Diabetes & Metabolism Journal

Original Articles

Effect of Red Ginseng Extract on Lipid Peroxidation in Streptozotocin-induced Diabetic Rats.: Hee Jong Jin, Sung Hee Ihm, Ja Hei Ihm; Korean Diabetes J. 2001;25(5):374-383. Published online October 1, 2001

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Abstract PDF: BACKGROUND
Diabetes mellitus is postulated to be associated with increased oxidative stress and lipid peroxidation which may contribute to vascular complications. Recently ginseng (Panax) has been shown to have an antioxidant effect by enhancing nitric oxide synthesis in endothelial cells and by directly scavenging hydroxyl radicals. It is unknown whether ginseng might act as an antioxidant against lipid peroxidation in diabetes. METHODS: We studied the in vitro effect of red ginseng extract on lipid peroxidation employing phospholipid liposome and low-density lipoprotein (LDL) as a model system. To investigate the in vivo effect on lipid peroxidation in diabetes, we administered red ginseng extract (1 g/L in drinking water) to streptozotocin (STZ)- induced diabetic rats for 12 weeks and measured lipid peroxidation products in plasma, liver, kidneys and heart. RESULTS: The Fe(3+)- or Cu(2+)- mediated lipid peroxidation in phospholipid liposome and LDL, measured by the concentration of TBARS, was inhibited in the presence of red ginseng extract. MDA level in plasma measured by HPLC was higher in STZ-induced diabetic rats than in control rats. Plasma MDA level was lower by 41% in red ginseng-treated diabetic rats than in untreated diabetic rats. Tissue MDA levels measured by TBA method in liver, kidneys and heart were higher in STZ-induced diabetic rats than in control rats. In red ginseng-treated diabetic rats tissue MDA levels were lower by 14~30% than in untreated diabetic rats. CONCLUSION: We observed that red ginseng extract has an effect in inhibiting lipid peroxidation both in vitro and in STZ-induced diabetic rats. These results suggest that red ginseng might have a beneficial effect in diabetes as an antioxidant against lipid peroxidation and diabetic vascular complications.

Proliferative Ability of Aortic Smooth Muscle Cells and Lipid Peroxidation of Red Blood Cell Membrane in Diabetic Rats.: Sae Young Park, Hyung Joon Yoo, Kyun Soo Kim, Hyun Kyu Kim, Doo Man Kim, Jae Myung Yoo, Sung Hee Ihm, Moon Gi Choi, Sung Woo Park; Korean Diabetes J. 1999;23(6):785-792. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Diabetes mellitus is a known risk factor for atherosclerosis, and lipid peroxidation, expression of oxidative stress, is also known to related to diabetes mellitus. The purpose of this study was to investigate the proliferative behaviour of cultured vascular smooth muscle cells (VSMCs) and the alteration of lipid peroxidation in relation to the pathogenesis of diabetic atherosclerosis. METHODS: Seven streptozotocin-induced insulin dependent diabetic Sprague Dawley rats and 7 normal rats were studied. Using enzyme method, aortic VSMCs was cultured in diabetic rats. and proliferation was compared between normal and diabetic rat. The membrane lipid peroxidaton of erythrocytes was determined by measurement of malonyl- dialdehyde(MDA), an end-product of fatty acid peroxidation with thiobarbituric acid (TBA) reaction. MDA-TBA colored complex concentration was calculated with the extinction coefficient of MDA-TBA complex at 532nm = 1.56X105cm-lM-1. RESULT: 1. The proliferative ability of cultured VSMCs was much higher in diabetic rats than in nondiabetic ones (p<0.05). 2. Compared with normal control rats, MDA concentration of diabetic rats was significantly increased (p<0.05). CONCLUSION: We concluded that proliferation of cultured VSMCs is due to oxidative stress in diabetes mellitus as a result of the increased proliferative ability of cultured VSMCs combined with increased lipid pemxidation in diabetic rats.

Effects of Smoking on Plasma Lipid Metabolism in Patients with non-insulin Dependent Diabetes Mellitus.: Seon Min Jeon, Yeun Kyung Lee, Hye Sung Lee, Bo Wan Kim, Young Bok Park, Myung Sook Choi; Korean Diabetes J. 1997;21(4):457-468. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Diabetes mellitus has been identified as a risk factor in the development of coronary vascular disease. Smoking also has been known as an independent risk factor in the development of coronary artery disease, causing a dislipidemia. This study was carried out to examine the effects of smoking on plasma lipids and lipoproteins metabolism in patients with NIDDM and in normal healthy subjects among Korean population in Taegu. METHODS: The 80 patients with NIDDM and 60 normal subjects were suMivided into non-stnoker, ex-smoker, and smoker group. Antbropornetric assessments, mean intake of nutrients, and the levels of plasma lipids, Apo A-I, L,p(a), CETP activity, and antioxidant vitamins such as vitamin A, E were measured, RESULTS: WHR in non-smoker of patients with NIDDM was greater than that in non-smoker of normal control. There were no differences in the nutrient intakes among groups, but protein intake was even higher in smoker of NIDDM group than that of normal group. There were no smoking effect on total cholesterol, LDL-C, AI, Apo A-I, Lp(a) and lipid peroxide in plasma of two groups, but they were higher in NIDDM group than normal group. Plasma TG concentrations were higher in smoker group than other groups within normal group, HDL-C levels were lower in non-smoker group than other groups within NIDDM group. CETP activities were higher in smoker group than non-smoker within normal group. And CEPT activities in NIDDM group were mostly higher than those of normal group. Vit. A levels of non-smoker in normal group were higher than ex-smoker within same group, and were also higher than non-smoker in NIDDM group. Vit. E levels showed no difference within each group, but they were mostly lower in NIDDM group than normal group. CONCLUSION: It was concluded that smoking was not a major factor for changing lipid metabolism in NIDDM patients as well as normal subjects unlike others findings. Their abnormal lipid rnetabolism may be induced from other risk factors for NIDDM rather than smoking itself. However, present study was done only for a short period, thus more studies are needed for longer term to investigate the effects af smoking on lipid metabolism in NIDDM among Korean population.

Effect of Aminoguanidine on Lipid Peroxidation in Streptozotocin-induced Diabetic Rats.: Kwon Yeop Lee, Sung Hee Ihm, Hyung Joon Yoo, Sung Woo Park, Ja Hei Ihm; Korean Diabetes J. 1997;21(4):372-380. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Diabetes mellitus is postulated to be associated with increased lipid peroxidation which may contribute to vascular complications. One potential mechanism of the increased lipid peroxidation in diabetes is lipid-linked advanced glycosylation and oxidation. Aminoguanidine(AMGN), the prototype inhibitor of advanced glycosylation end-product formation, has been recently shown to prevent oxidative moditication of LDL in vitro at moderate concentration. It is unknown whether AMGN might act as an anti-oxidant against lipid peroxidation under hyperglycemia in vivo. METHODS: To investigate the in vivo effect of AMGN on lipid peroxidation in diabetes, we administered AMGN(1 g/L in drinking water) or vitamin E (400mg/day, 5 days/week) to streptozotocin(STZ)-induced diabetic rats for 9 weeks and measured plasma lipid hydroperoxides by ferrous oxidation with xylenol orange II method and RBC membrane malon-dialdehyde(MDA) by thiobarbituric acid method. RESULTS: Plasma lipid hydroperoxide level was higher in STZ-induced diabetic rats than in control rats(7.53+/-2.03 vs.5.62+/-0.44*pmol/L). RBC membrane MDA was also higher in STZ-induced diabetic rats than in control rats(2.67+/-0.46 vs. 1.81+/-0.19* nmol/mL). Plasma lipid hydroperoxide level was lower in AMGN-treated(6.23+/-0.59*umol/L) and vitamin E-treated(5.29+/-0.27*umol/L) diabetic rats than in untreated diabetic rats. RBC membrane MDA was also lower in AMGN-treated(1.93+/-0.12""'nmol/ mL) diabetic rats than in untreated diabetic rats. There was no significant difference in plasma glucose, triglyceride levels among diabetic groups(Mean +/-S.D; *, P<0.05 vs. untreated STZ-induced diabetic rats; n=8-14/group). CONCLUSION: Although the mechanisms of action of AMGN on lipid peroxidation in vivo should be studied further, these results suggest that AMGN might have an additional beneficial effect as an antioxidant against lipid peroxidation in prevention trial for diabetic vascular complications.

Effect of Dietary Polyunsaturated / Saturated Fatty Acid on Membrane Lipid Peroxidation of Red Blood Cells and Hepatic Intracellular Organelles in Streptozotocin Induced Diabetec Rats.: Hyung Joon Yoo; Korean Diabetes J. 1997;21(3):271-279. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Lipid peroxidation in tissues and in tissue fractions is a degradative free-radical process that primarily involves polyunsaturated fatty acids; it has been implicated as a major contribution to many types of tissue damage, especially in diabetes mellitus. This study was designed to investigate the effect of P/S dietary composition on the lipid peroxidation of biomembranes in streptozotocin-induced diabetic rats. METHODS: Diabetic Sprague Dawley rats weighing about 200g were randomly divided into 3 groups: Group L(n=8) fed with P/S ratio 0.4, Group M(n=8) fed with P/S ratio 1.2, and Group H(n=8) fed with P/S ratio 2.0. Diabetes was induced by daily intraperitoneal injection of streptozotocin(20mg/kg) for 5 days. After feeding for 6 weeks, plasma cholesterol, HDL-cholesterol, RBC membrane peroxidation and hepatic mitochondrial lipid peroxidation were measured. RESULTS: Total cholesterol(mmol/L) was decreased and HDL-cholesterol/total cholesterol % ratio was increased by increment of P/S ratio in a doseindependent manner(L 3.4+/-0.32 and 8.7; M 2.5+/- 0.29 and 12.6; H 2.5+/-0.29 and 12.3). RBC membrane lipid peroxidation(nmol/mI. packed RBC) was higher in H(3.21+/-0.20) than that in L(2.02+/-0.19) or M(2.40+/-0.21) (p<0.05). Hepatic mitoehondrial lipid peroxidation (nmol/g protein) was lower in L(7.5+/- 1.25) than that in M(11.7+1.57) or H(14.0+2.04) (p<0,05). CONCLUSION: P/S dietary increment increased the lipid peroxidation of biomembranes(RBC membrane an4 hepatic mitochondrial membrane) in streptozotocin-induced diabetic rats.

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