Lipoprotein (a) (Lp [a]) is a well-known risk factor for cardiovascular disease, but analysis on Lp (a) and renal dysfunction is scarce. We aimed to investigate prospectively the association of serum Lp (a) with the risk of reduced renal function, and further investigated whether diabetic or hypertensive status modified such association. 6,257 Chinese adults aged ≥40 years and free of reduced renal function at baseline were included in the study. Reduced renal function was defined as estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m2. During a mean follow-up of 4.4 years, 158 participants developed reduced renal function. Each 1-unit increase in log10-Lp (a) (mg/dl) was associated with 1.99-folds (95% confidence interval [CI] 1.15-3.43) increased risk of incident reduced renal function; multivariable-adjusted odds ratio (OR) for the highest tertile of Lp (a) was 1.61 (95% CI 1.03–2.52) compared to the lowest tertile (P for trend=0.03). The stratified analysis showed the association of serum Lp (a) and incident reduced renal function was more prominent in participants with prevalent diabetes (OR 4.04, 95% CI [1.42-11.54]) or hypertension (OR 2.18, 95% CI [1.22-3.89]). A stronger association was observed among group with diabetes and high Lp (a) (>25 mg/dl), indicating a combined effect of diabetes and high Lp (a) on the reduced renal function risk. Elevated Lp (a) level was independently associated with risk of incident reduced renal function, especially in diabetic or hypertensive patients.
Context Body composition may explain partially why non-obese individuals still at the risk of developing non-alcoholic fatty liver disease (NAFLD). The ratio of fat mass to fat-free mass (FM/FFM) has been proposed to assess the combined effect of different body compositions. Objective We aimed to investigate the associations of FM/FFM ratio with the risk of developing NAFLD and fibrosis and to identify the potential mediators according to obesity status. Methods This cohort study comprised 3419 adults age ≥ 40 years and free of NAFLD at baseline. Body composition was measured by bioelectrical impedance analysis. NAFLD was ascertained by ultrasonography and fibrosis was assessed by non-invasive score systems. Results For each 1 standard deviation increment in FM/FFM ratio, the odds ratio for the risk of NAFLD was 1.55 (95% confidence interval [CI] 1.23–1.95) in non-obese men, 1.33 (95% CI 1.08–1.65) in obese men, 1.42 (95% CI 1.44–1.67) in non-obese women, and 1.29 (95% CI 1.12–1.50) in obese women. Similar associations were also found between FM/FFM ratio and NAFLD with fibrosis. Mediation analysis showed that insulin resistance, triglycerides, high-density lipoprotein cholesterol, white blood cells, and total cholesterol mediated the association of FM/FFM ratio with NAFLD risk in specific sex and obesity subgroups. Conclusions The FM/FFM ratio significantly associated with the NAFLD and fibrosis risk in both non-obese and obese individuals. Different factors may mediate the association between body composition and NAFLD risk according to different obesity status.
Background: Prolonged heart rate corrected QT (QTc) interval was reported to be associated with cardiovascular diseases (CVDs). Objective: There exists little data on the association between QTc interval and cardiovascular risk in Asian populations. We prospectively investigated the association of QTc interval with CVDs and vascular traits in a large cohort of Chinese adults. Methods: A total of 7,605 participants aged 40 years or older from a well-defined community without CVDs at baseline were included and followed up for an average of 4.5 years. Association of baseline QTc interval with incident CVDs was evaluated using Cox regression analysis. Associations of QTc interval with brachial-ankle pulse wave velocity (baPWV), carotid intimamedia thickness (CIMT), and risk of microalbuminuria and peripheral arterial diseases (PAD) were secondarily examined. Results: Prolonged QTc interval (≥460 ms in women and ≥450 ms in men) was associated with 51% higher risk of total major CVDs (hazard ratio [HR] = 1.51, 95% confidence interval [CI] [1.20, 1.90]), particularly, 48% increased risk of stroke (95% CI [1.16, 1.88]). Prolonged QTc interval was positively associated with baPWV (β = 38.10 cm/s, standard error [SE] = 8.04, P < 0.0001) and CIMT (β = 0.01 mm, SE = 0.01, P = 0.04). Prolonged QTc interval was associated with increased risk of incident microalbuminuria (odds ratio [OR] = 1.65, 95% CI [1.21, 2.24]) and PAD (2.49, 95% CI [1.35, 4.59]). Conclusions: Prolonged QTc interval is positively and significantly associated with increased risk of CVDs and related vascular traits in Chinese population.
BackgroundThe performance of peripheral blood transcriptional markers in evaluating the risk of type 2 diabetes (T2D) with normal weight is unknown. We developed a whole blood-based transcriptional risk score (wb-TRS) for nonobese T2D and assessed its contributions to disease risk and dynamic changes in glucose metabolism.Methods and findingsWe developed the wb-TRS in 1105 participants aged ≥40 years and in normal weight for up to 10 years from a well-defined community-based cohort with blood transcriptome data and validated it in an external dataset (253 overweight/obese participants from a dietary intervention trial with 3 repeated transcriptome data). Potential biology significance and causal inference were also explored. The wb-TRS included 144 transcripts. Compared to the lowest tertile, wb-TRS in tertile 3 associated with 8.68-folds (95% confidence interval [CI], 3.51-21.5), and each 1-unit increment associated with 2.57-folds (95% CI, 1.86-3.56) higher risk of nonobese T2D, after adjustments for traditional risk factors. Furthermore, baseline wb-TRS was significantly associated with dynamic changes in average, daytime, nighttime and 24h glucose and HbA1c, and area under the curve of glucose measured in the continuous glucose monitoring during 6-month of intervention. The wb-TRS improved the predicting performance for nonobese T2D in a model with fasting glucose, triglycerides and demographic and anthropometric parameters. Mitch analysis implicated oxidative phosphorylation, cholesterol metabolism and mTORC1 signaling involved in nonobese T2D pathogenesis. Transcriptome-wide Mendelian randomization supported causal effects of gene transcripts such as RAB1A and GCC1-PAX4 on nonobese T2D risk.ConclusionsA whole blood based nonobese T2D associated TRS was validated to predict dynamic changes in glucose metabolism. These findings also suggested several genes and biological pathways that might involve in the pathogenesis of nonobese T2D.
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