International Journal of Computer Science & Network Security
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제21권2호
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pp.9-13
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2021
Type 2 diabetes mellitus (T2D) is a complex diabetes disease that is caused by high blood sugar, insulin resistance, and a relative lack of insulin. Many studies are trying to predict variant genes that causes this disease by using a sample disease model. In this paper we predict diabetic and normal persons by using fisher score feature selection, chi-2 feature selection and Logistic Regression supervised learning algorithm with best accuracy of 90.23%.
Purpose: This study focused on identifying the interaction effects of genetic and lifestyle-environmental factors on the development of type 2 diabetes mellitus (T2D). Methods: Study subjects were selected from the Korean Genome and Epidemiology Study (KoGES) from 2001 to 2014. Data on genetic variations, anthropometric measurements, biochemical data, and seven lifestyle factors (diet, physical activity, alcohol drinking, smoking, sleep, depression, and stress) were obtained from 4,836 Koreans aged between 40 and 59 years, including those with T2D at baseline (n = 1,209), newly developed T2D (n= 1,298) and verified controls (n = 3,538). The genetic risk score (GRS) was calculated by using 11 single-nucleotide polymorphisms (SNPs) related to T2D development and the second quartile was used as the reference category. A Cox proportional hazards regression model was used to evaluate the associations of GRS and lifestyle factors with T2D risk, controlling for covariates. Results: Multivariate regression analysis revealed that GRS was the strongest risk factor for T2D, and body mass index (BMI), smoking, drinking, and spicy food preference also increased the risk. Lifestyle/environmental factors that showed significant interactions with GRS were BMI, current smoking, current drinking, fatty food preference, and spicy food preference. Conclusions: Interactions between genetic factors and lifestyle/environmental factors were associated with an increased risk of T2D. The results will be useful to provide a new perspective on genetic profiling for the earlier detection of T2D risk and clues for personalized interventions, which might be more effective prevention strategies or therapies in individuals with a genetic predisposition to T2D.
Recent papers have shown that the initial event in the pathogenesis of autoimmune type 1 diabetes (T1D) comprises sensing of molecular patterns released from apoptotic ${\beta}$-cells by innate immune receptors such as toll-like receptor (TLR). We have reported that apoptotic ${\beta}$-cells undergoing secondary necrosis called 'late apoptotic' ${\beta}$-cells stimulate dendritic cells (DCs) and induce diabetogenic T cell priming through TLR2. The role of other innate immune receptors such as TLR7 or TLR9 in the initiation of T1D has also been suggested. We hypothesized that TLR2 blockade could inhibit T1D at the initial step of T1D. Indeed, when a TLR2 agonist, $Pam3CSK_4$ was administered chronically, the development of T1D in nonobese diabetic (NOD) mice was inhibited. Diabetogenic T cell priming by DCs was attenuated by chronic treatment with $Pam3CSK_4$, indicating DC tolerance. For the treatment of established T1D, immune tolerance alone is not enough because ${\beta}$-cell mass is critically reduced. We employed TLR2 tolerance in conjunction with islet transplantation, which led to reversal of newly established T1D. Dipeptidyl peptidase 4 (DPP4) inhibitors are a new class of anti-diabetic agents that have beneficial effects on ${\beta}$-cells. We investigated whether a combination of DPP4 inhibition and TLR2 tolerization could reverse newly established T1D without islet transplantation. We could achieve normoglycemia by TLR2 tolerization in combination with DPP4 inhibition but not by TLR2 tolerization or DPP4 inhibition alone. ${\beta}$-cell mass was significantly increased by combined treatment with TLR2 tolerization and DPP4 inhibition. These results suggest the possibility that a novel strategy of TLR tolerization will be available for the inhibition or treatment of established T1D when combined with measures increasing critically reduced ${\beta}$-cell mass of T1D patients such as DPP4 inhibition or stem cell technology.
Kim, Hyesook;Park, Seokyung;Yang, Hyesu;Choi, Young Ju;Huh, Kap Bum;Chang, Namsoo
Nutrition Research and Practice
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제9권5호
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pp.496-502
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2015
BACKGROUND/OBJECTIVES: This study was performed to investigate the association between the dietary intake of fish and shellfish, and omega-3 polyunsaturated fatty acids (PUFAs) and cardiovascular disease (CVD) risk factors in the middle-aged Korean female patients with Type 2 diabetes (T2D). SUBJECTS/METHODS: A cross-sectional analysis was performed with 356 female patients (means age: 55.5 years), who were recruited from the Huh's Diabetes Clinic in Seoul, Korea between 2005 and 2011. The dietary intake was assessed by a validated semi-quantitative food frequency questionnaire and analyzed using the Computer Aided Nutritional Analysis program (CAN-Pro) version 4.0 software. RESULTS: In a multiple regression analysis after the adjustment for confounding factors such as age, BMI, duration of diagnosed T2D, alcohol consumption, fiber intake, sodium intake, and total energy intake, fish and shellfish intake of the subjects was negatively associated with triglyceride and pulse wave velocity (PWV). Omega-3 PUFAs intake was negatively associated with triglyceride, systolic blood pressures, diastolic blood pressures, and PWV. The multiple logistic regression analysis with the covariates showed a significant inverse relationship between the omega-3 PUFAs consumption and prevalence of hypertriglyceridemia [OR (95% CI) for greater than the median compared to less than the median: 0.395 (0.207-0.753)]. CONCLUSIONS: These results suggest that the consumption of fish and shellfish, good sources of omega-3 PUFAs, may reduce the risk factors for CVD in the middle-aged female patients with T2D.
Park, Mi-Kyoung;Seo, Su-Yeong;Hong, Sook-Hee;Kim, Hye-Jin;Park, Eun-Jin;Kim, Duk-Kyu;Lee, Hye-Jeong
The Korean Journal of Physiology and Pharmacology
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제10권1호
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pp.39-44
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2006
Type I diabetes (T1D) is an organ-specific autoimmune disease caused by the T cell-mediated destruction of the insulin-producing ${\beta}$ cells in the pancreatic islets. The onset of T1D is the consequence of a progressive destruction of islet ${\beta}$ cells mediated by an imbalance between effector $CD4^+$ T helper (Th)1 and regulatory $CD4^+$ Th2 cell function. Since interferon-alpha (IFN-${\alpha}$) has been known to modulate immune function and autoimmunity, we investigated whether administration of adenoviralmediated IFN-${\alpha}$ gene would inhibit the diabetic process in NOD mice. The development of diabetes was significantly inhibited by a single injection of adenoviral-mediated IFN-${\alpha}$ gene before 8 weeks of age. Next, we examined the hypothesis that Th2-type cytokines are associated with host protection against autoimmune diabetes, whereas Th1-type cytokines are associated with pathogenesis of T1D. The expression of IFN-${\alpha}$ induced increase of serum IL-4 and IL-6 (Th2 cytokines) levels and decrease of serum IL-12 and IFN-${\gamma}$ (Th1 cytokines) levels. Therefore, overexpression of IFN-${\alpha}$ by adenoviralmediated delivery provides modulation of pathogenic progression and protection of NOD mice from T1D.
Hyun Jeong Cho;Akinkunmi Paul Okekunle ;Ga-Eun Yie ;Jiyoung Youn ;Moonil Kang;Taiyue Jin;Joohon Sung;Jung Eun Lee
Nutrition Research and Practice
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제17권4호
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pp.789-802
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2023
BACKGROUND/OBJECTIVES: Habitual coffee consumption was inversely associated with type 2 diabetes (T2D) and hyperglycemia in observational studies, but the causality of the association remains uncertain. This study tested a causal association of genetically predicted coffee consumption with T2D using the Mendelian randomization (MR) method. SUBJECTS/METHODS: We used five single-nucleotide polymorphisms (SNPs) as instrumental variables (IVs) associated with habitual coffee consumption in a previous genome-wide association study among Koreans. We analyzed the associations between IVs and T2D, fasting blood glucose (FBG), 2h-postprandial glucose (2h-PG), and glycated haemoglobin (HbA1C) levels. The MR results were further evaluated by standard sensitivity tests for possible pleiotropism. RESULTS: MR analysis revealed that increased genetically predicted coffee consumption was associated with a reduced prevalence of T2D; ORs per one-unit increment of log-transformed cup per day of coffee consumption ranged from 0.75 (0.62-0.90) for the weighted mode-based method to 0.79 (0.62-0.99) for Wald ratio estimator. We also used the inverse-variance-weighted method, weighted median-based method, MR-Egger method, and MR-PRESSO method. Similarly, genetically predicted coffee consumption was inversely associated with FBG and 2h-PG levels but not with HbA1c. Sensitivity measures gave similar results without evidence of pleiotropy. CONCLUSIONS: A genetic predisposition to habitual coffee consumption was inversely associated with T2D prevalence and lower levels of FBG and 2h-PG profiles. Our study warrants further exploration.
Purpose: This study was performed to identify lower urinary tract symptoms (LUTS), and to evaluate the factors affecting LUTS in patients with type 2 diabetes mellitus (T2DM). Methods: The cross sectional study was used with a structured questionnaire to collect data through interviews with 181 T2DM patients and their clinical data from a university hospital diabetes clinic from October 2010 to April 2012. LUTS were measured using the International Prostate Symptom Score (IPSS), depression using the Center for Epidemiologic Studies Depression Scale (CES-D), and glycosylated hemoglobin (HbA1c) from the clinical data. Results: Of all patients with T2DM, the mean IPSS of LUTS was $9.34{\pm}6.86$. Concerning the reported severity of LUTS, 53.6% of the subjects were in the moderate and severe group. In each symptom score of LUTS (range 0-5), nocturia was the highest 2.04, weak stream 1.62, and frequency 1.45. LUTS was significantly predicted by HbA1c and depression, and 14.3% of the variance in LUTS was explained. Conclusion: HbA1c and depression were found to be very important factors associated with LUTS in T2DM patients.
Background: It has been recently noticed that type 2 diabetes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3'-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells. Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and followed by FACS analysis for the surface molecules. Results: Cordycepin inhibited the production of NO and pro-inflammatory cytokines such as IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ in LPS-activated macrophages via suppressing protein expression of pro-inflammatory mediators. T2D regulating genes such as $11{\beta}$-HSD1 and PPAR${\gamma}$ were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration. In accordance with suppressed pro-inflammatory cytokine production lead to inhibition of diabetic regulating genes in activated macrophages. Cordycepin suppressed NF-${\kappa}B$ activation in LPS-activated macrophages. Conclusion: Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-${\kappa}B$ dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.
Montevecchi, Marco;Valeriani, Leoluca;Gatto, Maria Rosaria;D'Alessandro, Giovanni;Piana, Gabriela
Journal of Periodontal and Implant Science
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제51권6호
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pp.409-421
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2021
Purpose: The aim of this study was to compare the prevalence and bacterial load of 6 main periodontal pathogens between pairs of periodontal patients with and without type 2 diabetes mellitus. Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans genotypes were also investigated. Methods: Twenty patients affected by chronic periodontitis and type 2 diabetes were retrospectively selected and matched to 20 patients without diabetes on the basis of the degree and severity of periodontal disease. Microbiological data of subgingival biofilms were analysed and compared for the examined pathogens: A. actinomycetemcomitans, P. gingivalis, Prevotella intermedia, Treponema denticola, Fusobacterium nucleatum, and Tannerella forsythia. Results: The pairs were balanced in terms of demographic and clinical parameters, except for bleeding on probing and suppuration. In the microbiological test sites (4 for each patient), the mean probing pocket depth was 6.34±1.63 mm in patients with diabetes and 6.41±1.78 mm in patients without diabetes. No significant difference between pairs in the prevalence of P. gingivalis or the distribution of its genotypes was recorded. Patients with diabetes had a significantly greater amount of total bacterial load, P. gingivalis, T. denticola, T. forsythia, and F. nucleatum (P<0.05). Moreover, patients with diabetes had a higher number of sites with a greater cell count than patients without diabetes. When compared to the total bacterial load, only T. forsythia maintained its relative load in patients with diabetes (P=0.001). Conclusions: This retrospective matched study supports the hypothesis that microbiological differences exist among periodontal patients with and without diabetes mellitus.
Noviana Astuti Irna Sakir;Su Bin Hwang;Hyeon Ju Park;Bog-Hieu Lee
Nutrition Research and Practice
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제18권1호
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pp.132-148
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2024
BACKGROUND/OBJECTIVES: This study aimed to assess the current mean daily intake of 10 food groups, analyze the sociodemographic factors associated with food consumption, and determine the associations between food consumption/dietary intake and the prevalence rates of obesity, type 2 diabetes (T2D), and hypertension (HTN) in Jakarta, Indonesia. SUBJECTS/METHODS: A total of 600 participants aged 20-85 yrs were included in this cross-sectional study. Food consumption and dietary habits were assessed using a food frequency questionnaire. To determine the association between food consumption/dietary habits and the abovementioned diseases, logistic regression analysis was performed. RESULTS: The average vegetable and fruit intake was lower, while sugar and salt consumption were higher than that recommended by Indonesia's national dietary guidelines. A high intake of ultra-processed foods (UPFs) was associated with young age, men, "single" status, a high education level, and employment with a high monthly income. Obesity and T2D were positively correlated with high intakes of cereals and tubers, UPFs, sugars, fats, and oils. Conversely, an inverse association was found between legume, vegetable, and fruit consumption and obesity risk. An inverse correlation was also observed between vegetable consumption and T2D risk. Moreover, a high salt intake was inversely correlated with fruit consumption in terms of HTN risk. Non-indulgence in habitual late-night snacking and refrainment from consuming more than one dish at each meal were also negatively related to the prevalence of obesity, T2D, and HTN. Inverse correlations were also observed between the prevalence rates of T2D and HTN and abstaining from adding sugar to beverages. CONCLUSION: Foods high in fat, sugar, and sodium were strongly associated with the risks of obesity, T2D, and HTN. Additionally, poor eating habits were also associated with disease development.
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