Diabetes & Metabolism Journal

Original Articles

Effects of Insulin and Vitamin E on the Apoptosis of Pancreatic Islet Cells in Multiple Low dose Streptozotocin Induced Diabetic (LDSD) Mice.: Yong Hyun Kim, Jeong Hun Oh, Nan Hee Kim, Kyung Muk Choi, Sang Jin Kim, Sei Hyun Baik, Eung Seok Lee, Min Chul Lee, Dong Seop Choi; Korean Diabetes J. 1999;23(6):757-767. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Type 1 diabetes mellitus results from irreversible loss of beta cells in pancreatic islet. It is generally known that abnormal MHC expression and interaction of variable cytokines play a role in beta cell death, but the precise mechanism of beta cell death is unknown. Apoptosis is a physiological form of cell death and can play an important role in beta cell death in experimental diabetic animal models. Thus, in insulin and vitamin E treated LDSD mice and streptozotocin treated control mice. We attempted to comparing the levels of blood glucose (BG), the degree of insulitis, and number of apoptotic cells. Our study goal was to understand inhibition of apoptosis which thought to play an important mechanism in reducing the degree of hyperglycemia and insulitis. METHODS: In 3 LDSD mice groups (group 1: control group with streptozotocin only, group 2: streptozotocin plus insulin, group 3: streptozotocin plus vitamin E), the effects of insulin and vitamin E on the blood glucose levels and the degree of insulitis were evaluated. The number of apoptotic cells of pancreatic islet was compared using double staining immunohistochemical method. RESULT: The levels of BG, degree of insulitis and the rate of apoptosis of pancreatic islet cells were decreased in insulin and vitamin E treated groups when compared to the control group. There was no difference in number of apoptotic cells between insulin and vitamin E treated group, but levels of BG and degree of insulitis were higher in vitamin E treated group than insulin treated group as time elapsed. CONCLUSION: Insulin and vitamin E can decrease the elevation of BG and the degree of insulitis via inhibition of apoptosis in LDSD mice.

Effect of Protein Kinase C Inhibitors on Expression of TGF-betamRNA in Cultured Mesangial Cells Under High Glucose Concentration.: Yoon Sang Choi, Dong Seop Choi; Korean Diabetes J. 1999;23(5):635-646. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Diabetic nephropathy is characterized by hypertrophy of both glomerular and tubular elements, thickening of the glomerular and tubular basement membranes, progressive accumulation of extracellular matrix components in mesangium, and tubulointerstitial fibrosis. Hyperglycemia increases the level of diacylglycerol (DAG) and activates protein kinase C (PKC) in mesangial cells and other vascular tissues. PKC activation regulates a number of vascular functions such as vascular permeability, contractility, cellular proliferation, basement membrane synthesis, signal transduction mechanisms for hormones and growth factors, In addition, glomerular mesangial cells play an important role in the development of diabetic nephropathy. Mesangial cells have many functions such as contractile properties, phagocytosis of macromolecules, synthesis of matrix proteins, and production of and response to growth factors (e.g., PDGF, TGF beta). Also, these growth factors play important roles for mesangial cell proliferation and in pathophysiology of diabetic nephropathy. Specifically, TGF beta is a key mediator in development of diabetic nephropathy. This study was performed to evaluate the relationship between PKC activation and TGF f3 production in mesangial cells under high glucose condition. METHODS: The expression of the TGF beta mRNA was evaluated in cultured human mesangial cells by semiquantitive RT-PCR, under varying degree of glucose concentrations (5 mM, 10 mM, 30 mM) with and without treatment of PKC inhibitors (calphostin C, Vitamin-E). RESULT: In control group (no treatment), ratio of TGF beta/beta-aetin mRNA in 5mM, 10mM, 30mM glucose were 1.694+/-0.223, 3.383+/-2.089, 5,474+/-1.74S, respectively. In calphostin C treated group, ratio of TGF beta/beta-actin mRNA in 5mM, 10mM, 30mM glucose were 1.457+/-0,322, 1.379+/-0.138, 1.205+/-0.050, respectively. In vitamin E treated group, ratio of TGF beta/beta-actin mRNA in 5mM, 10rnM, 30mM glucose were 1.198+/-0.081, 1.995+/-1.625, O.S04+/-0.570, respectively. In 10mM glucose concentration, ratios of TGF beta/beta-actin mRNA were reduced in calphostin C and vitamin E treated groups, compared with those in control group. But, there were no statistical significancies (p=0.191, 0.208). In high glucose concentration (30mM), ratios of TGF /3/f3-actin mRNA were significantly reduced in calphostin C and vitamin E treated groups compared with those in control group (p<0.05), respectively. CONCLUSIONS: These results indicate that high glucose concentration induce TGF beta expression in eultured mesangial cells through PKC activation. This suggests that selective PKC beta isoform inhibitors may be useful for treatment and prevention of diabetie nephropathy.

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.

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