47 research outputs found

    Hazard ratios (95% Confidence interval) for incident CKD according to the FLI groups.

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    <p>Hazard ratios (95% Confidence interval) for incident CKD according to the FLI groups.</p

    <strong>Long-term effectiveness of the national diabetes quality assessment program in South Korea</strong>

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    Objective: This study examined the long-term effectiveness of the national diabetes quality assessment program (NDQAP) in diabetes. Research Design and Methods: From the Health Insurance Review and Assessment Service database, 399,984 individuals with diabetes who visited a primary care clinic from July 1, 2012, to June 30, 2013, were included and followed up until May 31, 2021. The NDQAP included five quality assessment indicators: regular outpatient visits, continuity of prescriptions, regular testing of glycated hemoglobin and lipids, and regular fundus examination. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for diabetes complications and all-cause mortality by the achievement of quality assessment indicators. Results: During the mean follow-up duration of 7.6 ± 1.8 years, 20,054 (5.0%) cases of proliferative diabetic retinopathy (PDR), 6,281 (1.6%) end-stage kidney diseases (ESKD), 1,943 (0.5%) amputations, 9,706 (2.4%) myocardial infarctions (MI), 26,975 (6.7%) strokes, and 35,799 (8.9%) all-cause mortality occurred. Each achievement of quality assessment indicator was associated with a decreased risk of diabetes complications and all-cause mortality. Individuals who were managed in high-quality institutions had a lower risk of PDR (HR, 0.82; 95% CI, 0.80–0.85), ESKD (HR, 0.77; 95% CI, 0.73–0.81), amputation (HR, 0.75; 95% CI, 0.69–0.83), MI (HR, 0.85; 95% CI, 0.82–0.89), stroke (HR, 0.86; 95% CI, 0.84–0.88), and all-cause mortality (HR, 0.96; 95% CI, 0.94–0.98) than those who were not managed in high-quality institutions. Conclusions: In Korea, the achievement of NDQAP indicators was associated with a decreased risk of diabetes complications and all-cause mortality.  </p

    Study populations.

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    <p>CKD, chronic kidney disease; NSAIDs, nonsteroidal anti-inflammatory drugs.</p

    Lower Serum Creatinine Is Associated with Low Bone Mineral Density in Subjects without Overt Nephropathy

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    <div><p>Background</p><p>Low skeletal muscle mass is associated with deterioration of bone mineral density. Because serum creatinine can serve as a marker of muscle mass, we evaluated the relationship between serum creatinine and bone mineral density in an older population with normal renal function.</p><p>Methods</p><p>Data from a total of 8,648 participants (4,573 men and 4,075 postmenopausal women) aged 45–95 years with an estimated glomerular filtration rate >60 ml/min/1.73 m2 were analyzed from the Fourth Korea National Health and Nutrition Examination Survey (2008–2010). Bone mineral density (BMD) and appendicular muscle mass (ASM) were measured using dual-energy X-ray absorptiometry. Receiver operating characteristic curve analysis revealed that the cut points of serum creatinine for sarcopenia were below 0.88 mg/dl in men and 0.75 mg/dl in women. Subjects were divided into two groups: low creatinine and upper normal creatinine according to the cut point value of serum creatinine for sarcopenia.</p><p>Results</p><p>In partial correlation analysis adjusted for age, serum creatinine was positively associated with both BMD and ASM. Subjects with low serum creatinine were at a higher risk for low BMD (T-score ≤ –1.0) at the femur neck, total hip and lumbar spine in men, and at the total hip and lumbar spine in women after adjustment for confounding factors. Each standard deviation increase in serum creatinine was significantly associated with reduction in the likelihood of low BMD at the total hip and lumbar spine in both sexes (men: odds ratio (OR) = 0.84 [95% CI = 0.74−0.96] at the total hip, OR = 0.8 [95% CI = 0.68−0.96] at the lumbar spine; women: OR = 0.83 [95% CI = 0.73–0.95] at the total hip, OR=0.81 [95% CI = 0.67–0.99] at the lumbar spine).</p><p>Conclusions</p><p>Serum creatinine reflected muscle mass, and low serum creatinine was independently associated with low bone mineral density in subjects with normal kidney function.</p></div

    Adjusted odds ratios with 95% confidence interval for the presence of low bone mineral density for each standard deviation (SD) increase in serum creatinine.

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    <p>*Data were adjusted for age, current smoking status, regular exercise, daily calcium intake (mg/d), HOMA-IR, vitamin D, body fat (%) and estrogen replacement therapy (in women).</p

    Multivariate odds ratio and 95% confidence interval for low bone mineral density<sup>a</sup> according to serum creatinine.

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    <p><sup>a</sup>Low bone mineral density: T-score ≤ –1.0</p><p><sup>b</sup>Data are presented using a Chi-square test</p><p>Model 1: adjusted for age; Model 2: Model 1+ further adjusted for regular exercise, alcohol intake, current smoking status, 25(OH)D and estrogen replacement therapy (women); Model 3: Model 2+ further adjusted for HOMA-IR, daily calcium intake and body fat (%).</p><p>Multivariate odds ratio and 95% confidence interval for low bone mineral density<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0133062#t003fn001" target="_blank"><sup>a</sup></a> according to serum creatinine.</p

    α-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition C-C chemokine receptor 2

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    <div><p>Obesity induces various metabolic diseases such as dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. Fat expansion in adipose tissue induces adipose tissue dysfunction and inflammation, insulin resistance, and other metabolic syndromes. α-Mangostin (α-MG) has been previously studied for its anti-cancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the effects of α-MG on adipose tissue inflammation and hepatic steatosis. We categorized study animals into four groups: regular diet control mice, RD mice treated with α-MG, high fat diet-induced obese mice, and HFD mice treated with α-MG. α-MG treatment significantly reduced not only the body, liver, and fat weights, but also plasma glucose, insulin, and triglyceride levels in HFD mice. Additionally, adiponectin levels of α-MG-treated mice were significantly higher than those of control HFD mice. Immunohistochemistry of liver and adipose tissue showed that CD11c expression was reduced in α-MG fed obese mice. α-MG treatment of HFD mice down-regulated the adipose-associated inflammatory cytokines and CCR2 in both liver and adipose tissue. Moreover, glucose tolerance and insulin sensitivity were significantly improved in α-MG fed obese mice. α-Mangostin ameliorates adipose inflammation and hepatic steatosis in HFD-induced obese mice.</p></div
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