American Journal of Medical Sciences and Medicine
ISSN (Print): 2327-6681 ISSN (Online): 2327-6657 Website: Editor-in-chief: Apply for this position
Open Access
Journal Browser
American Journal of Medical Sciences and Medicine. 2014, 2(1), 21-24
DOI: 10.12691/ajmsm-2-1-5
Open AccessArticle

Role of Antioxidant Enzymes in Glucose and Lipid Metabolism in Association with Obesityand Type 2 Diabetes

Kandi Sabitha1, , B. Venugopal1, Md Rafi1 and K V Ramana2

1Chalmeda AnandRao Institute of Medical Sciences, Bommakal, Karimnagar, Andhra Pradesh

2Prathima institute of Medical Sciences, Nagnur, Karimnagar, Andhra Pradesh

Pub. Date: February 21, 2014

Cite this paper:
Kandi Sabitha, B. Venugopal, Md Rafi and K V Ramana. Role of Antioxidant Enzymes in Glucose and Lipid Metabolism in Association with Obesityand Type 2 Diabetes. American Journal of Medical Sciences and Medicine. 2014; 2(1):21-24. doi: 10.12691/ajmsm-2-1-5


Introduction: Obesity is a state of excess adipose tissue mass. It can be calculated by BMI or waist circumference. Waist circumference more than 88cm in female and 102cm in males make them overweight and these overweight increases 2.9 times the risk of metabolic syndrome, type 2 diabetes. The antioxidant enzymes SOD (Superoxide Dismutase), MDA (Malondialdehyde) levels are assayed in these overwight and risk category (gentic risk). Materials & Methods: 25 obese and overweight are included with age matched controls who came to chalmeda anadrao institute of medical sciences hospital. The Fasting blood glucose (FBS), lipid profile, SOD, MDA levels are measured. Results: The mean ± SD values of FBS of samples with history of diabetes (146.3 ± 11.68) and without history of diabetes (95 ± 4.02) compared to controls are (88.33 ± 6.78) which is significant with p<0.001. The antioxidant enzyme levels in controls and samples are SOD mean ± SD samples (50 ± 4.96) controls (100 ± 4.62), MDA samples are (619.12 ± 0.91) controls (240.4 ± 1.14). The comparison of lipid profile of samples with controls are also significant with p value <0.001. Discussion: In normal healthy condition there is always redox homeostasis occurring in cell, any imbalance to this redox homeostasis leads to oxidative stress (OS). OS leads to overproduction of ROS and impairs antioxidant defense mechanism. Increased metabolic and mechanical load on myocardium, large body mass, nutritious diet leads to formation of lipid peroxidation, freeradical and reactive oxygen species generation which inturn impairs insulin receptors functioning leads to insulin resistance, metabolic syndrome, type 2 diabetes. Conclusion: From this study we conclude that regular physical activity, diet restriction, and early assessment of SOD, MDA levels we can prolong the complications of type 2 diabetes.

obesity antioxidant enzymes reactive oxygen species (ROS) oxidative stress type 2 Diabetes

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit


[1]  Hurst R, Bao Y, Jemth P, Mannervik B, Williamson G. Phosholipid hydroperoxide glutathione peroxidase activity of rat class theta glutathione transferase T2-2. Biochem Soc Trans 1997; 25: S559.
[2]  Jornot L, Petersen H, Junod AF. Hydrogen peroxide - induced DNA damage is independent of nuclear calcium but dependent on redox-active ions. Biochem J 1998; 335: 85-94.
[3]  Mills EM, Takeda K, Yu Zx, et al, Nerve growth factor treatment prevents the increase in superoxide produced by epidermal growth factor in PC 12 cells. J Biol Chem 1998; 273: 22165-8.
[4]  Chopra S, Wallace HM. Induction of spermidine / spermine N1-acetyl transferase in human cancer clls in response to increased production of reactive oxygen species. Biochem Pharmacol 1998; 55: 1119-23.
[5]  Czen S, Tiback M, Harms – Ringdahl M. pH dependent DNA cleavage in permeabilized human fibroblasts. Biochem J 1997; 323: 337-41.
[6]  Scott MD, Eaton JW, Kuypers FA, Chiu DT, Lubin BH. Enhancement of erythrocyte superoxide dismutase activity: effects on cellular oxidant defense. Blood 1989; 74: 2542-9.
[7]  Stahl W, Junghans A, de Boer B, Driomina ES et al. Carotenoid mixtures protect multilamellar liposomes against oxidative damage: Synergistic effects of lycopene and lutein. FEBS Lett 1998; 427: 305-8.
[8]  Hall L, Williams K, Perry ACF, Frayne J, Jury JA. The majority of human glutathione peroxide type 5 (GPX 5) transcripts are incorrectly spliced: implications for the role of GPX5 in the male reproductive tract. Biochem J 1998: 333: 5-9.
[9]  Grazoli V, Schiavo R, Casari E, et al. Antioxidant enzymatic activities and lipid peroxidation in cultured human chondrocytes from vertebral plate cartilage. FEBS Lett 1998; 431: 149-53.
[10]  Jeffrey S. Flier, Eleftheria Maratos Flier. Harrisons Principles of Internal Medicine: chapter 64: Obesity; 16th edition; McGraw Hill Medical Publishing division: 2005; vol I: 422.
[11]  National Institutes of Health Consensus Development Panel on the Health Implications of Obesity. 1985. Health implications of Obesity: National Institutes of Health Consensus Development Conference statement. Ann Intern Med; 103: 1073-77.
[12]  Ramachandran A. 2005. Epidemiology of diabetes in India – 3 decades of research. JAPI; 53: 34-38.
[13]  Bannister J, Bannister W, Rotilio G. 1987. “Aspects of the structure,function and applications of SOD. Critical Rev Biochem 22: 111-180.
[14]  Dourerdjou P, Koner B.C (2008), Effects of different cooking vessels on heat induced lipid peroxidation of different edible oils. Journal of Food Biochemistry, 32: 740-751.
[15]  V. Nair, C.L.O Neil, P.G.Wang. ‘Malondialdehyde, Encyclopedia of reagents for organic synthesis, 2008. Johnweily & Sons. Newyork.
[16]  Jose M Mates, Cristins perez-Gomez, Ignacio nunez de castro. ‘Antioxidant enzymes and human diseases’. Clinical Biochemistry, 32: 8: 5 95-603, 1999.
[17]  Furukawa S, Fujiti T, Shimabukuro M, Iwaki M, Yamada Y et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. The Journal of clinical Investigation 114 (12): 1752-1761, 2004.
[18]  Turrens JF: Superoxide production by the mitochondrial respiratory chain. Bio Sci Rep 17: 3-8, 1997.
[19]  Lechieitner M, KochT, Harold M, Dzien A, Hoppiahler F; TNF-α plasma levele in patients with type 1 Diabete mellitus and its association with glycemic control & cardiovascular risk factors. J Intern Med; 248: 67- 76, 2000.
[20]  Moor de Burgos A, Wartonowics M, Ziemlanski S : Blood vitamin & lipid levels in overweight & obese women. Eur J Clin Nutr 46: 803-808, 1992.
[21]  Alexander CM, Landsman PB, Teutsch SM: Diabetes melliteus impairing fasting glucose, atherosclerotic risk factors & prevelance of coronary heart disease. Am J Cardiol 86; 897-902, 2000.
[22]  Redinger RN.2007, Pathophysiology of obesity and its clinical manifestations. Gastroenterology & Hepatology, 3: 856-863.
[23]  Evans RM, Barish GD, Wang YX.2004.PPARS and the complex journey to obesity. Nat Med 10: 355-361.
[24]  Hutley L, Prins JB.2005. fat as an endocrine organ: relationship to the metabolic syndrome. Am J Med Sci 330; 280-289.
[25]  Boden G, ChenX, Riuz J, White JV, Rosseti L.1994. Mechanism of fattyacid induced inhibition of glucose uptake. J Clin Invest, 93: 2438-2446.