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Volume 31(1); January 2007
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Review
The Roles of Clusterin on Morphogenesis of Beta Cells During Pancreas Regeneration.
Seok Woo Hong, KC Ranjan, Song Lee, Yong Jae Shin, Bon Hong Min, In Sun Park
Korean Diabetes J. 2007;31(1):1-8.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.1
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  • 27 Download
  • 1 Crossref
AbstractAbstract PDF
Clusterin is a highly glycosylated heterodimeric glycoprotein that plays diverse biological roles in various organs. The secreted clusterin has been established as a major form of the protein that exerts diverse tissue effects. For instance, clusterin is known to act in cell protection through the actions of extra-cellular molecular chaperones. In the extracellular milieu, clusterin participates in specific interactions with a diverse array of native biological molecules including LRP-2 (Lipoprotein receptor-related protein 2, also known as gp330 or megalin), which is involved in ligand endocytosis at the surfaces of certain epithelia. Clusterin is expressed transiently in developing and differentiating endocrine pancreatic cells and might be involved in pancreas development. This transient expression of clusterin at specific time points of pancreas development and cell differentiation during pancreas regeneration implies that the protein is a regulatory factor for cytodifferentiation as well as for replication. A specific action of the clusterin in the reconstruction and remodeling of the endocrine pancreas has been demonstrated. It also strongly stimulates duct cell differentiation into insulin-secreting cells under in vitro culture conditions. Clusterin appears thus as a potent regulator of insulin cell morphogenesis.

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  • Effect of African Mango (Irvingia gabonesis, IGOB 131TM) Extract on Glucose Regulation in STZ-Induced Diabetes
    Yejin Ha, Minhee Lee, Han Ol Kwon, Yoo-Hyun Lee
    Journal of the Korean Society of Food Science and Nutrition.2015; 44(11): 1607.     CrossRef
Original Articles
Glucose-dependent Insulin Secretion from Genetically Engineered K-cells Using EBV-based Episomal Vector.
Ju Hee Kim, Sung Dae Moon, Seung Hyun Ko, Yu Bai Ahn, Ki Ho Song, Hyang Sook Lim, Sook Kyung Lee, Soon Jip Yoo, Hyun Shik Son, Kun Ho Yoon, Bong Yun Cha, Ho Young Son, Sung Joo Kim, Je Ho Han
Korean Diabetes J. 2007;31(1):9-21.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.9
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  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Type 1 diabetes mellitus is an autoimmune disease resulting in destruction of the pancreatic beta cells. Insulin gene therapy for these patients has been vigorously researched. The strategy for achieving glucose-dependent insulin secretion in gene therapy relies on glucose-responsive transcription of insulin mRNA and the constitutive secretory pathway of target non-beta cells. We observed that genetically engineered K-cells using Epstein-Barr virus (EBV)-based episomal vector can produce glucose-regulated insulin production. METHODS: Green fluorescent protein (GFP) or rat-preproinsulin (PPI) expression cassette transcriptionally controlled by the promoter of glucose dependent insulinotropic peptide (GIPP) is fused to pCEP4 containing the origin of replication (oriP) and Epstein-Barr virus nuclear antigen 1 (EBNA-1). CMV promoter was replaced by subcloning the GIPP into pCEP4 to generate pGIPP/CEP4. Two recombinant EBV-based episomal vectors, pGIPP/GFP/CEP4 and pGIPP/PPI/CEP4, were constructed. pGIPP/GFP/CEP4 and pGIPP/PPI/CEP4 containing K-cell specific GIPP were co-transfected into STC-1. K-cell was isolated from the clonal expansion of the fluorescent cells selected by hygromycin treatment in STC-1, and were analyzed for the expression of glucokinase (GK) or transcription factors involved in pancreas development. K-cells concurrently transfected with pGIPP/PPI/CEP4 and pGIPP/GFP/CEP4 were analyzed for the transcripts of PPI by RT-PCR, and for the glucose dependent insulin expression by immunocytochemistry or insulin assay using ultra-sensitive rat-specific insulin ELISA kit. RESULT: STC-1 was stably-transfected with pGIPP/GFP/CEP4 along with pGIPP/PPI/CEP4. Genetically selected fluorescent K-cells expressed GK and transcription factors involved in pancreas development. And K-cells transfected with pGIPP/PPI/CEP4 contained detectable levels of PPI transcripts and showed glucose-dependent immunoreactive insulin secretion. CONCLUSION: We identified genetically engineered K-cells which exert a glucose-dependent insulin expression using EBV-based episomal vector. The similarities between K-cells and pancreatic beta cells support that K-cells may make effective and ideal targeting cells for insulin gene therapy or alternative cell therapy.

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  • Relationship of traditional and nontraditional cardiovascular risk factors to coronary artery calcium in type 2 diabetes
    Ju-Yeon Sim, Ju-Hee Kim, Yu-Bae Ahn, Ki-Ho Song, Je-Ho Han, Bong-Yun Cha, Sook-Kyung Lee, Sung-Dae Moon
    Korean Diabetes Journal.2009; 33(6): 466.     CrossRef
  • Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells
    Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung-Hyun Ko, Yu-Bae Ahn, Sung-Dae Moon, Ki-Ho Song
    Korean Diabetes Journal.2009; 33(6): 475.     CrossRef
Oxidative Stress Causes Vascular Insulin Resistance in OLETF Rat Through Increased IRS-1 Degradation.
Jung Lae Park, Young Sil Lee, Bo Hyun Kim, Yang Ho Kang, In Ju Kim, Yong Ki Kim, Seok Man Son
Korean Diabetes J. 2007;31(1):22-32.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.22
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AbstractAbstract PDF
BACKGROUND
Insulin resistance and oxidative stress have been reported to play essential pathophysiological roles in diabetic cardiovascular complication. The relationship between insulin resistance and oxidative stress in vasculature remains unclear. The study was conducted to assess whether oxidative stress induce vascular insulin resistance in OLETF rat, a model of type 2 diabetes METHODS: We used OLETF rats (20/30/40 weeks, n = 5/5/5), as models of type 2 DM, and LETO rats (20/30/40 weeks, n = 5/5/5) as controls. Aortas of each rats were extracted. Superoxide anion production was detected by NBT assay and lucigenin assay. 8-hydroxyguanosine (OHdG) and nitrotyrosine were detected as markers of oxidative stress in 20 and 40 weeks groups. The glucose uptake of aortas was measured by detecting 2-deoxyglucose uptake in both groups. The expression of IR, IRS-1, PI3-K and Akt/PKB were detected by immuno precipitation and immunoblotting in 20, 30 and 40 weeks groups RESULTS: Superoxide anion production and markers of oxidative stress (8-OHdG, nitrotyrosine) were significantly increased in aortas of OLETF rats compared with controls. Aortas of OLETF rats exhibited decreased IRS-1 content and increased phosphorylation of IRS-1 at Ser307 compared with LETO rats. There were no significant differences in expressions of IR, PI3-K and Akt/PKB between two groups CONCLUSION: These results suggest that oxidative stress induces insulin resistance in vasculature of OLETF rat specifically through increasing serine phosphorylation of IRS-1 and its degradation by a proteasome-dependent pathway, providing an alternative mechanism that may explain the association with insulin resistance and diabetic vascular complications.

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  • Anti-diabetic effects of benfotiamine on an animal model of type 2 diabetes mellitus
    Kang Min Chung, Wonyoung Kang, Dong Geon Kim, Hyun Ju Hong, Youngjae Lee, Chang-Hoon Han
    Korean Journal of Veterinary Research.2014; 54(1): 21.     CrossRef
Thiazolidinediones on Insulin Resistance and Insulin Secretion in Obese Diabetic OLETF Rats.
Jung hyun Noh, Seung hyun Hong, Kyoung hee Lee, Kyoung Min Min, Tae young Yang, Myung shik Lee, Kwang won Kim, Moon kyu Lee
Korean Diabetes J. 2007;31(1):33-43.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.33
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AbstractAbstract PDF
BACKGROUND
Thiazolidinediones are synthetic peroxisome proliferator-activated receptor-gamma agonists that decrease insulin resistance but, as in vitro and in vivo studies suggest, may have direct beneficial effects on pancreatic beta cells. Here, we investigated the effects of thiazolidinediones (TZDs) on the insulin resistance, beta-cell mass and insulin secretion in obese diabetic OLETF rats. METHODS: We studied insulin resistance (by hyperinsulinemic euglycemic clamp) and insulin secretion (by hyperglycemic clamp) in TZDs administered OLETF and LETO rats. Histologic alterations of the islets were observed and beta-cell mass was also measured by point counting method. RESULTS: Chronic administration of troglitazone (TGZ, 0.15%) or pioglitazone (PGZ, 0.02%) prevented the development of glucose intolerance in OLETF rats, as assessed by oral glucose tolerance test. There was significant difference in submaximal glucose infusion rate between TGZ-treated and untreated OLETF rats during euglycemic clamp studies at 24 weeks of age. At 16 and 24 weeks of ages, beta-cell mass significantly increased in TGZ-treated OLETF rats compared to untreated animals. At 19 weeks and 30 weeks of age, first-phase insulin secretion was not different in PGZ-treated OLETF rats from untreated OLETF rats during hyperglycemic clamp study. At 30 weeks of age, late-phase insulin secretion was decreased in PGZ-treated OLETF rats compared to untreated OLETF rats. The expression of alpha-smooth muscle actin, a marker of activated pancreatic stellate cells that are involved in the fibrosis of the pancreas, in the islets was suppressed by TGZ treatment at 24 weeks of age. CONCLUSION: The treatment of TGZ prevented the development of diabetes, and increased insulin sensitivity and pancreatic beta-cell mass in OLETF rats. These results might be related with the suppression of pancreatic stellate cells. Insulin secretion was not affected by PGZ treatment.
Activin A and Glucose Derived Human Pancreatic Ductal Cells into Insulin-producing Cells.
Seung Hyun Hong, Chul Han, Hyo Sup Kim, Mi Kyung Park, Young Jin Lee, Jae Hoon Jeong, Yong Ki Min, Myung Shik Lee, Kwang Won Kim, Moon Kyu Lee
Korean Diabetes J. 2007;31(1):44-50.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.44
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AbstractAbstract PDF
BACKGROUND
Cellular replacement therapy holds promise for the treatment of diabetes mellitus but donor tissue is severely limited. Human postnatal pancreatic ductal cells are a potential source of new beta cells. Therefore, we investigated the potential of human pancreatic ductal cells could be differentiated into endocrine cells that would be capable of secreting insulin in response to glucose. METHODS: Cell fractions enriched with pancreatic ductal cells after human islet isolation were treated with streptozotocin to remove residual beta cells, grown in monolayer culture, changed the media for differentiation in the presence of activin A and glucose, supplemented with 10% FCS. The differentiation markers, insulin secretion and cell proliferation were examined. RESULT: No insulin was detectable in cell preparations after 5 days of treatment with streptozotocin. In monolayer culture, 80% of the streptozotocin-treated pancreatic ductal cells expressed cytokeratin-19. Cell cultures with a high proportion of cytokeratin-19 cells had greater plasticity for differentiation into cells with phenotypic and functional markers of beta cells. This property were significantly enhanced by treatment of activin A and glucose. The differentiated human pancreatic ductal cells secreted insulin sensitively responded with high glucose. CONCLUSION: Human pancreatic ductal cells are a potential source of new glucose -induced insulin producing cells that may be developed further for clinical use. Therefore, the present data support a possible role for human adult pancreatic ductal cells, following expansion and differentiation, as a source of insulin by transplantation cells to type I diabetes patients.
PDX-1/VP16 Overexpression Induce the Transdifferentiation of Canine Adult Pancreatic Cells into Beta-cells.
Young Hye You, Sun Cheol Park, Seung Hwan Lee, Heon Seok Park, Dong Sik Ham, Marie Rhee, Ji Won Kim, Ki Ho Song, Kun Ho Yoon
Korean Diabetes J. 2007;31(1):51-62.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.51
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AbstractAbstract PDF
BACKGROUND
A major obstacle of islet transplantation is an inadequate supply of insulin-producing tissue. Ad-PDX-1/VP16 overexpression and Exendin-4 treatment have been proved the effects on differentiation and proliferation of pancreatic stem cells. But, the study is insufficient using adult animal pancreatic stem cells. METHODS: Pancreatic cells were prepared from the non-endocrine fraction of canine pancreases. This cells were cultivated free floating state and monolayer culture after dispersion. The floating pancreatic cells were transplanted under the kidney capsule of normoglycaemic nude mice. The dispersed pancreatic cells were infected with Ad-PDX-1/VP16 or Ad-GFP. After infection, those cells were transplanted of nude mice. After transplantation, mice were treated with either 1 nmol/kg exendin-4 or saline solution by intraperitoneal injection for 10 days. RESULTS: The relative volume of the beta-cells in the grafts of the free floating cultured pancreatic cells were 23.4 +/- 13.1% at two weeks and 5.2 +/- 2.0% at eight weeks. At two weeks after transplantation, the relative volume of insulin-positive cells in the grafts of dispersed pancreatic cells were 28 +/- 5.7%, 20.5 +/- 0.7% and 31 +/- 1.4% in control, GFP and PDX-1/VP16 treated groups respectively. At eight weeks after transplantation, the relative volume of insulin-positive cells in the grafts were 11.8 +/- 5.9%, 8 +/- 7.3% and 16.6 +/- 7.4% in control, GFP and PDX-1/VP16 treated groups respectively. Exendin-4 treatment didn't show any additive effects on transdifferentiation of pancreas stem cell into beta-cells. CONCLUSION: The expansion and transdifferentiation were not observed after the transplantation of the free floating cultured pancreatic cells. PDX-1/VP16 overexpression induces the transdifferentiation of adult pancreatic cells into beta-cells. However Exendin-4 treatment hasn't any effects on the expansion and transdifferentiation of the cells in the grafts.

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  • Generation of Functional Insulin-Producing Cells from Neonatal Porcine Liver-Derived Cells by PDX1/VP16, BETA2/NeuroD and MafA
    Dong-Sik Ham, Juyoung Shin, Ji-Won Kim, Heon-Seok Park, Jae-Hyoung Cho, Kun-Ho Yoon, Kathrin Maedler
    PLoS ONE.2013; 8(11): e79076.     CrossRef
  • Adenoviruses Expressing PDX-1, BETA2/NeuroD and MafA Induces the Transdifferentiation of Porcine Neonatal Pancreas Cell Clusters and Adult Pig Pancreatic Cells into Beta-Cells
    Young-Hye You, Dong-Sik Ham, Heon-Seok Park, Marie Rhee, Ji-Won Kim, Kun-Ho Yoon
    Diabetes & Metabolism Journal.2011; 35(2): 119.     CrossRef
  • Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells
    Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung-Hyun Ko, Yu-Bae Ahn, Sung-Dae Moon, Ki-Ho Song
    Korean Diabetes Journal.2009; 33(6): 475.     CrossRef
Prevention of Diabetes by Fenofibrate in OLETF Rats: Hepatic Mechanism for Reducing Visceral Adiposity.
Hye Jeong Lee, Mi Kyoung Park, Kyung Il Lee, Young Jun An, Ji Min Kim, Ja Young Park, Young Han, Sook Hee Hong, Sun Seob Choi, Young Hyun Yoo, Joon Duk Suh, Duk Kyu Kim
Korean Diabetes J. 2007;31(1):63-74.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.63
  • 2,235 View
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  • 4 Crossref
AbstractAbstract PDF
BACKGROUND
The aim of this study is to evaluate the hepatic mechanism of fenofibrate that has the diabetes protective action in rats. METHODS: We chose OLETF rats and divided them into three groups. Fenofibrate (DF) group was fed with diet and fenofibrate (300 mg/kg/day). Paired feeding (Dd) group and free diet (DD) group were fed with diet. After 36 weeks of treatment, all the rats were sacrificed. RESULTS: The fasting blood glucose level of DF group (8.5 +/- 0.9 mmol/L) showed normal. The fasting blood glucose level of Dd group (22.4 +/- 3.0 mmol/L) and DD group (16.9 +/- 3.7 mmol/L) showed significantly increased than that of DF group (P < 0.01, respectively). The body weight, visceral adipose tissue and subcutaneous adipose tissue of DF group were significantly decreased compared to those of Dd and DD groups (P < 0.01, P < 0.05, P < 0.05). DF group showed significantly increased state-3 respiration rate, ATP synthetic activity, state-4 respiration rate and their blood beta-keton body levels than those of control groups (P < 0.01, respectively). DF group showed normal morphology of hepatocytes but DD and Dd groups showed hepatic steatosis with mitochondrial swellings. CONCLUSION: Chronic fenofibrate treatment prevents the development of diabetes in OLETF rats with inhibiting gain of body weight and abdominal adiposity. The hepatic mechanism for reducing visceral adiposity is that fenofibrate leads to increasing oxidative phosphorylation, uncoupling and ketogenesis as well as increasing beta-oxidation of fatty acids. Moreover, fenofibrate treatment prevents the development of hepatic steatosis.

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  • The Differences of Metabolic Syndrome Risk Factors according to Obesity and Abdominal Obesity in Elderly Korean Women
    Kyung-A Shin
    The Korean Journal of Clinical Laboratory Science.2016; 48(4): 304.     CrossRef
  • Effects of Soybean and DJI Chungkukjang Powder on Blood Glucose and Serum Lipid Reduction in db/db Mice
    Jae-Joon Lee, Ah-Ra Kim, Hae-Choon Chang, Hae-Ok Jung, Myung-Yul Lee
    Journal of the Korean Society of Food Science and Nutrition.2012; 41(8): 1086.     CrossRef
  • Comparative analysis of fat and muscle proteins in fenofibratefed type II diabetic OLETF rats: the fenofibrate-dependent expression of PEBP or C11orf59 protein
    Jong-Ryeal Hahm, Jin-Sook Ahn, Hae-Sook Noh, Seon-Mi Baek, Ji-Hye Ha, Tae-Sik Jung, Yong-Jun An, Duk-Kyu Kim, Deok-Ryong Kim
    BMB Reports .2010; 43(5): 337.     CrossRef
  • Comparative analysis of fat and muscle proteins in fenofibratefed type II diabetic OLETF rats: the fenofibrate-dependent expression of PEBP or C11orf59 protein
    Jong-Ryeal Hahm, Jin-Sook Ahn, Hae-Sook Noh, Seon-Mi Baek, Ji-Hye Ha, Tae-Sik Jung, Yong-Jun An, Duk-Kyu Kim, Deok-Ryong Kim
    BMB Reports.2010; 43(5): 337.     CrossRef
Blood Leptin, Anthropometric and Biochemical Parameters in Type 2 Diabetics.
Seong su Moon, Jae han Jeon, Jung eun Lee, Soon hong Park, Hee kyung Kim, Jeong yun Doh, Ye dal Jung, In kyu Lee, Bo wan Kim, Jung guk Kim
Korean Diabetes J. 2007;31(1):75-82.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.75
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Leptin is a hormone which is produced in adipose tissue and regulates food intake and body weight. Leptin is known to correlate with body adiposity such as body mass index. Blood leptin concentration is not different between non-diabetics and diabetics. And It affect not only food intake but may be one of the key factors in the developement of insulin resistance. Recent studies suggest a complex relationship between leptin and insulin resistance or insulin. Therefore we examined the relationship between leptin and anthropometric, biochemical parameters, and insulin resistance in type 2 diabetics. METHOD: The study subjects were 144 patients with type 2 diabetes who visited Kyungpook national university hospital. Anthropometric parameters such as body fat mass, soft lean mass, BMI, arm circumference, skin fold thickness of several sites were measured. Percent body fat were calculated from Brozek fomula, body density were calculated from Jackson and Pollock fomula. Fasting blood leptin and metabolic varables such as C-peptide, HbA1C, insulin, HDL, LDL, TG, total cholesterol, FFA, HOMA-IR were measured. The relationships of blood leptin concentration with clinical data were analyzed with SPSS program. RESULT: Blood leptin concentrations were 8.2 +/- 5.39 ng/mL in women with type 2 diabetes and 5.1 +/- 5.55 ng/mL in men with type 2 diabetes (P-value: 0.01). Percent body fat, FFA were higher in women than men but arm circumference, soft lean mass, waist circumference were higher in men than women (P-value < 0.05). Leptin concentration correlated with BMI, percent body fat, insulin, TG, body fat mass, waist circumference, HOMA-IR. And insulin, C-peptide, total cholesterol, TG were also correlated with leptin only in women with type 2 diabetes. Waist circumference and percent body fat were independent variables which influence blood leptin concentration in multiple regression analysis. CONCLUSION: Blood leptin concentrations are related to parameters such as percent body fat, waist circumference, BMI, body fat mass, insulin, TG, HOMA-IR in type 2 diabetics. The relationship between leptin and obesity or HOMA-IR suggests that leptin may be a one of factors in developement of insulin resistance.

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  • Prognostic Value of Leptin in Terminally Ill Cancer Patients
    Ji Hyun Hong, So Jin Lee, Sang Mi Kwak, Youn Seon Choi, June Yeong Lee
    The Korean Journal of Hospice and Palliative Care.2012; 15(2): 99.     CrossRef
Pedometer-Determined Physical Activity in Type 2 Diabetes in Korea.
Sang Ah Chang, Jung Min Lee, Tae Seo Sohn, Hyun Shik Son, Sung Woo Park, Sei Hyun Baik, Jae Myung Yu, Yeon Ah Sung, Chul Woo Ahn, Kyung Wan Min, Kyung Ah Han
Korean Diabetes J. 2007;31(1):83-88.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.83
  • 1,809 View
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AbstractAbstract PDF
BACKGROUND
Walking is a popular, convenient and relatively safe form of exercise. However, there is few objective data for walking exercise. The aim of this study was to evaluate pedometer-determined physical activity defined as steps/day in type 2 diabetes mellitus. Therefore, it could be the basic data for programming walking exercise in diabetes mellitus. METHODS: Participants with type 2 diabetes who visited in 6 university hospitals on February, 2006 in Seoul and Kyung-gi area were recruited. The participants were asked their ambulatory activity with the given pedometer and calorimeter for 1 week. Total 240 (Male 122, Female 118) subjects who walked above 1000 steps/day were analyzed. We also collected their biochemical data from the medical records. RESULTS: Participants took 8532 +/- 4130 steps for day (step/day) and energy expenditure were 320 +/- 161 Cal/day. Steps/day was not significantly different between male and female, but energy expenditure was higher in male than female ( P < 0.05). Steps/day was significantly lower in obese patients than non-obese patients (P < 0.001). BMI (r = -0.325, P < 0.001), waist circumference (r = -0.287, P < 0.001), triglyceride (r = 0.164, P < 0.018) showed significant inverse correlation with steps/day, but BUN (r = 0.165, P = 0.019) and HDL-cholesterol (r = 0.164, P = 0.018) were positive correlated with steps/day significantly. BMI (r = -0.14, P < 0.032) and cholesterol (r = -0.139, P < 0.041) showed significantly inverse correlation with energy expenditure and BUN (r = 0.187, P = 0.008) and HDL cholesterol (r = 0.145, P < 0.037) positively correlated with energy expenditure. Pedometer-determined steps/day was positively associated with energy expenditure (r2 = 0.824, P < 0.001). CONCLUSION: This study showed the objective quantification of physical activity measured by simple and inexpensive pedometers. It could be used to recommend walking exercise since the practitioners can estimate steps/day for required energy expenditure.
A Clinical Study on the Diabetic Foot Wound.
J Young Kim, Kyung Tai Lee, Ki Won Young, Seung Keun Hwang
Korean Diabetes J. 2007;31(1):89-95.   Published online January 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.1.89
  • 1,959 View
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  • 5 Crossref
AbstractAbstract PDF
PURPOSE: To make protocol on diabetic foot ulcer, with making use of this protocol, investigate hospitalized patients who have had diabetic foot wound and define pattern, characteristics and problems of diabetic foot in hospitalized patients MATERIALS AND METHODS: From Oct. 2002 to Sep. 2003, Seventy-two patients who had been admitted to our hospital due to treatment of diabetic foot wound studied with use of the protocol designed by the authors. RESULTS: The mean age of patients was 64.3 years and male patients were twice as many as female. The most common cause of hospitalization was infection of diabetic foot (77.7%). As a basic pathology of diabetic foot, the main pathology of diabetic foot was the neuropathy that is four times more than vasculopathy. The causations of wound were infection with no specific cause (40.0%). No statistical difference was found between timing of hospitalization and the results of treatment in vasculopathic group but in neuropathic ulcer group, the major procedure such as amputation, and the times of debridement in operation room and are more common in patients who were hospitalized after 3rd days of beginning of symptoms than within 3rd day. CONCLUSION: The education that the patient having a foot symptom have to visit the hospital as soon as possible on patients is important to prevent morbidity of diabetic foot wound, long hospitalization and amputation. The protocol that we are presenting can be modified for other study related to diabetic foot.

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  • Educational Needs Associated with the Level of Complication and Comparative Risk Perceptions in People with Type 2 Diabetes
    Youngji Hwang, Dongsuk Lee, Yeon Sook Kim
    Osong Public Health and Research Perspectives.2020; 11(4): 170.     CrossRef
  • The Changes of Trends in the Diagnosis and Treatment of Diabetic Foot Ulcer over a 10-Year Period: Single Center Study
    Choong Hee Kim, Jun Sung Moon, Seung Min Chung, Eun Jung Kong, Chul Hyun Park, Woo Sung Yoon, Tae Gon Kim, Woong Kim, Ji Sung Yoon, Kyu Chang Won, Hyoung Woo Lee
    Diabetes & Metabolism Journal.2018; 42(4): 308.     CrossRef
  • Factors Contributing to Diabetic Foot Ulcer among Patients with Type 2 Diabetes Mellitus
    Seo Jin Park, Taeyoung Yang, Jun Young Lee, Jinhee Kim
    Korean Journal of Adult Nursing.2018; 30(1): 106.     CrossRef
  • Prevalence and Current Status of Treatment of Diabetic Foot in South Korea
    Jae-Ik Bae, Je Hwan Won, Jun Su Kim, Man Deuk Kim, Chang Jin Yoon, Yun Ku Cho
    Journal of the Korean Society of Radiology.2016; 74(3): 169.     CrossRef
  • Diabetic Foot
    Kwang-Won Kim
    Journal of the Korean Medical Association.2007; 50(5): 447.     CrossRef

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