About Authors:
Samudrala Lahari
St.Peters Institute Of Pharmaceutical Sciences,
Kakatiya University
plushylahari@gmail.com
Abstract
Background: Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia and abnormalities in carbohydrate, fat and protein metabolism. It results from defects in insulin secretion, insulin sensitivity or both. Oxidative stress may play an important role in the itiology of diabetes and Diabetic complications. So, during Diabetes hyperglycemia causes increased production of free radical especially reactive oxygen species(ROS) for all tissues from glucose auto-oxidation and protein glycosylation.
METHODS: This is a prospective observational case-control study. Data were collected and venous blood samples were collected from the patients and centrifuged, estimating the parameters such as SOD, CAT, GPx. The statistical analysis was done.
RESULTS: A Total number of 70 patients were enrolled into the study, out of which 50 were grouped as Diabetic subjects and 20 were healthy human volunteers named as controls. SOD levels were normal in controls (mean 202.0±6.760). There was a significant decrease in SOD of diabetic patients(P<0.0001) compared to that of controls.CAT levels were normal in controls (mean 54.10±1.083). There was a significant decrease in CAT of diabetic patients (p<0.0001)compared to that of controls.GPx levels were normal in controls (mean 65.05±1.144). There was a significant decrease in GPx of diabetic patients(P<0.0001) compared to that of controls.
CONCLUSION: If ROS production overcomes the antioxidant defences of the cell, either because of abundant production of oxidants or depletion of antioxidant defences, many cellular components can be damaged. The key cellular targets are lipids, proteins and DNA. This leads to complications such as Microvascular and macrovascular complications like Nephropathy, Neuropathy, Retinopathy, Atherosclerosis, stroke and Cardiovascular disease. Need of this study is to determine the levels of antioxidants such as SOD, CAT, GPx in type II Diabetic patients. Low levels of antioxidants such as CAT, SOD, GPx are observed in Type II Diabetic patients where the administration of antioxidants supplements is needed for the patients and it merits the serious consideration to reduce the risk of future cardiovascular complications
REFERENCE ID: PHARMATUTOR-ART-2024
1. INTRODUCTION
1.1. DIABETES MELLITUS
“Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia and abnormalities in carbohydrate, fat and protein metabolism. It results from defects in insulin secretion, insulin sensitivity or both.”(Kangralkar et.al.,2010)
Type I DM accounts for up to 10% of diabetic cases. It generally attacks in the childhood and finally results from the destruction of pancreatic β-cells by immune system resulting in lack of insulin. Hyperglycemia occurs when 80% to 90% of β-cells are destroyed. The autoimmune process is mediated by macrophages and T-lymphocytes with autoantibodies to β-cell antigens. Type II DM accounts for 90% of diabetic cases and it is characterized by presence of both insulin resistance and insulin deficiency. Insulin resistance gets by the processes such as increased lipolysis and free fatty acid production, increased hepatic glucose production, decreased skeletal muscle uptake of glucose. Progression of β-cell dysfunction takes place. Risk factors of Type II DM are Age, Obesity, Physical Inactivity, Family history, Race, Gestational Diabetes, Polycystic Ovarian Syndrome, High Blood Pressure, Abnormal Cholesterol levels.(Desmond et.al.,2005)
When defects in glucose metabolizing activity there will be consistent efforts of the physiological system to correct the imbalance of metabolism by the endocrine system. A defect of such endocrine control exacerbates the metabolic disturbances and leads to primarily to hyperglycemia. Initially, it results with insulin resistance, which progress gradually with the passage of time. Prolonged exposure to elevated glucose induces both repeated acute changes in intracellular metabolism and long-term changes in the structure and function. Both type I and type II diabetes exhibit hyperglycemia as their hallmark.(Desmond et.al.,2005)
Secondary hyperinsulinism develops to counter it, but it too at one point of time fails to maintain glucose homeostasis resulting in glucose intolerance. In progress, β-cells fail to cope up with requirement and insulin secretion goes down. Hyperglycemia may develop and may be accompanied with glycosuria. These perturbations are accompanied with changes in a variety of biochemical processes and are exacerbated by overweight and obesity, altered lipid profile, degree of hyperglycaemia, smoking and genetic profile. In diabetes, oxidative stress impairs glucose uptake in muscle and fat and decreases insulin secretion from pancreatic β-islet cell failure with resulting insulin deficiency.(Maharajan et.al.,2008)
Type II diabetes encompasses 90% of diabetics and is characterized by insulin resistance and it is often accompanied by obesity and dyslipidemia. Gestational diabetes accounts for a small percentage of diabetes and usually resolves after delivery. However, patients who have had gestational diabetes are 50% more likely to develop overt diabetes within 10 years of diagnosis. Both type I and Type II diabetes increase the risk of complications such as microvascular and macrovascular complications.(Michael et.al.,2008)
Microvascular complications, focuses on dysfunction in capillary bed of tissues, and include the retinopathy, nephropathy and neuropathy that eventually affect nearly all patients with DM. Diabetic Retinopathy(DR) is major cause of adult blindness. Diabetic neuropathy(DN) which affects half of all diabetic patients, is themost common cause of nontraumatic amputations and diabetic nephropathy(DNf) is the major cause of end-stage renal disease. Macrovascular complications due to atherosclerosis remain the leading cause of death. Myocardial infarction, stroke, and pheripheral vascular disease are more prevalent in diabetic patients. Hyperglycemia, a characteristic feature of DM, predisposes to vascular complications, both microvascular and macrovascular and also an indicator of endothelial dysfunction.(Paulescu et.al.,2008)
1.2.OXIDATIVE STRESS
Oxidative stress may play an important role in the itiology of diabetes and Diabetic complications. So, during Diabetes hyperglycemia causes increased production of free radical especially reactive oxygen species(ROS) for all tissues from glucose auto-oxidation and protein glycosylation. These ROS are capable of chemically altering all major classes of biomolecules eg:lipids,proteins and nucleic acids by changing their structure and function thus leading to cell damage in Diabetes Mellitus. Diabetes is associated with several mechanisms, one of which is oxidative stress. Oxidative stress is a general term used to describe the imbalance between the production and manifestation of ROS and a biological system’s ability to ready detoxify or to repair the resulting damage. The imbalance may be due to either decrease production of antioxidants or excessive production of free radicals.(Fatmah et.al.,2012)
Oxidative stress(OS) is defined as the tissue damage resulting from an imbalance between an excessive generation of oxidant compounds (super oxide, hydrogen peroxide, alkoxy radical and hypochlorous acids etc) and insufficient anti?oxidant (vitamin E and C, N-acytyl cystein, L-arginine, Glutathione and GlutathioneS-transferase etc) defense mechanisms.(Ilaiah et.al.,2013)
Abnormality high levels of free radicals and the simultaneous decline of antioxidant defence mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation and development of insulin resistance. These all consequences of oxidative stress can promote the development of complications. Oxidative damage to unsaturated lipids is a well-established general mechanism for oxidative stress mediated cellular injury, and in addition to increased lipid peroxidation. The occurrence of lipid peroxidation causes considerable changes in the cell membrane. Evidence suggested that oxidative stress is increased in diabetes, because of excessive production of ROS and an impaired antioxidant defence mechanism. The important causes of cell malfunction are ROS induced membrane lipid peroxidation and the toxicity of generated fatty acids peroxides. Antioxidants can be defined as substances whose presence is relatively high in concentration and significantly inhibits the rate of oxidation of lipids, proteins, carbohydrates and DNA. Antioxidants such as uric acid, SOD and GSH act as potent electron donors. They convert reactive free radicals into inactive substances.(Natheer et.al., 2011)
Humans are exposed to many carcinogens, but the most significant may be the reactive species derived from the metabolism of oxygen and nitrogen known as ROS and RNS. The formation of ROS and RNS in the human body can cause oxidative damage to especially plasma membrane which may contribute to the development of Cancer, Cardiovascular diseases and other oxidative stress-mediated dysfunctions. ROS are a heterogenous group of molecules that are generated by mature myeloid cells during innate immune responses, and are also implicated in normal intracellular signaling. When phagocytes are activated, they produce ROS in high amounts enough to kill bacteria. On the other hand, leads to oxidative stress, loss of cell function, and ultimately to apoptosis or necrosis.(Ajay et.al.,2009)
ROS are produced by oxidative phosphorylation, NADPH, xanthine oxidase, the uncoupling of lipoxygenases, cytochrome P450 monooxygenases, and glucose autoxidation. Once formed, ROS deplete antioxidant defences, rendering the affected cells and tissues more susceptible to oxidative damage by reacting with lipids in cellular membranes, nucleotides in DNA, sulphydryl groups in proteins leading to changes in cellular structure and function.
Levels of ROS are under control by the protective actions of antioxidant enzymes and non-enzymatic antioxidants in normal and healthy cells. In Diabetes, excessive cellular levels of ROS are induced by hyperglycemia causing a major complication of DM.(Dana et.al.,2005)
1.2.1. Sources of oxidative stress
There are multiple sources of oxidative stress in diabetes including non enzymatic, enzymatic and mitochondrial pathway.
Non enzymatic sources of oxidative stress originate from the oxidative biochemistry of glucose. Hyperglycemia can directly cause increased ROS generation. Glucose can undergo autooxidation and generate hydroxyl radicals. In addition, glucose reacts with proteins in a non enzymatic manner leading to the formation of advanced glycation end products (AGE’s). ROS is generated at multiple steps during this process. In hyperglycemia, there is enhanced metabolism of glucose through the polyol pathway (sorbitol pathway), which also results in enhanced production of superoxides. Enzymatic sources of augmented generation of reactive species in diabetes include Nitrous Oxide Species(NOS), NAD(P)H oxidase and xanthine oxidase.
(Natheer et.al.,2011)
The mitochondrial respiratory chain represents the most powerful cellular source of oxidants in the body. Mitochondrial oxidants may exert deleterious effects and are thought to
contribute to neurodegenerative diseases. However, to date, there is no method available to determine their potential contribution to cellular pathology. The oxidant generation system is based on the inducible production of reactive oxygen species (ROS) via univalent reduction of molecular oxygen (O2) following exposure to appropriate stimuli, both polymorphonuclear neutrophils (PMNs) and monocyte– macrophages activate and increase their O2 consumption. The NADPH-oxidase enzyme system, which is bound to cellular membranes, reduces O2 to superoxide anion (O2−), which is highly unstable and, as soon as it is formed, is converted into hydrogen peroxide (H2O2). Both O2− and H2O2 are precursors for the production of more powerful oxidants. O2− interacts with nitric oxide (NO) to form highly reactive nitrogen species (nitrostative stress), while H2O2 reacts with intracellular iron to form hydroxyl radicals (OH−), that are heavily implicated in cell membrane lipid degradation, protein aggregation and DNA damage. Moreover, H2O2 is the substrate for myeloperoxidase (MPO) to produce the chlorinated oxidants. In the presence of Cl−, MPO converts H2O2 into hypochlorous acid (OCl−), a powerful compound capable of oxidizing a number of molecules, such as lipids, proteoglycans and other membranous or intracellular constituents, particularly the thiol groups of membrane proteins (chlorinative stress). In addition, it may react with endogenous amines to produce chloramines.(Natheer et.al.,2011)
1.2.2.Mechanisms for increased oxidative stress in diabetes:
1.2.2.1. Advanced glycation end products (AGEs):
AGEs are products of glycation and oxidation, which are increased with age, and at accelerated rate in diabetes. The formation of AGEs is an important biochemical abnormality that accompanies diabetes mellitus. AGEs initiate oxidative reactions that promote the formation of oxidized LDL. Interaction of AGEs with endothelial cells as well as other cells accumulating within the atherosclerotic plaque, such as mononuclear phagocytes and smooth muscle cells provides a mechanism to augment vascular dysfunction.
AGEs measurement is useful to evaluate diabetes complications and it is done in skin, serum and saliva of diabetic patients.(Natheer et.al.,2011)
1.2.2.2. Alteration in glutathione metabolism:
Reduced glutathione detoxify reactive oxygen species such as hydrogen peroxide and lipid peroxide directly or in a glutathione peroxidase (GPX) catalyzed mechanism. Glutathione reductase (GRD) catalyzes the NAD(P)H dependent reduction of oxidized glutathione.
Blood GSH was significantly decreased in different phases of type 2 diabetes mellitus such as: glucose intolerance and early hyperglycemia and poor glycemic control.Previous studies identified GSH activity in serum and saliva of patients with type 2 diabetes which was significantly low when compared with control group. This finding was explained on the basis that oxidative stress may consumes some naturally occurring local antioxidants such as reduced glutathione and this reflects the overwhelming adaptive response to the challenge of oxidative stress in the diabetic state with or without complications.(Natheer et.al.,2011)
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1.2.2.3. Impairment of SOD and catalase activity:
SOD and catalase are also major antioxidant enzymes, SOD exists in 3 different isoforms; Cu,Zn-SOD is mostly in the cytosol and dismutate superoxide to hydrogen peroxide, Extracellular SOD is found in the plasma and extracellular space and Mn-SOD is located in mitochondria.
Catalase is H2O2 decomposing enzyme mainly localized to peroxicomes or microperoxicomes. Superoxide may react with other reactive oxygen species such as Nitric Oxide to form highly toxic species such as peroxynitrite. The major reason for the decreased SOD activity is the glycosylation of Cu, Zn-SOD which has been shown to lead to enzyme inactivation both in vivo and in vitro. Increased free oxygen radicals by glycated proteins on SOD activity in diabetes which could lead to oral complications in diabetic patients. The previous studies have demonstrated an increase in the level of SOD in serum and saliva of diabetic patients, this increase could be due to the existance or increased free radicals production which could enhance the antioxidant defense system.(Natheer et.al.,2011)
1.2.2.4. Polyol Pathway:
The polyol pathway consists of two enzymes. The first enzyme, aldose reductase (AR), reduces glucose to sorbitol with the aid of its co-factor NADPH, and the second enzyme, sorbitol dehydrogenase (SDH), with its co-factor NAD+, converts sorbitol to fructose. In animal models, treatment with AR inhibitors (ARI) was shown to be effective in preventing the development of various diabetic complications, including cataract, neuropathy, and nephropathy. The possibility of determination of sorbitol and fructosamine in saliva has been studied in healthy volunteers and patients with diabetes.(Natheer et.al.,2011)
1.2.2.5. Lipid peroxidation and protein oxidation in diabetes:
Lipid peroxidation:Lipid peroxidation end-products very commonly detected by the measurement of thiobarbituric acid reactive substance (TBARS). The use of TBARS as an index of lipid peroxidation has been increased in plasma of diabetic patients.
Thiobarbituric acid reacting substances (TBARS) are produced during lipoperoxidation oxidative stress-induced damage of lipids and are, thus, a widely used marker of oxidative stress. However, they represent a heterogeneous group of compounds – best known is malondialdehyde (MDA). TBARS is associated with parodontopathies when measured directly in the injured gingival tissue. The previous studies have shown that TBARS can be found in measurable concentrations in saliva and that these levels are higher in patients with parodontopathies and their origin is unlikely to be plasma.
MDA levels are directly affected by sytemic oxidative stress, since MDA levels were also elevated in saliva of diabtetic patients without parodontopathies. The Studies have conducted on diabetic rats and reported an increase in salivary and serum MDA with variable antioxidant activity. Studies by Reznick et.al., and Astaneie et.al., have shown both salivary and serum antioxidants to increase depending on HbA1C levels and severity of diabetes.(Natheer et.al., 2011)
1.2.3.Oxidative stress markers
ROS compounds are highly reactive with half-life of only seconds; hence, their in vivo measurement to assess oxidative stress is generally not possible. Instead, lipids, proteins, carbohydrate, and nucleic acid have lifetimes ranging from hours to weeks after being modified by ROS, which makes them ideal markers of oxidative stress.For example during lipid peroxidation, unstable hydroperoxides, resulting from peroxyl radical?dependent chain reactions among unsaturated fatty acyl moieties, break down to smaller and more stable products, e.g. aldehydes, such as acrolein, malonyldialdehyde (MDA), 4?hydroxynonenal (HNE) or thiobarbituric acid?reactive substances (TBARS). F2?isoprostanes are primarily products of arachidonic acid oxidation and may serve as stable markers of free?radical attack of the cell membrane phospholipids in vivo. Furthermore, increased levels of advanced lipid oxidation end?products (ALEs) and the presence of specific antibodies directed against oxidized low?density lipoproteins (LDLs) may represent useful markers of enhanced oxidative stress.(Scott et.al.,2008)
1.2.3.1.Superoxide Dismutase (SOD)
The SOD family of enzymes catalyse the conversion of O2- into H2O2 and oxygen in the first step of the antioxidant pathway thereby performing an important role in the removal of O2-Three isoforms exists in humans, Cu/Zn-SOD (also known as SOD1), Mn- SOD (also known as SOD2) and SOD3 with distinct cellular localisation, namely cytosolic, mitochondrial and extracellular, respectively. Diabetes is associated with a decrease in SOD activity in most animal studies. Lowered SOD levels are reported in serum, and decreased SOD1 and SOD3 levels are suggested to play a key role in the pathogenesis of diabetic nephropathy.
The significance of SOD2 was revealed where the overexpression of mitochondrial-specific SOD targeted to the endothelium prevented diabetic retinopathy. Furthermore, the targeted overexpression of Mn-SOD significantly attenuated morphological changes in diabetic hearts and improved contractility in diabetic cardiomyocytes. Collectively, these studies show that targeted removal of .O2-, leads to improved outcomes in diabetic nephropathy and retinopathy.(Sih Min Tan et.al.,2011)
1.2.3.2.Catalase
Catalase is present mainly in the peroxisomes of mammalian cells as a tetrameric enzyme of four identically arranged subunits; each containing a haeme group and NADPH at its active centre. A role for catalase in the protection against atherosclerosis comes from the analysis of mice overexpressing catalase. In those experiments, overexpression of catalasesignificantly reduced the severity of lesions in ApoE-deficient mice. However, the role of catalase in diabetes is debatable; studies have shown that onset and progression of diabetes is accompanied by reductions in catalase activity, while others report an increase in the activity of catalase. More recently, mutations within the catalase gene have been suggested to contribute to the increased risk of diabetes .
However, other studies report no such association with catalase gene polymorphisms and the development of diabetic complications.For example, one study reported that blood catalase activity was lowered due to the down regulation of catalase synthesis, rather than specific catalase gene mutations in type 2 diabetic patients. This was also associated with increased H2O2 levels and dysfunctional insulin receptor signalling. (Sih Min Tan et.al.,2011)
1.2.3.3. Glutathione peroxidase
Pre-clinical and clinical evidence are now mounting in support of an important role for GPx in the protection against diseases such as atherosclerosis, both in a non-diabetic and a diabetic setting. The selenocysteine-containing GPx family of antioxidant enzymes attenuates oxidative stress by utilising GSH to reduce hydrogen and lipid peroxides to water and their corresponding alcohol. Additionally, GPx also functions to remove harmful ONOO-. Thus the major role for GPx in the protection against pathogenesis may reside in the fact that it is the only antioxidant enzyme that metabolises three major ROS, H2O2, lipid peroxide (LOOH) and ONOO-(Sih Min Tan et.al.,2011)
Different isoforms of GPx: GPx1, also known as cellular GPx, was first identified as an erythrocyte enzyme that protects haemoglobin from oxidative injury. Its ubiquitous expression in almost all tissues, together with its abundant expression in organs such as the kidney and liver have meant that this isoform is one of the most well-characterised of the GPx family. GPx2 is most prominent in the gastrointestinal tract and its role is mainly to protect intestinal epithelium from oxidative stress. GPx3 is secreted by the kidney and is the main source of plasma GPx; however GPx3 is also expressed in other tissues, for example in the heart. GPx4 reduces phospholipid hydroperoxides and is thought to play a protective role in oxidative stress-induced apoptosis, possibly through the mitochondrial death pathway.(Sih Min Tan et.al.,2011)
METHODOLOGY
Study site: This study was conducted in Out patient wards of Mahatma Gandhi Memorial (MGM) hospital and In Patients wards of Rohni hospital, Warangal. MGM hospital is a 1100 bed tertiary care teaching hospital under the Govt. of Andhra Pradesh located in Warangal, Andhra Pradesh. Rohini is a Super Speciality hospital, Hanamkonda, Warangal.
PHASE-I:
Step1. Study Design: This was a prospective observational case-control study.
Step2. Study Duration:The study was conducted over a period of eight months from January 2013 to August 2013.
Step3. Study Criteria:
Inclusion criteria:
- Patients with Type II DM at MGM hospital, Warangal.
- Patients of either sex aged 18 to 75 years.
- Patients willing to give the informed consent.
Exclusion criteria:
- Patients with Type I DM.
- Patients with pregnancy.
- Patients with chronic infections like HIV and TB.
Step4. Sources of data
The data including demographics, previous illness, past history, drug usage pattern, and details of patients were collected from the patients’ case notes, treatment chart, nurses notes, laboratory reports, out patient records, by interviewing patients and/or their care takers and healthcare professionals wherever necessary. All the collected data was documented in a suitably designed data collection form.
Step5. Ethical committee Approval
The protocol of the study including the introduction, objectives, data collection form and methodology was submitted to the Principal, Kakatiya Medical College, Warangal. After the agreement of ethical committee members, the study was approved by the Institutional Human Ethical Committee of MGM hospital, Warangal.
Step 6. Designing of Data Collection form
A suitable data collection form (Annexure I) was designed to collect, document and analyze the data. Informed consent section was also incorporated in the data collection form. Data collection form included the provision for collection of information related to demographic details of patients (name, age, sex, weight, contact details, address), diagnoses, medication usages before hospital admission and during the patients’ stay in wards, past medical history.
Step7. Study procedure:
All patients were reviewed intensively in the OP department. Those patients who met the study criteria were enrolled. The enrolled patients were reviewed from the first day. Demographic details of the patient, reason for admission, diagnosis, past medical and medication history, medications used at admission, were documented in the data collection form.
The patients history was carefully collected by gathering details like hypertension, shortness of breath, duration of problems, socio-economic status, marital status, representative area (Rural/Urban), mode of development of disease (diabetes, hypertension etc.,) were collected, documented and analyzed. Wherever required, assistance from the patient attendants, nurses and clinicians was obtained.
PHASE II
Step 1: Literature Survey
The literature supporting the study was collected and from different sources like Micromedex drug information databases, various websites like pubmed, science direct, DOAJ, Medline, Google scholaretc.
Step 2: Data collection: Data were collected from inpatients record available in department and Medical record department of the hospital, including the clinical characteristics such as nausea, vomiting, pedal Oedema, headache, dizziness, body temperature, blood pressure, pulse rate,etc.
Step 3: Sample Collection:Venous blood samples were collected from the patients after obtaining the Informed consent from the patient or the attendee. The samples were collected in 5 ml EDTA vials for serum. The samples were immediately centrifuged at 3000 rpm for 30 mins and upper layer is separated in labeled effendroff’s tubes and kept at 40C till biochemical analysis.
ESTIMATION OF PARAMETERS:
I) Superoxide Dismutase assay: The activity of SOD was measured at 500nm with a commercially available kit (Sura Labs ) by testing the inhibition degree of a tetrazolium salt oxidation reaction. The results were expressed in graphs.
Procedure: Standard kits were taken so as to prepare standard concentrations for the concentration of standard graph. Test samples were placed in the instrument by using instrument cells supplied by the instrument manufacturer. Test samples were observed for their respective concentrations of antioxidants.
Normal Values: SOD : 170-240µg/dl.
II) Glutathione Peroxidase Assay: The activity of GPx was measured with a commercially available kit (Sura Labs) by measuring the decrease of NADPH absorbance. GPx content was estimated spectrophotometrically at 412nm.
Procedure: Standard kits were taken so as to prepare standard concentrations for the concentration of standard graph. Test samples were placed in the instrument by using instrument cells supplied by the instrument manufacturer. Test samples were observed for their respective concentrations of antioxidants.
Normal Values : GPx : 64.4µg/dl.
III) Catalase Assay: The activity of serum catalase was determined by using the commercially available kit (Sura Labs). Catalase content was estimated spectrophotometrically.
Procedure: Standard kits were taken so as to prepare standard concentrations for the concentration of standard graph. Test samples
were placed in the instrument by using instrument cells supplied by the instrument manufacturer. Test samples were observed for their respective concentrations of antioxidants.
Normal Values: CAT : 50 - 60µg/dl.
STATISTICALANALYSIS:
The results were expressed in mean ± standard deviation(SD).P<0.0001 was considered to be statistically significant. Statistical analysis was performed using Graph pad PRISM version 6.03.
Independent sample t-test was used to compare mean values.
Results
A Total number of 70 patients were enrolled into the study, out of which 50 were grouped as Diabetic subjects and 20 were healthy human volunteers named as controls. Among 50 diabetic treated patients 23 were males and 27 were females.
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Table 1: Number of DIABETIC PATIENTS with gender difference
|
Males |
Females |
Total |
|||
|
No. of Patients |
% |
No. of Patients |
% |
No. of Patients |
% |
|
23 |
46% |
27 |
54% |
50 |
100 |
Table 2 : Distribution of DiABETIC patients in different age groups
|
Age group in years |
Number of Patients |
||
|
Male |
Female |
Total |
|
|
30-40 |
3 |
5 |
08 |
|
41-50 |
5 |
3 |
08 |
|
51-60 |
6 |
7 |
13 |
|
61-70 |
9 |
2 |
06 |
|
71-80 |
4 |
2 |
06 |
Distribution of DIABETIC PATIENTS in different Age group:
Table 3: HbA1C LEVELS of DIABETIC SUBJECTS.
HbA1c levels were significantly higher in diabetic patients when compared with controls.
|
HbA1C RANGE |
Number of Patients |
||
|
Male |
Female |
Total |
|
|
5-7 |
5 |
5 |
10 |
|
7-9 |
10 |
10 |
20 |
|
9-11 |
5 |
8 |
13 |
|
11-13 |
3 |
4 |
07 |
|
TOTAL |
23 |
27 |
50 |
Table 4: HbA1C LEVELS IN CONTROLS
|
HbA1C RANGE |
Number of Patients |
||
|
Male |
Female |
Total |
|
|
5-7 |
7 |
10 |
17 |
|
7-9 |
1 |
2 |
3 |
|
9-11 |
0 |
0 |
00 |
|
11-13 |
0 |
0 |
00 |
|
TOTAL |
8 |
12 |
20 |
SOD: One of the parameters estimated to assess the antioxidant status was SOD. These SOD levels were normal in controls (mean 202.0±6.760). There was a significant decrease in SOD of diabetic patients(P<0.0001) compared to that of controls.
The levels of SOD in diabetic cases and controls were compared and were shown below.
Table 5 : MEAN VALUES OF SOD IN CASES AND CONTROLS:
|
SNO |
Test group |
Total SOD |
|
1 |
controls |
202.0±6.760 |
|
2 |
cases |
13.57±1.073 |
Comparision of SOD levels between Diabetic subjects and controls
CAT: The second parameter estimated to assess the antioxidant status was CAT. These levels were normal in controls (mean 54.10±1.083).
There was a significant decrease in CAT of diabetic patients(p<0.0001)compared to that of controls.
Table 6:The levels of CAT in cases and controls:
|
SNO |
Test group |
Total SOD |
|
1 |
controls |
54.10 ± 1.083 |
|
2 |
cases |
15.80 ± 1.207 |
Comparision of CAT levels between Diabetic subjects and controls.
GPx:The third parameter estimated to assess the antioxidant status was GPx. These levels were normal in controls (mean 65.05±1.144). There was a significant decrease in GPx of diabetic patients(P<0.0001) compared to that of controls.
Table 7: Mean values of GPx in cases and controls:
|
SNO |
Test group |
Total GPx |
|
1 |
controls |
65.05 ± 1.144 |
|
2 |
cases |
11.22± 0.7408 |
Comparision of GPx levels between Diabetic subjects and controls
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