1, fasting blood glucose was significantly higher in 
females than in males in the diabetic   population. The table   
revealed a significantly (P<0.05) higher levels of serum total 
cholesterol, trialytglycerol, LDL-cholesterol, in females than 
males, except low HDL cholesterol (P<0.05) compared to male 
matched patients. Glycated haemoglobin was significantly 
(P<0.05) higher in female than male. Creatinine was 
significantly (P<0.05) higher in male. Urea was also 
significantly (P<0.05) higher in female. Potassium was 
significantly  

(P<0.05) higher in females. Bicarbonate was significantly 
(P<0.05) lower in female.  

Table 1: Comparing the biochemical parameters between 
males and females 

TREATMENTS MALE FEMALE 

Sodium 144.23±47.34 123.08±32.11 

FBS 129.54±10.73 133.71± 9.42 

Potassium  3.95 ± 5.71 4.53± 0.60 

Chloride 87.50± 9.58 90.33± 9.90 

Bicarbonate 21.50± 3.35 22.25± 3.19 

Urea 32.6923 ± 14.33532 29.1250 ± 14.02579 

Creatinine 0.85± 0.26 0..89± 0.21 

Total 
Cholesterol 

210.77±24.09 191.92±30.15 

High Density 
Lipoprotein 

41.62± 8.23 46.21± 14.26 

TG 134.54±21.99 140.08±26.02 

Glycated 
Haemoglobin 

6.54± 0.54 6.49± 0.64 

LDL 136.58±25.88 114.10±41.64 



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Table 2: Comparing of biochemical parameters between 
age ranges 57-74 years and 40- 56 years 

AGE 57 – 74 YEARS  40 – 56 YEARS 

Bicarbonate 21.86 ± 3.65 21.86 ± 2.8 

Sodium 128.92 ± 16. 28 132.24 ± 6.91 

Potassium  4.88 ± 0.70 4.70 ± 0.57 

Chloride 87.86 ± 11.02 89.06 ± 9.33 

FBS 160.38 ± 59.14 127.68 ± 27.89 

Urea 33.79 ± 20.48 30.72 ± 13.33 

Creatinine 0.93 ±0. 27 0.86 ±0. 24 

Cholesterol 205.58 ± 32.02 202.50 ± 33.74 

HDL 43.19 ± 11.45 45.43 ± 12.38 

TG 151.43 ± 35.29 146.11 ± 19.85 

HBA/C 6.64 ± 53 6.47 ± 0.61 

LDL 126.9429 ± 
38.82065 

124.9806 ± 
39.92871 

 

Table 2 showed a significantly (P<0.05) higher levels of total 
cholesterol, trialyglycerol, LDL- cholesterol in patient’s aged 
between 57-74years, except low HDL-cholesterol (P<0.05) 
compared to those aged between 40-56years.   

Fasting blood glucose and HbAIC were significantly (P<0.05) 
higher in age limit 57-74years than 40-56years. Urea and 
creatinine were significantly (P<0.05) low in patients aged 57-
74years when compared to age 40-56years.  However, HDL 
concentration was significantly (P<0.05) high in the 40-
56years when compared to 57-74years.  

Result for HbAIC showed an increase in 57-74years when 
compared to the 40-56years group.  

DISCUSSION  

In this study, fasting blood glucose was significantly higher in 
females than in males in the diabetic population. This may be 
as a result of the fact that after menopause, there is loss of 
ovarian function.  

This results in adverse changes in glucose and insulin 
metabolism 18. Nutrition may also be a contributory factor of 
higher glucose levels in females. Females have a higher body 
mass index than males.  The results revealed a significantly 
(P<0.05) higher levels of serum total cholesterol, 
triacylglycerol, LDL-cholesterol, in females than males, except 
low HDLcholesterol (P<0.05) compared to male matched 
patients. The higher prevalence of hyperlipidaemia in females 
was due to their higher body mass index. A number of changes 
occur in the lipid profile after menopause 19. Lack of estrogen 
is an essential factor in this mechanism. A part from 
maintaining friendly lipid profile, estrogen change vascular 
tone by increasing nitric oxide production.  Glycated 
haemoglobin was significantly (P<0.05) higher in female than 
male.  

Bicarbonate was significantly (P<0.05) lower in female and 
male. This may be due to hormonal changes which lead to 
increased cardiovascular risk 19.              

This study observed a significantly (P<0.05) higher levels of 
total cholesterol, trialyglycerol, LDL- cholesterol in patient’s 
aged between 57-74years, except low HDL-cholesterol 

(P<0.05) compared to those aged between 40-56years. This 
may be due to hormonal changes and aging.   

Fasting blood glucose and HbAIC were significantly (P<0.05) 
higher in age limit 5774years than 40-56years. The ensuing 
hyperglycernia lead to increase protein glycation hence high 
levels of glycated haemoglobin serum 20. The increased levels 
may be due to diminishing body function because of aging.   

Urea and creatinine were significantly (P<0.05) low in patients 
aged 57-74years when compared to age 40-56years. This can 
be attributed to the rapid break down of proteins during 
aging. Also, consulting the activity of muscle mass, the 
concentration of creatinine may be affected.   

Generally, in diabetic conditions, high level of cholesterols is 
observed. From the result obtain from this study, cholesterol 
concentration was significantly (P<0.05) higher in the 57-
74years group when compared to the 40-56years. This can be 
attributed to reduction in physical activity in aged patients 
and also the impairment in her to carry out its metabolic 
function during aging. TG and LDL were also high in the 57-74 
years when compared to the 40-56years and this corroborated 
on result for total cholesterol.   

However, HDL concentration was significantly (P<0.05) high 
in the 40-56years when compared to 57-74years. HDL has 
been reported to transport cholesterol, from the walls of the 
artery to the heart degradation. The increase in HDL in the 40-
56years group can be attributed to high physical activities and 
also proper functioning of the liver. Diabetic complication may 
increase as aging progresses.   

Result for HbAIC showed an increase in 57-74years when 
compared to the 40-56years group. As diabetes progresses, 
hyperlipidemia or hypercholesteronaemia may set in.  

Increase in cholesterol concentration is related to the onset of 
obesity.   

From the result of the study, cholesterol concentration was 
higher in the older patients. Obesity has been linked to the 
increase in HbAIC and this was ending net in our study.   

  Difference in electrolytes in the study can be attributed to the 
psychological change that is bond to occur during aging and 
also membrane disorder associated with aging.  

Diabetes is a group of conditions linked by an inability to 
produce enough insulin and/or to respond to insulin. This 
causes high blood glucose levels (hyperglycemia). Diabetes 
mellitus (DM) is a group of metabolic disorders characterized 
by a chronic hyperglycaemic condition resulting from defects 
in insulin secretion, insulin action or both. Permanent 
neonatal diabetes is caused by glucokinase deficiency, and is 
an inborn error of the glucose-insulin signaling pathway 8. The 
estimated worldwide prevalence of diabetes among adults in 
2010 was 285 million (6.4%) and this value is predicted to 
rise to around 439 million (7.7%) by 2030 11.  

The body tries to rid the blood of excess glucose by flushing it 
out of the system with increased urination. This process can 
cause dehydration and upset the body’s electrolyte balance as 
sodium, potassium is lost in the urine. The statistical result 
above (bar chart), compares the lipid profile and kidney 
function parameters in diabetic and normal patients. A sharp 
increase in fasting blood sugar is seen in diabetic patients (test 
group) compared with non-diabetic patients (control group).   

This is as a result of the body not being able to process 
glucose, the body’s primary energy source, effectively. 
Normally, after meal carbohydrates are broken down into 
glucose and other simple sugars. This causes blood glucose 
levels to rise and stimulates the pancreas to release insulin 



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[36]                                                                                                                                                                                                   AJDHS.COM 

into the blood stream. The basic effect of insulin lacks or 
insulin resistance on glucose metabolism is to prevent the 
efficient uptake and utilization of glucose by most cells of the 
body, except those of the brain 6.  

CONCLUSION 

Elevated levels of triglyceride (TG), total cholesterol (TC), and 
glycated haemoglobin (Glyc.Hb) and reduced levels of HDL 
with either normal or elevated levels of LDL compared with 
non-diabetic patients was noted.  

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