Relationship between Dietary Pattern And Level of Antioxidant Enzymes in Diabetic Patients

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IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-issn: 2279-0853, p-issn: 2279-0861.Volume 15, Issue 11 Ver. VII (November. 2016), PP 161-165 www.iosrjournals.org Relationship between Dietary Pattern And Level of Antioxidant Enzymes in Diabetic Patients Maigari, F.U. 1*, Shu aibu Isa 2, Alkali, Y.S 1., Maigari, M.U 3, Sadau Y 1., Musa Abubakar 4 1 College Of Medical Sciences, Gombe State University, 2 Department Of Microbiology, Gombe State University, 3 Federal College Of Education (T)Gombe, 4 Ministry Of Health, Gombe. Abstract Background: Diabetes mellitus is a medical condition affecting many with incidence rapidly growing worldwide. Approximately, 7.1 million Africans were said to be suffering from diabetes at the end of 2000, a figure that was expected to rise to 18.6 million by 2030 (Wild et al., 2004). Materials and Methods: This study determined the relationship between the dietary pattern and level of antioxidant enzymes of some diabetic patients attending the Federal Teaching Hospital Gombe. The patients are registered with the hospital and have their glycated haemoglobin level above normal and their informed consent was sought. The hospital also gave an ethical clearance for the research. Results and Conclusion: There was no significant difference in the levels of glycated hemoglobin, superoxide dismutase, catalase, GPx and malondialdehyde levels (p>0.05) against the breakfast levels of the study subjects. The results also showed no significant difference (p>0.05) in the mean levels of the antioxidant enzymes of superoxide dismutase, catalase and GPx in the pattern of lunch of the subjects but a significant difference exists in the level of glycated hemoglobin and malondialdehyde (p<0.05). With respect to dinner consumption among the study subjects, a significant difference in the levels of glycated hemoglobin and GPx also exist. It can be concluded from the study that relationship between the level of antioxidant enzymes of GPx, superoxide dismutase and catalase with the selected breakfast and lunch pattern of is not to a significant level, however level of GPx is significantly affected by eating rice during dinner. Keywords: Diabetes mellitus, Dietary pattern, Antioxidant enzymes, Glycated haemoglobin, Diabetic subjects. I. Introduction The term oxidative stress is used when the body s natural defence mechanism are exceeded by the production of deleterious reactive oxygen species (ROS), resulting in damage to susceptible cell components such as DNA, proteins and lipids. Features of the brain that cause it to be particularly sensitive to oxidative stress include a high rate of oxidative metabolic activity, relatively low levels of antioxidant enzymes (e.g. catalase, glutathione peroxidase), a high concentration of unsaturated fatty acids, large iron and copper stores, and a low mitotic index (Lynch et al.,2000). Superoxide dismutase is one of the key antioxidant enzymes which provide an essential defence against oxygen toxicity to the cell. Superoxide dismutase is the antioxidant enzyme that catalyses the conversion of O 2.- to O 2 and to the less reactive species H 2 O 2.There are three forms of SOD in humans (Landis and Tower, 2005); CystolicCu,Zn-SOD, Mitochondrial Mn-SOD, Extracellular SOD EC- SOD. Catalase is a heme containing redox enzyme, found in high concentration in the peroxisomes. The enzyme is present in the cells of plants, animals and aerobic bacteria (Mates et al., 1999).The enzyme very efficiently promotes the conversion of H 2 O 2 to water and molecular oxygen. Glutathione metabolism is one of the most essential of antioxidative defence mechanisms. GPx acts in conjunction with the tripeptide glutathione (GSH), which is present in cells in high concentration (micro molar). The substrate for the catalytic reaction of GPx is H 2 O 2, or organic peroxide ROOH. GPx decomposes peroxides to water (or alcohol) while simultaneously oxidising GSH. The incidence of diabetes, especially type 2, is rapidly growing in the world. In 1985, an estimated 30 million people suffered with this chronic disease, which, by the end of 2006, had increased to 230 million, representing 6% of the world population. Of this number, 80% is found in the developing world (Roglic et al., 2005).It is estimated that during the next 35 years, diabetic world-wide prevalence will reach 25%, with India being the hardest hit. For a long time, Africa was considered safe from many of the diseases that are called diseases of affluence, which plague the Western world. Similarly, there was a time when Africa was thought to be a continent, relatively free of diabetes mellitus illnesses. Indeed, from 1959 to the mid-1980s, medical statistics showed that the prevalence rate of diabetes in Africa was equal to or less than 1.4%, with the exception of South Africa, where the rate was estimated to be as high as 3.6% in 2001 ( Motala, 2002; Motala et al., 2003; DOI: 10.9790/0853-151107161165 www.iosrjournals.org 161 Page

Rheeder, 2006). But, by 1994, the continent-wise prevalence of diabetes mellitus stood at 3 million and was then predicted to double or triple by the year 2010 (Sobngwi et al., 2001; International Diabetes Federation, 2003). Approximately, 7.1 million Africans were said to be suffering from diabetes at the end of 2000, a figure that was expected to rise to 18.6 million by 2030 (Wild et al., 2004). By far the most investigated diet component is cow milk protein and its effect on auto-immunity or diabetes outcome; several reviews are available (Kolb and Pozzilli, 1999; Schrezenmeir and Jagla, 2000).Human milk contains approximately four times more insulin as cow milk. This has prompted the suggestion that human insulin should be added to infant formulas to increase the oral immune tolerance to insulin and possibly prevent diabetes (Shehadeh et al., 2001). II. Methodology This study was conducted in Gombe State. It is one of Nigeria's 36 states with an area, having its state capital Gombe.Subjects for this study were drawn from Diabetic patients attending the Medical clinic of Federal Teaching Hospital Gombe (FTHG). The subjects were registered with the clinic and their informed consent was sought. The patients were previously diagnosed with diabetes for more than a year, and they were treated for the disease but still had their glycated haemoglobin above normal range. They were free from other diseases and chronic diabetic complications. The institutional ethical board granted the approval of the research protocol. The procedure for estimation of Glycated haemoglobin was as described by Gonen and Rubenstein (1978), plasma malondialdehyde was measured by the method of Ohakawa et al. (1979), Superoxide dismutase (SOD) activity was measured according to the method of Maier and Chan (2002), Reagents for catalase activity were obtained from Cell Biolabs, Inc USA and the method for assay of the enzyme activity in the diabetic patients and apparently healthy subjects employed was as described by Zamocky and Koller (1999).Glutathione peroxidase (GPx) activity was measured according to the method of Paglia and Valentine (1967) using reagents purchased at Cayman, MI, USA. III. Results There was no significant difference in the levels of glycated hemoglobin, superoxide dismutase, catalase, GPx and malondialdehyde levels (p>0.05) against the breakfast levels of the study subjects (table 1). The number of subjects consuming tea and bread were highest (N=50) and has a mean level of glycated hemoglobin (6.57±1.263), superoxide dismutase (0.19±0.228), catalase (44.06±14.707), GPx (87.87±31.703), malondialdehyde (7.81±5.242nmol/min/L). Table 2 shows the frequency and mean± standard deviation of subjects against their lunch consumption. The table showed no significant difference (p>0.05) in the mean levels of the antioxidant enzymes of superoxide dismutase, catalase and GPx in the pattern of lunch of the subjects. However, there is significant difference in the levels of glycated hemoglobin and malondialdehyde (p<0.05). The mean levels of glycated hemoglobin (7.36±0.31) was highest in the subjects that consume pasta (N=5) with the lowest level (6.19±1.372) in the subjects that consume rice (N=50). From the table, the subjects that consumed rice (N=50) have the lowest level of malondialdehyde (6.42±5.004µmol/L) with those consuming Tuwo (N=5) having the highest level of malondialdehyde (14.09±5.357µmol/L). There was a significant difference in the levels of glycated hemoglobin and GPx in the different pattern of dinner consumption among the study subjects (table 3). The level of GPx is higher in the subjects (N=16) that consume Rice (7.19±0.223) and lowest among the subjects (N=26) that consumed Pasta (6.13±1.435). The mean level of GPx was significantly highest in subjects (N=16) that consumed rice (110.79±44.929) with the lowest level of GPx in subjects (N=66) that consumed Tuwo (84.13±28.470). From the table, there was no significant difference (p<0.05) in the mean levels of superoxide dismutase, catalase and malondialdehyde in relation to the dinner pattern of the subjects. Table 1: Breakfast of Subjects against Glycated Hb, Antioxidant Enzymes and MDA Levels Breakfast N Mean± Std. Dev Glycated Hb Koko/Kosai 28 6.41±1.345 Tea/ Bread 50 6.57±1.263 Tuwo 39 6.85±0.966 Chips 3 5.39±1.649 Total 120 6.59±1.212 SOD(u/ml) Koko/Kosai 28 0.19±0.025 Tea/Bread 50 0.19±0.228 Tuwo 39 0.19±0.026 Chips 3 0.21±0.173 Catalase(u/ml) Koko/Kosai 28 46.94±14.195 Tea/Bread 50 44.06±14.707 Tuwo 39 44.69±12.887 DOI: 10.9790/0853-151107161165 www.iosrjournals.org 162 Page

GPx(nmol/min/ml ) (µmol/l) Chips 3 56.87±7.422 Total 120 45.26±13.917 Koko/Kosai 28 96.42±28.696 Tea/ Bread 50 87.87±31.703 Tuwo 39 92.73±33.478 Chips 3 65.37±11.483 Total 120 90.88±31.454 Koko/Kosai 28 6.88±4.147 Tea/Bread 50 7.81±5.242 Tuwo 39 8.51±4.599 Chips 3 8.19±6.028 Table 2: Lunch of Subjects against Glycated Hb, Antioxidant Enzymes and MDA Levels N N Mean± Std. Dev Glycated Hb Couscous 20 6.65±1.165 Pasta 45 6.92±0.972 Rice 50 6.19±1.372 Tuwo 5 7.36±0.31* Total 120 6.59±1.216 SOD(u/ml) Couscous 20 0.19±0.019 Pasta 45 0.19±0.026 Rice 50 0.19±0.021 Tuwo 5 0.18±0.049 Total 120 0.19±0.002 Catalase(u/ml) Couscous 20 43.82±16.469 Pasta 45 43.13±12.888 Rice 50 47.53±13.988 Tuwo 5 47.53±10.598 GPx(nmol/min/ ml) Malondialdehyd e (µmol/l) Couscous 20 85.19±40.019 Pasta 45 92.48±34.654 Rice 50 92.81±25.558 Tuwo 5 79.98±15.131 Total 120 90.88±31.454 Couscous 20 8.37±4.242 Pasta 45 8.46±4.068 Rice 50 6.42±5.004 Tuwo 5 14.09±5.357 * Table 3: Dinner of Subjects against Glycated Hb, Antioxidant Enzymes and MDA Levels Dinner N Mean±Std. Dev Glycated Hb Couscous 12 6.53±1.237 Pasta 26 6.13±1.435 Rice 16 7.19±0.223 Tuwo 66 6.64±1.209 Total 120 6.59±1.216* SOD(u/ml) Couscous 12 0.191±0.023 Pasta 26 0.20±0.020 Rice 16 0.18±0.020 Tuwo 66 0.19±0.026 Catalase(u/ml) Couscous 12 46.68±13.000 Pasta 26 49.52±12.271 Rice 16 40.04±12.829 Tuwo 66 44.59±14.662 GPx(nmol/min/ml) Couscous 12 82.35±25.868 Pasta 26 99.72±24.617 Rice 16 110.79±44.929 Tuwo 66 84.13±28.470 DOI: 10.9790/0853-151107161165 www.iosrjournals.org 163 Page

(µmol/l) Values with * are significantly different at p< 0.05 Total 120 90.88±31.454* Couscous 12 7.82±6.089 Pasta 26 5.81±4.159 Rice 16 8.09±2.846 Tuwo 66 8.56±5.002 Table 34: In between meals Consumption of Subjects against glycated hemoglobin, antioxidant enzymes and malondialdehyde Levels N Mean± Std. Dev Glycated Hb water 47 6.45±1.339 tea nd bread 26 7.02±0.840 juice 27 6.29±1.326 Pasta 20 6.76±1.056 Total 120 6.59±1.216 SOD(u/ml) water 47 0.19±0.027 tea nd bread 26 0.19±0.025 juice 27 0.19±0.023 Pasta 20 0.19±0.179 Catalase(u/ml) water 47 46.71±15.243 GPx(nmol/min/ml ) (umol/l) tea nd bread 26 42.67±13.968 juice 27 44.18±14.976 Pasta 20 46.66±8.230 water 47 79.17±20.635 tea nd bread 26 101.68±40.353 juice 27 88.86±29.256 Pasta 20 107.09±32.717 Total 120 90.88±31.454* water 47 8.64±5.638 tea nd bread 26 8.15±3.501 juice 27 6.57±4.927 Pasta 20 7.21±3.603 IV. Discussion The different lunch pattern of the study subjects in relation to glycated hemoglobin and malondialdehyde differed significantly (p<0.05). The study found that those subjects consuming Tuwo during lunch (table 28) had a higher level of glycated hemoglobin (7.36±1.372) and malondialdehyde (14.09±5.357µmol/L). Most of the subjects consume the tuwo with different kinds of soups which may have high lipid content that may be susceptible to lipid peroxidation. The dinner pattern of the subjects showed significant rise in the level of glycated hemoglobin (table 29) with those consuming rice having a higher level of glycated hemoglobin (7.19±0.223). The level of GPx in the subjects was also significantly higher (110.79±44.929nmol/min/ml). The study found an increase in the level of GPx in diabetic subjects, with higher level of glycated hemoglobin indicating a poor management of blood sugar. Subjects consuming rice (table 32) during dinner had a significantly higher content of Cu (105.57±14.362µg/dl) (p<0.05). From the food composition table (FAO, 2012) rice whole, polished and boiled has a high retention factor for copper. Serum copper level in the study subjects may be implicated due to diabetic condition since increase in serum copper was found to be higher in diabetic subjects as reported by Maigari et al. (2015). DOI: 10.9790/0853-151107161165 www.iosrjournals.org 164 Page

The result showed a significant difference (p<0.05) in the mean level of GPx in those subjects consuming Pasta in between their meals. Level of the antioxidant enzyme GPx was found to be high in diabetics (Maigari et al., 2015) References [1]. Gonen, B. And Rubenstein, A.H. (1978). Haemoglobin A1 and diabetes mellitus. Diabetologia15:1-8 [2]. International Diabetes Federation. (2003)Diabetes Atlas. 3rd ed. Belgium: IDF, Brussels. [3]. Kolb, H. andpozzilli, P.(1999). Cow s milk and type I diabetes: the gut immune system deserves attention. Immunol Today 20: 108 10. [4]. Landis, G.N. and Tower, J. (2005) Superoxide dismutase evolution and life span regulation, Mech. Ageing Dev. 126:365 379. [5]. Maier, C.M. and Chan, P.H. (2002). Role of superoxide dismutases in oxidative neurodegenerative disorders. The Neuroscientist8 (4): 323-334. [6]. Mates, J.M., Perez-Gomez, C. and De Castro, I.N. (1999). Antioxidant enzymes and human diseases, Clin. Biochem. 32:595 603. [7]. Maigari, F.U., Atiku, MK, Wudil, AM and Goje, LJ (2015) Determination of trace elements level in diabetes mellitus patients attending the Federal Teaching Hospital, Gombe. International Journal of Scienific Innovation and Sustainable Development 5(2)232-236. [8]. Motala, A.A. (2002). Diabetes trends in Africa. Diabetes Metab Res Rev.18:S14 20. [9]. Motala, A.A., Omar, M.A.K., Pirie, F.J. (2003). Epidemiology of type 1 and type 2 diabetes in Africa.J Cardiovasc Risk.10:77 83. [10]. Ohakawa H, Oshishi N. and Yagi K.(1979). Assay for Lipid Peroxidation in Animal Tissue by Thiobarbituric Acid Reaction. Anal. Biochem. 75:351-358. [11]. Paglia, D,E., and Valentine, W, N. (1967) Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J. Lab. Clin. Med.70: 158-169. [12]. Rheeder, P. (2006). Type 2 diabetes: The emerging epidemic. South AfrFamPract. 48:20. [13]. Roglic, G., Unwin, N., Bennett, P.H., Mathers, C., Tuomilehto, J., Nag, S.(2005). The burden of mortality attributable to diabetes: Realistic estimates for the year 2000. Diabetes Care.28:2130 5. [14]. Schrezenmeir, J., and Jagla, A.(2000).Milk and diabetes. J Am CollNutr19 (Suppl. 2): 176S 190S. [15]. Sobngwi, E., Mauvais-Jarvis, F., Vexiau, P., Mbanya, J.C., Gautier, J.F. (2001). Diabetes in Africans: Part 1: Epidemiology and clinical specificities. Diabetes Metab.27:628 34 [16]. Wild, S., Roglic, G., Green, R., and King, H. (2004) Global prevalence of diabetes: Estimates for year 2000 and projections for 2030. Diabetes Care27:1047-1053. DOI: 10.9790/0853-151107161165 www.iosrjournals.org 165 Page