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BACKGROUND AND AIMS: Longitudinal change in income is crucial in explaining cardiovascular health inequalities. However, there is limited evidence for cardiovascular disease (CVD) risk associated with income dynamics over time among individuals with type 2 diabetes (T2D). METHODS: Using a nationally representative sample from the Korean National Health Insurance Service database, 1 528 108 adults aged 30-64 with T2D and no history of CVD were included from 2009 to 2012 (mean follow-up of 7.3 years). Using monthly health insurance premium information, income levels were assessed annually for the baseline year and the four preceding years. Income variability was defined as the intraindividual standard deviation of the percent change in income over 5 years. The primary outcome was a composite event of incident fatal and nonfatal CVD (myocardial infarction, heart failure, and stroke) using insurance claims. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated after adjusting for potential confounders. RESULTS: High-income variability was associated with increased CVD risk (HRhighest vs. lowest quartile 1.25, 95% CI 1.22-1.27; Ptrend < .001). Individuals who experienced an income decline (4 years ago vs. baseline) had increased CVD risk, which was particularly notable when the income decreased to the lowest level (i.e. Medical Aid beneficiaries), regardless of their initial income status. Sustained low income (i.e. lowest income quartile) over 5 years was associated with increased CVD risk (HRn = 5 years vs. n = 0 years 1.38, 95% CI 1.35-1.41; Ptrend < .0001), whereas sustained high income (i.e. highest income quartile) was associated with decreased CVD risk (HRn = 5 years vs. n = 0 years 0.71, 95% CI 0.70-0.72; Ptrend < .0001). Sensitivity analyses, exploring potential mediators, such as lifestyle-related factors and obesity, supported the main results. CONCLUSIONS: Higher income variability, income declines, and sustained low income were associated with increased CVD risk. Our findings highlight the need to better understand the mechanisms by which income dynamics impact CVD risk among individuals with T2D.
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Enfermedades Cardiovasculares , Diabetes Mellitus Tipo 2 , Renta , Humanos , Femenino , Masculino , Persona de Mediana Edad , Diabetes Mellitus Tipo 2/epidemiología , Diabetes Mellitus Tipo 2/complicaciones , Renta/estadística & datos numéricos , Adulto , Enfermedades Cardiovasculares/epidemiología , República de Corea/epidemiología , Incidencia , Factores de RiesgoRESUMEN
BACKGROUND: Individuals with type 2 diabetes (T2D) have increased colorectal cancer (CRC) risk, but it is unknown whether income dynamics are associated with CRC risk in these individuals. We examined whether persistent low- or high-income and income changes are associated with CRC risk in non-elderly adults with T2D. METHODS: Using nationally representative data from the Korean Health Insurance Service database, 1,909,492 adults aged 30 to 64 years with T2D and no history of cancer were included between 2009 and 2012 (median follow-up of 7.8 years). We determined income levels based on health insurance premiums and assessed annual income quartiles for the baseline year and the four preceding years. Hazard ratios(HRs) and 95% confidence intervals(CIs) were estimated after adjusting for sociodemographic factors, CRC risk factors, and diabetes duration and treatment. RESULTS: Persistent low income (i.e., lowest income quartile) was associated with increased CRC risk (HRn=5years vs. n=0years 1.11, 95% CI 1.04-1.18; P for trend=0.004). Income declines (i.e., a decrease≥25% in income quantile) were also associated with increased CRC risk (HR≥2 vs. 0 declines 1.10, 95% CI 1.05-1.16; p for trend=0.001). In contrast, persistent high income (i.e., highest income quartile) was associated with decreased CRC risk (HRn=5years vs. n=0years 0.81, 95% CI 0.73-0.89; p for trend<0.0001), which was more pronounced for rectal cancer (HR 0.64, 95% CI 0.53-0.78) and distal colon cancer (HR 0.70, 95% CI 0.57-0.86). CONCLUSIONS: Our findings underscore the need for increased public policy awareness of the association between income dynamics and CRC risk in adults with T2D.
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Alcohol consumption exacerbates liver abnormalities in animal models, but whether it increases the severity of liver disease in early diabetic or prediabetic rats is unclear. To investigate the molecular mechanisms underlying alcohol-induced liver steatosis or hepatitis, we used a prediabetic animal model. Otsuka Long-Evans Tokushima Fatty (OLETF) and Long-Evans Tokushima Fatty (LETO) rats were pair-fed with an ethanol-containing liquid diet for 6 weeks. Compared with controls, OLETF and LETO rats displayed more pronounced liver steatosis and higher plasma levels of serum glutamic oxaloacetic transaminase (SGOT) and serum glutamate pyruvate transaminase (SPGT), indicating liver injury. Ethanol-fed LETO (Pd-L-E) rats showed mild liver steatosis and no inflammation compared with ethanol-fed OLETF (Pd-O-E) rats. Although precursor and active SREBP-1 levels in the liver of ethanol-fed OLETF rats significantly increased compared with control diet-fed OLETF rats (Pd-O-C), those of Pd-L-E rats did not. Bone morphogenetic protein (BMP) and TGF-ß1 balance in Pd-O-E rats was significantly altered because BMP signaling was upregulated by inducing BMP2, BMP4, BMP7, BMP9, Smad1, and Smad4, whereas TGF-ß1, Smad3, and Erk were downregulated. Activation of TGF-ß/Smad signaling inhibited BMP2 and BMP9 expression and increased epithelial-mesenchymal transition (EMT) marker levels (Hepcidin, Snail, and Twist) in the liver of LETO rats. Livers of ethanol-fed OLETF rats showed increased levels of vimentin, FSP-1, α-SMA, MMP1, MMP13, and collagen III compared with rats of other groups, whereas EMT marker levels did not change. Thus, BMP exerted anti- and/or pro-fibrotic effects in ethanol-fed rats. Therefore, BMP and TGF-ß, two key members of the TGF-ß superfamily, play important but diverse roles in liver steatosis in young LETO and OLETF rats.
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Diabetes Mellitus Tipo 2 , Enfermedad del Hígado Graso no Alcohólico , Estado Prediabético , Masculino , Ratas , Animales , Ratas Endogámicas OLETF , Estado Prediabético/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Factor de Crecimiento Transformador beta1 , Etanol/toxicidad , Enfermedad del Hígado Graso no Alcohólico/etiología , Factor de Crecimiento Transformador beta , Modelos Animales de EnfermedadRESUMEN
DA-9801, a plant-based drug used for the treatment of diabetic neuropathy, is known to improve angiotensin II (Ang II)-induced vascular endothelial cell dysfunction. However, the underlying mechanism is not fully understood. We aimed to determine whether the protective effect of DA-9801 against Ang II-induced endothelial cell dysfunction was mediated via inhibition of endothelial cell inflammation and apoptosis. Ang II-induced oxidative stress was attenuated by pretreatment of human dermal microvascular endothelial cells (HDMECs) with DA-9801. This prevented the Ang II-induced upregulation of NAD(P)H oxidase (the NOX4 and p22phox subunits) and reactive oxygen species. Further, pretreatment of HDMECs with DA-9801 ameliorated Ang II-mediated nuclear factor kappa B activity via prevention of the upregulation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase. It also decreased the Ang II-stimulated increase in inducible nitric oxide synthase (NOS) and decreased endothelial NOS protein expression. DA-9801 decreased Ang II-induced upregulation of intercellular adhesion molecule 1, vascular adhesion molecule, and E-selectin in HDMECs. Moreover, TUNEL and annexin V-FITC fluorescence staining for apoptosis and the activities of caspases 9, 7, and 3 decreased in HDMECs pretreated with DA-9801, indicating that the drug enhanced anti-apoptotic pathways. Thus, DA-9801 modulated Ang II-induced endothelial cell dysfunction via inflammatory and apoptotic pathways.
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Angiotensina II/efectos adversos , Apoptosis/efectos de los fármacos , Células Endoteliales/patología , Células Endoteliales/fisiología , Inflamación/metabolismo , Preparaciones de Plantas/farmacología , Células Cultivadas , Dermis/citología , Humanos , Molécula 1 de Adhesión Intercelular/metabolismo , NADPH Oxidasas/metabolismo , FN-kappa B/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismoRESUMEN
The objective of this study was to investigate molecular and physiological changes in response to long-term insulin glargine treatment in the skeletal muscle of OLETF rats. Male Otsuka Long-Evans Tokushima Fatty (OLETF) and Long-Evans Tokushima Otsuka (LETO) rats aged 24 weeks were randomly allocated to either treatment with insulin for 24 weeks or no treatment, resulting in three groups. Insulin glargine treatment in OLETF rats (OLETF-G) for 24 weeks resulted in changes in blood glucose levels in intraperitoneal glucose tolerance tests compared with age-matched, untreated OLETF rats (OLETF-C), and the area under the curve was significantly decreased for OLETF-G rats compared with OLETF-C rats (P < 0.05). The protein levels of MHC isoforms were altered in gastrocnemius muscle of OLETF rats, and the proportions of myosin heavy chain type I and II fibers were lower and higher, respectively, in OLETF-G compared with OLETF-C rats. Activation of myokines (IL-6, IL-15, FNDC5, and myostatin) in gastrocnemius muscle was significantly inhibited in OLETF-G compared with OLETF-C rats ( P < 0.05). MyoD and myogenin levels were decreased, while IGF-I and GLUT4 levels were increased, in the skeletal muscle of OLETF-G rats ( P < 0.05). Insulin glargine treatment significantly increased the phosphorylation levels of AMPK, SIRT1, and PGC-1α. Together, our results suggested that changes in the distribution of fiber types by insulin glargine could result in downregulation of myokines and muscle regulatory proteins. The effects were likely associated with activation of the AMPK/SIRT1/PGC-1α signaling pathway. Changes in these proteins may at least partly explain the effect of insulin in skeletal muscle of diabetes mellitus.
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AIMS/HYPOTHESIS: Asians have a propensity to develop type 2 diabetes with a lower BMI than Western populations. This discrepancy may be due to differences in body fat and muscle mass for a given BMI. However, unlike adiposity, it is unclear whether muscle mass affects the risk of type 2 diabetes in Asian populations. METHODS: We conducted a 2-yearly prospective assessment of 6895 participants who were free of diabetes at the baseline examination as part of the Korean Genome Epidemiology Study. The muscle mass index (MMI) was defined as the weight-adjusted appendicular skeletal muscle mass. Using Cox regression models, we evaluated the association between MMI and the risk of developing type 2 diabetes across sex-specific tertiles of MMI. Low muscle mass was defined as the sex-specific lowest tertile of MMI. Main covariates included age, sex, urban or rural residence, family history of diabetes, hypertension, smoking status, education level, monthly income, physical activity, alcohol consumption and diet. In addition, body fat mass, waist circumference and BMI were controlled as categorical variables. Obesity was defined as a BMI of ≥25 kg/m2 or a waist circumference of ≥90 cm for men and ≥85 cm for women. RESULTS: During a median follow-up of 9.06 years, 1336 participants developed type 2 diabetes. At baseline, the mean age was 52.1 years and the mean BMI was 24.4 kg/m2. The mean MMI for men and women was 32.1% and 26.0%, respectively. There was an inverse association between MMI and the risk of type 2 diabetes. Multivariate-adjusted HRs for the risk of developing type 2 diabetes were 2.05 (95% CI 1.73, 2.43), 1.39 (95% CI 1.17, 1.66) and 1.0 from the lowest to highest sex-specific MMI tertile, with an HR of 1.35 (95% CI 1.26, 1.45) per SD decline in MMI. Further adjustments for fat mass, waist circumference and BMI as categorical variables did not modify the relationship (each p < 0.01). In BMI-stratified analyses, the population-attributable fraction of the lowest tertile of MMI for developing type 2 diabetes was increased by 11.9% in the non-obese group and 19.7% in the obese group. CONCLUSIONS/INTERPRETATION: Low muscle mass as defined by MMI was associated with an increased risk of type 2 diabetes, independent of general obesity, in middle-aged and older Korean adults.
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Diabetes Mellitus Tipo 2/epidemiología , Diabetes Mellitus Tipo 2/metabolismo , Músculo Esquelético/fisiología , Factores de Edad , Pueblo Asiatico , Composición Corporal/fisiología , Índice de Masa Corporal , Peso Corporal/fisiología , Diabetes Mellitus Tipo 2/fisiopatología , Ejercicio Físico/fisiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Análisis Multivariante , Músculo Esquelético/metabolismo , Obesidad/metabolismo , Obesidad/fisiopatología , Modelos de Riesgos Proporcionales , Estudios Prospectivos , Circunferencia de la Cintura/fisiologíaRESUMEN
BACKGROUND: Element™ Auto-coding Blood Glucose Monitoring System (BGMS; Infopia Co., Ltd., Anyang-si, Korea) was developed for self-monitoring of blood glucose (SMBG). METHODS: Precision, linearity, and interference were tested. Eighty-four capillary blood samples measured by Element™ BGMS were compared with central laboratory method (CLM) results in venous serum. Accuracy was evaluated using ISO 15197:2013 criteria. RESULTS: Coefficients of variation (CVs; mean) were 2.4% (44.2 mg/dl), 3.7% (100.6 mg/dl), and 2.1% (259.8 mg/dl). Linearity was shown at concentrations 39.25-456.25 mg/l (y = 0.989 + 0.984x, SE = 17.63). Up to 15 mg/dl of galactose, ascorbic acid, and acetaminophen, interference > 10.4% was not observed. Element™ BGMS glucose was higher than CLM levels by 3.2 mg/dl (at 200 mg/dl) to 8.2 mg/dl (at 100 mg/dl). The minimum specification for bias (3.3%) was met at 140 and 200 mg/l glucose. In the Clarke and consensus error grids, 100% of specimens were within zone A and B. For Element™ BGMS values, 92.9% (78/84) to 94.0% (79/84) were within a 15 mg/dl (< 100 mg/dl) or 15% (> 100 mg/dl) of the average CLM value. CONCLUSION: Element™ BGMS was considered an appropriate SMBG for home use; however, the positive bias at low-to-mid glucose levels requires further improvement.
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Automonitorización de la Glucosa Sanguínea/métodos , Glucemia/análisis , Diabetes Mellitus/sangre , Adulto , Anciano , Diabetes Mellitus/diagnóstico , Femenino , Humanos , Modelos Lineales , Masculino , Persona de Mediana Edad , Valores de Referencia , Reproducibilidad de los Resultados , Estudios Retrospectivos , Sensibilidad y EspecificidadRESUMEN
Many studies have reported the frequency and distribution of haplogroups among various cattle breeds for verification of their origins and genetic diversity. In this study, 318 complete sequences of the mtDNA control region from four Korean cattle breeds were used for haplogroup classification. 71 polymorphic sites and 66 haplotypes were found in these sequences. Consistent with the genetic patterns in previous reports, four haplogroups (T1, T2, T3, and T4) were identified in Korean cattle breeds. In addition, T1a, T3a, and T3b sub-haplogroups were classified. In the phylogenetic tree, each haplogroup formed an independent cluster. The frequencies of T3, T4, T1 (containing T1a), and T2 were 66%, 16%, 10%, and 8%, respectively. Especially, the T1 haplogroup contained only one haplotype and a sample. All four haplogroups were found in Chikso, Jeju black and Hanwoo. However, only the T3 and T4 haplogroups appeared in Heugu, and most Chikso populations showed a partial of four haplogroups. These results will be useful for stable conservation and efficient management of Korean cattle breeds.
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Chronic ethanol consumption induces pancreatic ß-cell dysfunction through glucokinase (Gck) nitration and down-regulation, leading to impaired glucose tolerance and insulin resistance, but the underlying mechanism remains largely unknown. Here, we demonstrate that Gck gene expression and promoter activity in pancreatic ß-cells were suppressed by chronic ethanol exposure in vivo and in vitro, whereas expression of activating transcription factor 3 (Atf3) and its binding to the putative Atf/Creb site (from -287 to -158 bp) on the Gck promoter were up-regulated. Furthermore, in vitro ethanol-induced Atf3 inhibited the positive effect of Pdx-1 on Gck transcriptional regulation, enhanced recruitment of Hdac1/2 and histone H3 deacetylation, and subsequently augmented the interaction of Hdac1/Pdx-1 on the Gck promoter, which were diminished by Atf3 siRNA. In vivo Atf3-silencing reversed ethanol-mediated Gck down-regulation and ß-cell dysfunction, followed by the amelioration of impaired glucose tolerance and insulin resistance. Together, we identified that ethanol-induced Atf3 fosters ß-cell dysfunction via Gck down-regulation and that its loss ameliorates metabolic syndrome and could be a potential therapeutic target in treating type 2 diabetes. The Atf3 gene is associated with the induction of type 2 diabetes and alcohol consumption-induced metabolic impairment and thus may be the major negative regulator for glucose homeostasis.
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Factor de Transcripción Activador 3/metabolismo , Consumo de Bebidas Alcohólicas , Depresores del Sistema Nervioso Central/efectos adversos , Etanol/efectos adversos , Glucoquinasa/biosíntesis , Síndrome Metabólico , Transcripción Genética/efectos de los fármacos , Factor de Transcripción Activador 3/genética , Consumo de Bebidas Alcohólicas/efectos adversos , Consumo de Bebidas Alcohólicas/genética , Consumo de Bebidas Alcohólicas/metabolismo , Animales , Línea Celular , Depresores del Sistema Nervioso Central/farmacología , Diabetes Mellitus Tipo 2/inducido químicamente , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/metabolismo , Etanol/farmacología , Regulación Enzimológica de la Expresión Génica/efectos de los fármacos , Regulación Enzimológica de la Expresión Génica/genética , Glucoquinasa/genética , Glucosa/genética , Glucosa/metabolismo , Histona Desacetilasa 1/genética , Histona Desacetilasa 1/metabolismo , Histona Desacetilasa 2/genética , Histona Desacetilasa 2/metabolismo , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Humanos , Células Secretoras de Insulina/metabolismo , Masculino , Síndrome Metabólico/etiología , Síndrome Metabólico/genética , Síndrome Metabólico/metabolismo , Ratones , Ratas , Elementos de Respuesta , Transactivadores/genética , Transactivadores/metabolismo , Transcripción Genética/genéticaRESUMEN
Alcohol consumption increases the risk of type 2 diabetes. However, its effects on prediabetes or early diabetes have not been studied. We investigated endoplasmic reticulum (ER) stress in the pancreas and liver resulting from chronic alcohol consumption in the prediabetes and early stages of diabetes. We separated Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type-2 diabetic animal model, into two groups based on diabetic stage: prediabetes and early diabetes were defined as occurrence between the ages of 11 to 16 weeks and 17 to 22 weeks, respectively. The experimental group received an ethanol-containing liquid diet for 6 weeks. An intraperitoneal glucose tolerance test was conducted after 16 and 22 weeks for the prediabetic and early diabetes groups, respectively. There were no significant differences in body weight between the control and ethanol groups. Fasting and 120-min glucose levels were lower and higher, respectively, in the ethanol group than in the control group. In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the liver. In early diabetes rats, alcohol significantly increased most ER stress-marker levels in both the pancreas and liver. These results indicate that chronic alcohol consumption increased the risk of diabetes in prediabetic and early diabetic OLETF rats; the pancreas was more susceptible to damage than was the liver in the early diabetic stages, and the adaptive and proapoptotic pathway of ER stress may play key roles in the development and progression of diabetes affected by chronic alcohol ingestion.
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AIMS: The objective of this study was to demonstrate that sustained-release (SR) pregabalin is non-inferior to immediate-release (IR) pregabalin in attenuating diabetic peripheral neuropathic (DPN) pain along with patient satisfaction and compliance. METHODS: This was an 8-week, randomized, active-controlled, open-label, phase 4 study. Eligible subjects who had been on IR pregabalin for 4 weeks were randomized to 1:1 ratio to either continue with twice-daily IR pregabalin (75 mg), or to switch to once-daily SR pregabalin (150 mg). Primary efficacy endpoint was the change in visual analogue scale (VAS) scores after 8 weeks of treatment compared to baseline in both SR and IR pregabalin groups. RESULTS: Among 130 randomized subjects, 125 patients were included in full analysis set. For the change in VAS pain score, the least squares (LS) mean were -17.95 (SR pregabalin) and -18.74 (IR pregabalin) and the LS mean difference between both groups was 0.79, with the upper limit of the 95 % confidence interval [-5.99, 7.58] below the pre-specified non-inferiority margin of 9.2 mm. CONCLUSIONS: This study demonstrates that the new once-daily SR pregabalin formulation is not different to the twice-daily IR pregabalin in alleviating DPN pain, indicating its potential as a promising treatment for DPN pain with a comparable safety profile. TRIAL REGISTRATION: ClinicalTrials.gov, NCT05624853.
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Analgésicos , Preparaciones de Acción Retardada , Diabetes Mellitus Tipo 2 , Neuropatías Diabéticas , Neuralgia , Pregabalina , Humanos , Pregabalina/administración & dosificación , Pregabalina/uso terapéutico , Pregabalina/efectos adversos , Masculino , Persona de Mediana Edad , Femenino , Neuropatías Diabéticas/tratamiento farmacológico , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Anciano , Analgésicos/administración & dosificación , Analgésicos/uso terapéutico , Analgésicos/efectos adversos , Neuralgia/tratamiento farmacológico , Resultado del Tratamiento , Dimensión del Dolor , Adulto , Esquema de Medicación , Satisfacción del PacienteRESUMEN
OBJECTIVES: The aim of this study was to evaluate the effects of early intensive insulin therapy on body fat distribution, lean body mass and ß-cell function in patients with newly diagnosed type 2 diabetes. METHODS: Thirty-eight subjects with newly diagnosed type 2 diabetes participated in a 12-week course of intensive insulin therapy. Patients were administered a 75 g oral glucose tolerance test (OGTT), underwent measurement of visceral and subcutaneous adipose tissues (VAT and SAT) using computed tomography and appendicular skeletal muscle (ASM) mass was assessed using dual-energy X-ray absorptiometry. RESULTS: After intensive insulin therapy, fasting plasma glucose and HbA1c levels decreased. Homeostasis model assessment (HOMA)-B, the insulinogenic index, and the C-peptide-to-glucose area under the curve (AUC) ratio increased. The insulin sensitivity index and the glucose AUC decreased after 12 weeks. The body composition analysis revealed that the VAT and the ratio of VAT to SAT decreased, whereas body weight and total fat mass increased nonsignificantly. The ASM/weight and skeletal muscle mass index increased. The restoration of ß-cell function, as identified by HOMA-B, the insulinogenic index, and the C-peptide-to-glucose AUC ratio, was correlated with the changes in VAT when controlled for age and gender. In multiple regression analyses, the decrease in VAT was shown to independently contribute to improved HbA1c over the study period, after adjusting for confounding factors. CONCLUSIONS: These results suggest that a shift in fat distribution from visceral to subcutaneous fat after early intensive insulin therapy is associated with improvements in glycemic control and ß-cell function in patients with newly diagnosed type 2 diabetes.
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OBJECTIVE: There is limited evidence on the association of sustained low-income status, income changes, and all-cause mortality risk in individuals with type 2 diabetes (T2D). RESEARCH DESIGN AND METHODS: Using the Korean Health Insurance Service database, we studied 1,923,854 adults with T2D (aged ≥30 years) without cardiovascular disease and cancer, who were enrolled from 2009 through 2012 and followed to the end of 2020 (median 10.8 years of follow-up). We defined income levels based on the amount of health insurance premiums and categorized them into quartiles, the first being the low-income group, and assessed the income status annually in the preceding 5 years. Cox proportional hazards models were used to quantify the association of low-income status and income changes with mortality, with adjustment for sociodemographic factors, comorbidities, and diabetes duration and treatment. RESULTS: Participants who consecutively had low income showed a higher risk of mortality (hazard ratio [HR] 1.19; 95% CI 1.16-1.22), compared with those who had never been in the low-income group. This association was much stronger for consecutive recipients of Medical Aid, reflecting very-low-income status (HR 2.26; 95% CI 2.16-2.36), compared with those who had never been Medical Aid beneficiaries. Sustained low- and very-low-income status was associated with increased risk of mortality, specifically for younger adults (aged <40 years) and males. Those who experienced declines in income between the first (preceding 5 years) and the last (baseline) time points had an increased risk of mortality, regardless of baseline income status. CONCLUSIONS: Among Korean adults with T2D, sustained low-income status and declines in income were associated with increased risk of mortality.
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Enfermedades Cardiovasculares , Diabetes Mellitus Tipo 2 , Adulto , Masculino , Humanos , Diabetes Mellitus Tipo 2/epidemiología , Estudios de Cohortes , Renta , Factores Socioeconómicos , Pobreza , Factores de RiesgoRESUMEN
Importance: Evidence of the association between income fluctuation and risk of type 2 diabetes (T2D) is scarce. Objective: To investigate whether sustained low or high income and income changes are associated with incidence of T2D. Design, Setting, and Participants: In this population-based cohort study, more than 7.8 million adults without T2D aged 30 to 64 years from a nationally representative sample from the Korean Health Insurance Service database were enrolled in 2012 and followed up to 2019 (median follow-up, 6.3 years [IQR, 6.1-6.6 years]). Exposures: Twenty quantiles of monthly health insurance premiums determined income levels. Income quartiles were annually analyzed from 2008 to 2012. Beneficiaries of the Medical Aid Program were regarded as those with very low income. A decrease in income was indicated as a reduction of 25% or more in income compared with income in the previous year. Main Outcomes and Measures: The primary outcome was incident T2D based on the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision codes E11 to E14, 1 or more claims of antidiabetic medication, or a fasting glucose level of 126 mg/dL or higher. Multivariable Cox proportional hazards models were used to assess the association of low- or high-income status and income changes with incidence of T2D. Results: Of 7â¯821â¯227 participants (mean [SD] age, 46.4 [9.3] years; 54.9% men), 359â¯931 (4.6%) developed T2D at least 1 year after enrollment. Individuals who repeatedly experienced low and very low income for 5 years showed 22% (hazard ratio [HR], 1.22 [95% CI, 1.21-1.23]) and 57% (1.57 [95% CI, 1.53-1.62]) higher T2D risk compared with those who never experienced low and very low income, respectively. In contrast, individuals who were repeatedly in high-income quartiles showed lower T2D risk compared with those who never experienced high income (HR, 0.86 [95% CI, 0.85-0.86]). The number of income decreases was associated with elevated T2D risk (≥2 vs 0 income decreases: HR, 1.08 [95% CI, 1.06-1.11]; P < .001 for trend). When income quartile status was compared between 2008 and 2012, individuals who experienced an income increase had lowered T2D risk, while those who experienced an income decrease had elevated T2D risk in each income quartile group. Conclusions and Relevance: This cohort study found that individuals who experienced sustained low-income status or an income decrease had elevated T2D risk, while those who had sustained high-income status or an income increase had lowered T2D risk.
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Diabetes Mellitus Tipo 2 , Adulto , Masculino , Humanos , Persona de Mediana Edad , Femenino , Diabetes Mellitus Tipo 2/epidemiología , Estudios de Cohortes , Renta , Pobreza , Factores SocioeconómicosRESUMEN
BACKGROUND & AIMS: Inflammatory potential of diet may contribute to poor health outcomes in individuals with metabolic disorders. In a representative sample of the U.S. population, we investigated the association between consuming a pro-inflammatory diet and mortality risk in adults with normal range of body mass index (BMI) but with central obesity. METHODS: This prospective cohort study included 3521 adults 20-90 years of age with normal BMI who participated in the National Health and Nutrition Examination Survey III, 1988-1994 and did not have a history of cardiovascular disease (CVD) or cancer and did not change their dietary intake in the year preceding baseline measurements. Mortality from all causes, CVD, and cancer was ascertained from the National Death Index. Normal-weight central obesity (NWCO, n = 1777) was defined as those with BMI 18.5 to <25 kg/m2 and waist-to-hip ratio (WHR) ≥0.85 in women and ≥0.90 in men. Severe central obesity was defined as WHR ≥0.92 in women and ≥1.00 in men. The dietary inflammatory index (DII®) was computed based on baseline dietary intake using 24-h dietary recalls, and associations with mortality were estimated using multivariable Cox proportional hazards regression. RESULTS: In individuals with NWCO, DII score (i.e., more pro-inflammatory diet) was associated with increased risk of CVD mortality (HRT3 vs T1, 1.89 [95% CI, 1.01-3.53], P trend = 0.04; HR 1 SD increase 1.29 [95% CI, 1.06-1.57]). This association was stronger with more severe central obesity (HRT3 vs T1, 2.79 [95% CI, 1.10-7.03], P trend = 0.03; HR 1 SD increase 1.52 [95% CI, 1.05-2.21]). DII score was not associated with increased risk of mortality in normal-weight individuals without central obesity or with risk of cancer mortality in either group. CONCLUSION: Among individuals in the normal-weight range of BMI, a pro-inflammatory diet assessed by high DII scores was associated with increased risk of CVD mortality in those with central obesity.
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Enfermedades Cardiovasculares , Neoplasias , Masculino , Adulto , Humanos , Femenino , Obesidad Abdominal/epidemiología , Obesidad Abdominal/complicaciones , Factores de Riesgo , Estudios Prospectivos , Encuestas Nutricionales , Dieta/efectos adversos , Obesidad/epidemiología , Obesidad/complicaciones , Índice de Masa Corporal , Neoplasias/complicacionesRESUMEN
We evaluated the number of osteoporosis patients under treatment and secular trends in 2005-2008 in South Korea. We investigated nationwide data regarding the number of osteoporosis patients under treatment in South Korea using data from the Health Insurance Review and Assesment Service (HIRA), which includes nationwide information [corrected]. Reimbursement records from the HIRA database between 1 January 2004 and 31 December 2008 were investigated. Patients aged ≥30 years old with osteoporosis were identified based on a study-defined algorithm using prescription data and diagnostic codes. During the study periods, the number of patients receiving medical treatment related to osteoporosis increased from 1,034,399 to 1,392,189 for women and from 120,496 to 171,902 for men. The calculated proportion of osteoporosis patients under treatment in the general population over 50 years of age was 6.1% for men and 33.3% for women, and in the general population over 30 years of age was 2.7% for men and 16.6% for woman. More than 40% of patients (59.1% for women; 41.2% for men) were treated with medication indicated only for osteoporosis. About 4-7% of osteoporosis patients had a past medical history suggesting a secondary cause of osteoporosis. More than 80% of all osteoporosis patients were women older than 50 years, reflecting the pronounced burden of osteoporosis among postmenopausal women. This study demonstrated a substantial increasing trend in medical claims related to osteoporosis in 2005-2008 among adults in Korea and a pronounced burden of osteoporosis among postmenopausal women.
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Costo de Enfermedad , Bases de Datos como Asunto/estadística & datos numéricos , Programas Nacionales de Salud/estadística & datos numéricos , Osteoporosis/epidemiología , Adulto , Distribución por Edad , Femenino , Humanos , Masculino , Osteoporosis/terapia , República de Corea/epidemiología , Caracteres SexualesRESUMEN
Substantial evidence supports that metabolic syndrome (MetS) affects the incidence of several cancers, with different effects according to age group. We hypothesized that MetS has an age-specific effect on the occurrence of prostate cancer. We studied a National Health Insurance Service health checkup cohort. A total of 5,370,614 men in the cohort were categorized into three age groups in 2009 (20-39, 40-64, ≥65). Prostate cancer incidence was estimated on a cumulative basis from 2009 to 2018. We tried to identify the correlation of MetS components and prostate cancer by age group using this large retrospective cohort. MetS components included the body mass index (BMI), waist circumference (WC), hypertension, obesity, hyperlipidemia, cardiovascular disease, smoking, drinking, serum glucose, serum total cholesterol, serum triglyceride, serum high-density lipoprotein (HDL)-cholesterol and serum low-density lipoprotein (LDL)-cholesterol. A multivariate Cox proportional hazard model was used for the incidence of prostate cancer according to the MetS component. In the young age (20-39) group, the MetS component was not related to prostate cancer. In the middle-aged (40-64) group, the presence of MetS, WC, HDL cholesterol, and hypertension was significantly associated with an increased prevalence of prostate cancer. In the old age (≥65) group, the presence of MetS, WC, HDL cholesterol, triglycerides, and hypertension were significant factors for the incidence of prostate cancer. This tendency was marked in BMI>30 in the old age group (odds ratio: 1.32; P<0.0001). MetS components were age-specifically associated with an increased incidence of prostate cancer. Because the MetS components were related to prostate cancer from middle age to old age, preventing MetS for these age groups is crucial.
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Purpose: We sought to analyze the visual outcome and systemic prognostic factors for diabetic vitrectomy and predicted outcomes using these factors. Methods: This was a multicenter electronic medical records (EMRs) review study of 1504 eyes with type 2 diabetes that underwent vitrectomy for proliferative diabetic retinopathy at 6 university hospitals. Demographics, laboratory results, intra-operative findings, and visual acuity (VA) values were analyzed and correlated with visual outcomes at 1 year after the vitrectomy. Prediction models for visual outcomes were obtained using machine learning. Results: At 1 year, VA was 1.0 logarithm of minimal angle resolution (logMAR) or greater (poor visual outcome group) in 456 eyes (30%). Baseline visual acuity, duration of diabetes treatment, tractional membrane, silicone oil tamponade, smoking, and vitreous hemorrhage correlated with logMAR VA at 1 year (r = 0.450, -0.159, 0.221, 0.280, 0.067, and -0.105; all P ≤ 0.036). An ensemble decision tree model trained using all variables generated accuracy, specificity, F1 score (the harmonic means of which precision and sensitivity), and receiver-operating characteristic curve area under curve values of 0.77, 0.66, 0.85, and 0.84 for the prediction of poor visual outcomes at 1 year after vitrectomy. Conclusions: Visual outcome after diabetic vitrectomy is associated with pre- and intra-operative findings and systemic factors. Poor visual outcome after diabetic vitrectomy was predictable using clinical factors. Intensive care in patients who are predicted to result in poor vision may limit vision loss resulting from type 2 diabetes. Translational Relevance: This study demonstrates that a real world EMR big data could predict outcome after diabetic vitrectomy using clinical factors.
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Diabetes Mellitus Tipo 2 , Vitrectomía , Data Warehousing , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/cirugía , Humanos , Estudios Retrospectivos , Vitrectomía/métodos , Hemorragia Vítrea/cirugíaRESUMEN
AIMS: Heart failure (HF) is associated with obesity, but the relationship between weight change and HF is inconsistent. We examined the relationship between weight change and the incidence of HF in the Korean population. DESIGN: Retrospective cohort study design. METHODS AND RESULTS: A total of 11 210 394 subjects (6 198 542 men and 5 011 852 women) >20 years of age were enrolled in this study. Weight change over 4 years divided into seven categories from weight loss ≥15% to weight gain ≥15%. The hazard ratios (HRs) and 95% confidence intervals for the incidence of HF were analysed. The HR of HF showed a slightly reverse J-shaped curve by increasing weight change in total and >15% weight loss shows the highest HR (HR 1.647) followed by -15 to -10% weight loss (HR = 1.444). When using normal body mass index with stable weight group as a reference, HR of HF decreased as weight increased in underweight subjects and weight gain ≥15% in obesity Stage II showed the highest HR (HR = 2.97). Sustained weight for 4 years in the underweight and obesity Stages I and II increased the incidence of HF (HR = 1.402, 1.092, and 1.566, respectively). CONCLUSION: Both weight loss and weight gain increased HR for HF. Sustained weight in the obesity or underweight categories increased the incidence of HF.
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Insuficiencia Cardíaca , Índice de Masa Corporal , Femenino , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/epidemiología , Insuficiencia Cardíaca/etiología , Humanos , Incidencia , Masculino , Programas Nacionales de Salud , República de Corea/epidemiología , Estudios Retrospectivos , Factores de RiesgoRESUMEN
BACKGROUND: Obesity and diabetes mellitus (DM) are established risk factors for the development of chronic kidney disease. Visceral adiposity (VAT) and subcutaneous adiposity (SAT) may be associated with the differential metabolic risk. Our study was performed to determine whether VAT or SAT was associated with the decrease of renal function in people with type 2 DM. METHODS: Nine hundred and twenty-nine people with type 2 DM and who had undergone abdominal computed tomography assessment of the SAT and VAT areas were included. The estimated glomerular filtration rate (eGFR) was calculated using the Cockcroft-Gault equation and the Modification of Diet in Renal Disease (MDRD) four-variable equation at the time of the assessment of the SAT and VAT areas. RESULTS: VAT was negatively associated with eGFR using the MDRD equation after adjustment for the clinical variables (ß-coefficient = - 0.075, P = 0.034), while SAT was not significantly associated with eGFR. There was no significant association between the abdominal adiposity measurements and the eGFR using the Cockcroft-Gault formula. When stratifying the individuals by the body mass index groups, VAT was negatively associated with eGFR by the MDRD equation and the Cockcroft-Gault formula in the overweight and obese subjects after adjustment for the clinical variables, while there was no significant association between the VAT and the eGFR in the normal weight subjects. SAT was not significantly associated with eGFR in the normal weight, overweight and obese subjects. CONCLUSIONS: Our data suggest that VAT may be an additional prognostic factor for the decrease of renal function especially in the overweight or obese subjects with type 2 DM.