• Users Online: 292
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 15  |  Issue : 3  |  Page : 448-453

Evaluation of dyslipidemia and oxidative stress in type II diabetes patients


Department of Biochemistry, Santosh Medical College and Hospital, Ghaziabad, Uttar Pradesh, India

Date of Submission14-Sep-2020
Date of Decision25-Sep-2020
Date of Acceptance30-Sep-2020
Date of Web Publication1-Feb-2021

Correspondence Address:
Dr. Preeti Sharma
Department of Biochemistry, Santosh Medical College and Hospital, Ghaziabad - 201 009, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_366_20

Rights and Permissions
  Abstract 


Background: Diabetes mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia associated with impairment in the metabolism of carbohydrate, lipids, and proteins. The most common endocrine and metabolic disease in the world is Type II DM. Elevated glucose levels characterize a complicated combination of genes and environmental influences, contributing to decreased insulin secretions or resistance. Materials and Methods: This observational, case-control study was conducted in the Department of Biochemistry, Santosh Medical College and Hospital, Ghaziabad in collaboration with the Department of Medicine during the period from November 2016 to July 2018. A total of 316 subjects between the age of 30 and 60 years were enrolled in the study and they were divided into two groups-Cases: One hundred and fifty eighty Type-II diabetic patients and Controls: One hundred and fifty eighty healthy adults volunteers. Results: The mean age of Type 2 diabetic subjects had higher 44.52 ± 8.17 years and in 40.20 ± 7.42 years for healthy controls. Similarly, the mean body mass index of the Type II Diabetes subjects was higher 25.28 ± 2.55 as compared to 23.07 ± 1.49 healthy controls. Large changes have been observed in fasting blood sugar, Glycated Haemoglobin (HbA1c), and total cholesterol (TC), along with triglycerides. Low-density lipoprotein cholesterol (LDL-C) was also elevated, along with very low-density lipoprotein cholesterol (VLDL-C) and Malondialdehyde (MDA). With TG, LDL-C, and VLDL-C, fasting blood glucose with TC shows a favorable correlation between MDA and negative interaction with high-density lipoprotein cholesterol. Good interaction of MDA with HbA1c. Conclusion: Increased blood glucose levels lead to the generation of oxygen free radicals and decreased levels of antioxidants, which causes erythrocyte fragility in type 2 diabetes. As a step for the prevention of vascular complications along with macrovascular problems in Type II Diabetes subjects, early detection of dyslipidemia and oxidative stress may be used.

Keywords: Dyslipidemia, Oxidative stress, Malondialdehyde and type II diabetes


How to cite this article:
Yadav MK, Kumar P, Sharma P, Mohapatra TK. Evaluation of dyslipidemia and oxidative stress in type II diabetes patients. J Datta Meghe Inst Med Sci Univ 2020;15:448-53

How to cite this URL:
Yadav MK, Kumar P, Sharma P, Mohapatra TK. Evaluation of dyslipidemia and oxidative stress in type II diabetes patients. J Datta Meghe Inst Med Sci Univ [serial online] 2020 [cited 2021 Mar 4];15:448-53. Available from: http://www.journaldmims.com/text.asp?2020/15/3/448/308568




  Introduction Top


Diabetes mellitus (DM) is one of the main chronic health conditions of the 21st century. Between the worldwide population, 425 million people and 352.1 million people are estimated to have diabetes and impaired tolerance test for glucose, respectively. Prediabetes or impaired glucose in fasting is midway between normal glucose levels and diabetes diagnostic levels.[1] Prediabetes is also associated with central obesity, dyslipidemia, and hypertension.[2] According to an ICMR-INDIAB study, prediabetes was 10.3%.[3] Owing to the diagnostic reliance of patients on blood glucose tests, hyperglycemia is an evident characteristic of diabetes.[4] However, plenty of the populations could also bear unnoticed hyperlipidemia, marked by higher triglycerides (TG) levels, along with low density lipoprotein cholesterol (LDL-C) against lower high-density lipoprotein cholesterol (HDL-C).[5] Dyslipidemia is often coupled with diabetes, and is really the primary cause for atherosclerosis. It is interpreted as a lipid triad, which involves the survival of small but dense, sdLDL, lower HDL, and higher TG.[6],[7],[8] A commonly used predictor for sugar control in the long-term is the glycated hemoglobin (HbA1c). In conjunction with its role as a predictor for the mean blood glucose level, HbA1c forecasts the risk for the occurrence of diabetic complications in diabetes patients.[9],[10] Apart from classical risk factors like dyslipidemia, exceedingly high HbA1c has now been regarded as an autonomous threat for vascular disease in cardiac patients.[11] Studies in man have also demonstrated increased MDA with progressive hyperlipidemia.[12] Studies also reported that the induction of acute hyperlipidemia increases the oxidative stress marker.[13] Oxidative stress is the equilibrium between the generation and elimination of reactive oxygen species (ROS). In healthy conditions, cellular antioxidant enzymes are responsible for the regulation of ROS productions.[14] Because of the unique molecular structure, lipids are more vulnerable to oxidation. Malondialdehyde (MDA) is produced through peroxidation of polyunsaturated fatty acids, and it is atherogenic.[15] As? TBARS (ThioBarbituric Acid Reactive Substances), MDA is commonly used in Type II Diabetes patients to assess the prooxidant/antioxidant balance as they are safe and readily visible items for lipid peroxidation. Hyperactivity of the hezosamine pathway, increased transfer of glucose in polyol path, and further generates of advanced glycation end products within the cell[16] are some pathways involved in inducing oxidative stress in diabetes. Several studies have identified high oxidative stress and antioxidant defense in people who metabolize glucose differently.[17],[18] We also investigated the relationship between fasting blood glucose (FBG), glycated hemoglobin, serum lipid profile, and MDA in people with Type II diabetes in this current review.


  Materials and Methods Top


Study design

An observational, case-control study.

Study setting

Department of Biochemistry, Santosh Medical College and Hospital, Ghaziabad in collaboration with Department of Medicine during the period from November 2016 to July 2018.

Sample size

Total 316 subjects between the age of 30 and 60 years were enrolled in the study and they were divided into two groups:

Cases: One hundred and fifty eight Type-II diabetic patients

Controls: One hundred and fifty eight healthy adults volunteers.

Sample size calculation

SS = Z2 × (p) × (1 - P)/c2

Where,

SS = sample size.

Z = Z-value A (e.g.; 1.96 for a 5% level of significance).

P = Prevalence percentage of population, expressed as decimal.

C = Precision or margin of error, expressed as decimal (0.05).

Sampling technique

Convenience sampling was used to enrol cases from Type II diabetic patients attending outpatient department (OPD) who fit into the inclusion and exclusion criteria. Healthy volunteers among hospital staff and persons accompanying patients were included as controls.

Source of data

All the Type-2 diabetic subjects attending OPD in the Department of Medicine at Santosh Medical College and Hospital, Ghaziabad, Uttar Pradesh, India were included in the study till the desired sample size was reached. All the ethical measures were taken from the respected Institution. The written consent of the patient was also taken before starting the study. A record of clinical history and family history were compiled in a Performa. A Performa containing the relevant findings of clinical, biochemical, and physical investigations were recorded on preset questionnaire as baseline record.

Inclusion criteria:

  • Patients with type II DM.


Exclusion criteria

Other endocrinological problems, infectious illnesses, malignancies, other environmental conditions, patients with a history of cerebrovascular accidents or patients with myocardial infarction. All the parameters under investigation were determined in the serum of the subjects using commercially available reagent kits. The suggestions of the National Cholesterol Education Program and also of Adult Treatment Panel III were considered for serum lipid reference level. As per guidance, total cholesterol (TC) was reported to be > 200 mg/dl, LDL-C to > 100 mg/dl, high TG to > 50 mg/dl and low HDL-C to < 40 mg/dl. Dyslipidemia is noticeable by the appearance of abnormal serum lipids. Fasting glucose and lipid profile values were given in mg/dl, while all MDA values were given in nmol/ml.

Sample collection and biochemical analysis

Ten ml of venipuncture blood sample was drawn under aseptic conditions. Two h post prandial blood was also collected. Sample was allowed to stand at room temperature for 3 min for clotting. Then serum was separated by centrifugation at 3000 rpm for 5 min. The following parameters were estimated:

  1. Fasting Glucose (serum) by Glucose oxidase-peroxidase methods[19]
  2. HbA1c by cation exchange methods[20]
  3. Cholesterol by? Cholesterol Oxidase-presence of peroxides enzymatic endpoint methods[21]
  4. TG by enzyme-mediated glycerol phosphate oxidase/peroxidase method[22]
  5. By direct enzymatic end point process, HDL-C[23],[24]
  6. Friedewald's Formula's LDL-C[25]
  7. Friedewald 's Equation: LDL-C = TC-HDL-C (TG/5)
  8. MDA by Thobarbituric acid reactive substances (TBARS) Kei Satoh method.[26]


Statistical analysis

The results were expressed as mean ± standard deviation (SD) values. Data analysis was performed with Microsoft Excel. The statistical differences between cases and controls were determined by student independent sample t-test, and Pearson's correlation coefficient was calculated to determine the correlation between parameters. The P < 0.05 was considered as significant.

Ethical clearance

The Institutional Ethics Committee of Santosh Medical College and Hospital, Ghaziabad, Uttar Pradesh, India has approved the Research work proposed to be carried out at Santosh Medical College and Hospital, Ghaziabad, Uttar Pradesh, India Date: 17th March 2016 with Reference no SMCH/EC/2016/186.


  Observation and Results Top


The present study, 316 subjects were studied of which 158 Type II Diabetes cases, whereas 158 healthy subjects as controls. The mean age of type 2 diabetic subjects had higher 44.52 ± 8.17 years and in 40.20 ± 7.42 years for healthy controls. Similarly, the mean body mass index (BMI) of the Type II Diabetes subjects was higher 25.28 ± 2.55 as compared to 23.07 ± 1.49 healthy controls [Table 1].
Table 1: Anthropometric criterion of with type II diabetes subjects and normal subjects

Click here to view


Blood glucose, Lipid parameters, along with HbA1c level were evaluated. The mean and SD of all variables were registered.

In Type II Diabetes mean considered at (P < 0.05) higher than for nondiabetic respondents. In Type II diabetes, serum lipids along with lipoproteins were substantially higher when compared to normal participants, with the exception of HDL-C, which was noticeably smaller in Diabetics relative to people without diabetes [Table 2]. The mean cholesterol level was slightly higher in Diabetics than normal participants (P < 0.001). When valued against controls, the mean triglyceride level of diabetes patients was substantially higher (P < 0.001). The average score of LDL-C in diabetics was distinctly higher (P < 0.001) than the mean value of controls. The HDL-C mean was prominently lower (P < 0.01) in diabetics compared to the mean value of controls. Again in comparison to controls, the mean level of very low-density lipoprotein (VLDL) cholesterol in diabetics was clearly elevated (P < 0.001). Likewise, with contrast to mean values of controls, the mean volume of MDA was slightly increased in diabetes (P < 0.01).
Table 2: Comparison in diabetes and normal participants for blood glucose, glycated hemoglobin, lipid profile and malondialdehyde

Click here to view


MDA associated with Glucose (r = 0.03), Glycated haemoglobin (r = 0.07), TC (r = 0.008), TG (r = 0.005), LDL-C (r = 0.034) and VLDL cholesterol (VLDL-C) (r = 0.002) and HDL-C (r = 0.006), as seen in [Table 3] and [Figure 1],[Figure 2],[Figure 3],[Figure 4].
Table 3: Correlation fasting blood glucose, glycated hemoglobin and lipid profile with malondialdehyde in type II diabetes subjects

Click here to view
Figure 1: Correlation between malondialdehyde and glycated hemoglobin

Click here to view
Figure 2: Correlation between total cholesterol and malondialdehyde

Click here to view
Figure 3: Correlation between high-density lipoprotein and malondialdehyde

Click here to view
Figure 4: Correlation between low-density lipoprotein and malondialdehyde

Click here to view



  Discussion Top


Diabetes is a big health issue in the world. It produces serious health-related and socioeconomic impact on individual person and also on populations. In addition, the pandemic increase of diabetes is spurred on by transitioning demographic like population aging, socioeconomic, nutritional and lifestyle patterns and migratory cause and a joined proliferation in overweight an obese adults and in children.[27],[28] Diabetes is a common endocrine metabolic disorder. Due to reduced insulin secretions or aversion or both, it is characterized by elevated glucose levels from a multiple association of biological and epigenetic factors.[29] The mean age of subjects with Type II diabetes was 44.52 ± 8.17 and for controls were 40.20 ± 7.42. This was in accordance with previous research of Sabzwari et al.[30] This present research shows that the BMI was observed to be elevated in Type II diabetess as compared to on diabetic subjects which was statistically significant. These findings were in accordance to the study of Shahid and Mahboob.[31] In Type II diabetes and controls, the mean ± S.D.s and P values of blood sugar were in the range of 151.58 ± 20.09 mg/dl and 81.08 ± 7.86 mg/dl (P < 0.001). In Type II Diabetes subjects, the mean value of fasting serum glucose was higher compared to nondiabetic subjects. It was observed that the rise was highly noteworthy (P < 0.001), which is consistent with Amanullah et al,[32] Mahajan et al.[33] and Meshram et al.[34] Hyperglycemia in D.M. is caused by both overproduction and underutilization of glucose. There is a relative excess of glucagon levels also. AS a consequence, glucose production is increased rather than it's consumption by the liver and also there is a drastic reduction of uptake of glucose into muscle and adipose tissue, finally contributing to hyperglycemia.[35] The mean of HbA1c in diabetic type 2 and normal individuals were in the range 7.46% ± 1.24% and 4.65% ± 0.40%, respectively. Valued against Controls, the mean value of HbA1c was stronger in Diabetics. The increase was statistically highly significant (0.01). This is in accordance with Shetty et al.,[36] Sathiyapriya et al.,[37] Ren Y, et al.,[38] Dalan et al.[39] and Singer et al.[40] As the tempo of development of HbA1c is straightaway linked to the concentration of sugar, glycated hemoglobin level reflects the integrated glucose levels over the intervening 6–8 weeks. The relationship is well known between dyslipidemia and DM. In previous research, complex lipoprotein defects had been identified in DM. The outcome of our study reveals substantially higher levels of TC (P < 0.001) along with TG (P < 0.001), LDL-C (P < 0.001) and VLDL-C (P < 0.001) while HDL-C (P < 0.01) decreased relative to normal subjects in subjects with Type II Diabetes. These research results were concordant with Smaoui et al. 2004;[41] Garg and Grundy, 1990;[42] Dzien et al.;[43] 1991; Howard,[44] 1978. Diabetic dyslipidemia is well known in various studies, including the Heart Protection Study,[45] Anglo-Scandinavian Heart Results Trial-Lipid-Lowering Arm,[46] the Collaborative Atorvastatin Diabetes Research,[47] the Lescol Intervention Prevention Study[48] and the Cholesterol and Recurrent Events study. Type II Diabetes subjects have higher MDA levels than non-diabetic subjects; MDA represents the oxidative damage products of lipids and proteins, respectively.[49] DM is a progressive condition marked by progressive peaks in glucose, nonesterified fatty acids and oxidative stress. High values of MDA indicate elevated oxidative stress in Type II Diabetess. In this study, the lipid peroxidation product, MDA measured as TBARS, is significantly increased in diabetes type 2 against nonnormal subjects. This finding was concordant with Rani et al.[50] and Moussa.[51]


  Conclusion Top


We identified that blood glucose, glycated hemoglobin, lipid profile and MDA increased while HDL-C levels were significantly decreased. MDA had a significant correlation with FBG, TC, TG, LDL-C, VLDL-C, while no link with HDL-C. HbA1c positively correlated with MDA and erythrocyte fragility in diabetic patients. Increased blood glucose levels lead to the generation of oxygen free radicals and decreased levels of antioxidants, which causes erythrocyte fragility in type 2 diabetes. Accurate intervention of dyslipidemia as well as oxidative stress can be used as a prevention tool for the occurrence of microvascular and macrovascular problems in Type II Diabetes topics. Yet more research with a bigger sample size are required to verify this proposal.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Diabetes Atlas. 8th ed. Brussels, Belgium: International Diabetes Federation International Diabetes Federation; 2017.  Back to cited text no. 1
    
2.
Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2018.Diabetes Care: American Diabetes Association; 2018. p. S13-27.   Back to cited text no. 2
    
3.
Anjana RM, Deepa M, Pradeepa R, Mahanta J, Narain K, Das HK, et al. Prevalence of diabetes and prediabetes in 15 states of India: Results from the ICMR-INDIAB population-based cross-sectional study. Lancet Diabetes Endocrinol 2017;5:585-96.  Back to cited text no. 3
    
4.
Haffner SM, Lehto S, Ronnemma T, Pyorala K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in non-diabetic subjects with or without prior myocardial infarction. N Engle J Med 1998;339:229-34.  Back to cited text no. 4
    
5.
Rader DJ. Effects of insulin resistance, dyslipidemia and intra-abdominal adiposity on the development of cardiovascular disease and diabetes mellitus. Am J Med 2007;120:s12-8.  Back to cited text no. 5
    
6.
Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol 1998;81:18B-25B.  Back to cited text no. 6
    
7.
Taskinen MR. Diabetic dyslipidaemia: From basic research to clinical practice. Diabetologia 2003;46:733-49.  Back to cited text no. 7
    
8.
Ginsberg HN, Zhang YL, Hernandez-Ono A. Metabolic syndrome: Focus on dyslipidemia. Obesity 2006;14:41-9.  Back to cited text no. 8
    
9.
Sicree R, Shaw J, Zimmet P. Diabetes and Impaired Glucose Tolerance. In: Gan D, editor. Diabetes Atlas. International Diabetes Federation. 3rd ed. Belgium: International Diabetes Federation; 2006. p. 15-103.   Back to cited text no. 9
    
10.
Sultan A, Thuan JF, Avignon A. Primary prevention of cardiovascular events and type 2 diabetes: Should we prioritize our interventions? Diabetes Metab 2006;32:559-67.  Back to cited text no. 10
    
11.
Selvin E, Marinopoulos S, Berkenblit G, Rami T, Brancati FL, Powe NR, et al. Meta-analysis: glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Intern Med 2004;141:421-31.  Back to cited text no. 11
    
12.
Yang RL, Shi YH, Hao G, Li W, Le GW. Increasing oxidative stress with progressive hyperlipidemia in human: Relation between malondialdehyde and atherogenic index. J Clin Biochem Nutr 2008;43:154-8.  Back to cited text no. 12
    
13.
Lopes HF, Morrow JD, Stojiljkovic MP, Goodfriend TL, Egan BM. Acute hyperlipidemia increases oxidative stress more in African Americans than in white Americans. Am J Hypertens 2003;16:331-6.  Back to cited text no. 13
    
14.
Tangvarasittichai S. Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus. World J Diabetes 2015;6:456.  Back to cited text no. 14
    
15.
Ho E, Galougahi KK, Liu CC, Bhindi R, Figtree GA. Biological markers of oxidative stress: Applications to cardiovascular research and practice. Redox Biol 2013;1:483-91.  Back to cited text no. 15
    
16.
Brownlee M. The pathobiology of diabetic complications: A unifying mechanism. Diabetes 2005;54:1615-25.  Back to cited text no. 16
    
17.
Su Y, Liu XM, Sun YM, Jin HB, Fu R, Wang YY, et al. The relationship between endothelial dysfunction and oxidative stress in diabetes and prediabetes. Int J Clin Pract 2008;62:877-82.  Back to cited text no. 17
    
18.
Bandeira SD, Guedes GD, Fonseca LJ, Pires AS, Gelain DP, Moreira JC, et al. Characterization of blood oxidative stress in type 2 diabetes mellitus patients: Increase in lipid peroxidation and SOD activity. Oxid Med Cell Longev 2012;2012: 819310.  Back to cited text no. 18
    
19.
Bergmayer HV. “Methods of Enzymatic Analysis”. AP, NY: 1974. p. 1196.  Back to cited text no. 19
    
20.
Gabbay KH, Hasty K, Breslow JL, Ellison RC, Bunn HF, Gallop PM. Glycosylated hemoglobin. J Clin End Met 1977;44:859.   Back to cited text no. 20
    
21.
Richmond W. Preparation and properties of cholesterol oxidase from Nocardia sp. and its application to the enzymatic assay of total cholesterol in serum. Clin Chem 1973;19:1350-6.  Back to cited text no. 21
    
22.
Foosati P, Prencipe L. Serum triglyceride determined colorimetrically with an enzyme that produce hydrogen peroxide. Clin Chem 1982;28:2077-80.  Back to cited text no. 22
    
23.
Rifai N, Warnick GR. Laboratory Measurements of Lipids, Lipoproteins and Apolipoproteins. Washington, DC, USA: AACC press; 1994.  Back to cited text no. 23
    
24.
Burtis CA, Ashwood ER. Tietz Textbook of Clinical Chemistry, 2nd ed. Philadelphia: Saunders; 1994.  Back to cited text no. 24
    
25.
Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18:499-502.  Back to cited text no. 25
    
26.
Placer ZA, Cushman LL, Johnson BC. Estimation of product of lipid peroxidation (malonyl dialdehyde) in biochemical systems. Anal Biochem 1966;16:359-64.  Back to cited text no. 26
    
27.
Lardenson P, Kim M. Cecil Medicine. 23rd ed. Philadelphia: Saunders Elsevier; 2004. p. 1658-713.  Back to cited text no. 27
    
28.
Davies TF, Larsen PR, Williams Text Book of Endocrinology. 11th ed. Philadelphia: Elsevier; 2008. p. 333-68.  Back to cited text no. 28
    
29.
Al-Wazzan HT, Daban AH, AA Raffa, El-Shazly MK. Prevalance and associated factor's of thyroid dystunction among type 2 diabetic patients. Kuwait Bull Alex Fac Med 2010;46:141-8.  Back to cited text no. 29
    
30.
Sabzwari M.J, Ahmad M, Majeed M.T, Riaz M, Umair M. Serum sialic acid concentration and type 2 diabetes mellitus. Professional Med J 2006;13:508-10.  Back to cited text no. 30
    
31.
Shahid MS, Mahboob T. Clinical correclation between frequent risk factors of diabetic nephropathy and serum sialic acid. Int J Diabetes metab 2006;14:138-44.  Back to cited text no. 31
    
32.
Amanullah S, Jarari A, Govindin M, Basha MI, Khatheeja S. Association of hs-CRP with diabetic and non-diabetic individuals. Jordon J Biol Sci 2010;3:7-12.  Back to cited text no. 32
    
33.
Mahajan A, Tabassum R, Chavali S, Dwivedi OP, Bharadwaj M, Tandon N, et al. High-sensitivity C-reactive protein levels and type 2 diabetes in urban North Indians. J Clin Endocrinol Metab 2009;94:2123-7.  Back to cited text no. 33
    
34.
Meshram A, Agrawal U, Dhok A, Adole P, Meshram K, Khare R. HbA1c, hs-CRP and anthropometric parameters evaluation in the patients of Diabetes Mellitus of Central Rural India. Int J Med Sci Public Health 2013; 2:293-296.  Back to cited text no. 34
    
35.
Puri D. Text Book of Medical Biochemistry. 3rd ed. New Delhi: Elsevier; 2011. p. 324.  Back to cited text no. 35
    
36.
Shetty JK, Prakash M, Ibrahim MS. Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications. Indian J Clin Biochem 2008;23:67-70.  Back to cited text no. 36
    
37.
Sathiyapriya V, Bobby Z, Agrawal A, Selvaraj N. Protein glycation, insulin sensitivity and pancreatic beta cell function in high-risk, non-diabetic, first degree relatives of patients with type 2 diabetes. Indian J Physiol Pharmacol 2009;53:163-8.  Back to cited text no. 37
    
38.
Ren Y, Tian H, Li X, Liang J, Zhao G. Elevated serum ferritin concentrations in a glucose-impaired population and in normal glucose tolerant first-degree relatives in familial type 2 diabetic pedigrees. Diabetes Care 2004;27:622-3.  Back to cited text no. 38
    
39.
Dalan R, Earnest A, Leow MK. Ethnic variation in the correlation between fasting glucose concentration and glycated hemoglobin (HbA1c). Endocr Pract 2013;19:812-7.  Back to cited text no. 39
    
40.
Singer DE, Nathan DM, Anderson KM, Wilson PW, Evans JC. Association of HbA1c with prevalent cardiovascular disease in the original Framingham heart study. Diabetes 1992;41:202-8.  Back to cited text no. 40
    
41.
Smaoui M, Hammami S, Chaaba R, Attia N, Ben Hamda K, Masmoudi AS, et al. Lipids and lipoprotein concentration in Tunisian type II diabetic patients. J Diabetes Complic 2004;18:258-63.  Back to cited text no. 41
    
42.
Garg A, Grundy SM. Management of dyslipidemia in NIDDM. Diabetes Care 1990;13:153-69.  Back to cited text no. 42
    
43.
Dzien A, Lechleitner M, Hopferwieiser T, Drexel H, Patsh JR, Braunstecine H. Long –term effect of intensified insulin treatment on lipid parameters in diabetes mellitus type 1. J Klin Wochenschr 1991;69:483-5.  Back to cited text no. 43
    
44.
Howard BV. Lipoprotein metabolism in diabetes mellitus. J Lipid Research 1978;28:613-28.  Back to cited text no. 44
    
45.
Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, Caulfield, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the anglo-scandinavian cardiac outcomes trial-lipid lowering arm (ASCOT-LLA): A multicentre randomised controlled trial. Lancet 2003;361:1149-58.  Back to cited text no. 45
    
46.
Garcia MJ, McNamara PM, Gordon T, Kannel WB. Morbidity and mortality in diabetics in the Framingham population. Sixteen year follow-up study. Diabetes 1974;23:105-11.  Back to cited text no. 46
    
47.
Ulvenstam G, Aberg A, Bergstrand R, Johansson S, Pennert K, Vedin A, et al. Long-term prognosis after myocardial infarction in men with diabetes. Diabetes 1985;34:787-92.  Back to cited text no. 47
    
48.
Herlitz J, Malmberg K, Karlson BW, Rydén L, Hjalmarson A. Mortality and morbidity during a five-year follow-up of diabetics with myocardial infarction. Acta Med Scand 1988;224:31-8.  Back to cited text no. 48
    
49.
Tosukhowong P, Sangwatanaroj S, Jatuporn S, Prapunwattana P, Saengsiri A, Rattanapruks S, et al. The correlation between markers of oxidative stress and risk factors of coronary artery disease in Thai patients. Clin Hemorheol Microcirc 2003;29:321-9.  Back to cited text no. 49
    
50.
Rani AJ, Mythili SV, Nagarajan S. Serum nitrite levels in relation to malondialdehyde in type 2 diabetes mellitus. Recent Res Sci Technol 2012;4:11-2.  Back to cited text no. 50
    
51.
Moussa SA. Oxidative stress in diabetes mellitus. Romanian J Biophys Bucharest 2008;18:225-36.  Back to cited text no. 51
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and Me...
Observation and ...
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed56    
    Printed8    
    Emailed0    
    PDF Downloaded12    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]