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Background: Obesity is a global public health concern linked to chronic diseases such as cardiovascular disease and type 2 diabetes (T2D). Emerging evidence suggests that epigenetic modifications, particularly DNA methylation, may contribute to obesity. However, the molecular mechanism underlying the longitudinal change of BMI has not been well-explored, especially in East Asian populations. Methods: This study performed a longitudinal epigenome-wide association analysis of DNA methylation to uncover novel loci associated with BMI change in 533 individuals across two Chinese cohorts with repeated DNA methylation and BMI measurements over four years. Results: We identified three novel CpG sites (cg14671384, cg25540824, and cg10848724) significantly associated with BMI change. Two of the identified CpG sites were located in regions previously associated with body shape and basal metabolic rate. Annotation of the top 20 BMI change-associated CpGs revealed strong connections to obesity and T2D. Notably, these CpGs exhibited active regulatory roles and located in genes with high expression in the liver and digestive tract, suggesting a potential regulatory pathway from genome to phenotypes of energy metabolism and absorption via DNA methylation. Cross-sectional and longitudinal EWAS comparisons indicated different mechanisms between CpGs related to BMI and BMI change. Conclusion: This study enhances our understanding of the epigenetic dynamics underlying BMI change and emphasizes the value of longitudinal analyses in deciphering the complex interplay between epigenetics and obesity. [ABSTRACT FROM AUTHOR]

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease that affects over 30% of the world's population. For decades, the heterogeneity of non-alcoholic fatty liver disease (NAFLD) has impeded our understanding of the disease mechanism and the development of effective medications. However, a recent change in the nomenclature from NAFLD to MASLD emphasizes the critical role of systemic metabolic dysfunction in the pathophysiology of this disease and therefore promotes the progress in the pharmaceutical treatment of MASLD. In this review, we focus on the mechanism underlying the abnormality of hepatic lipid metabolism in patients with MASLD, and summarize the latest progress in the therapeutic medications of MASLD that target metabolic disorders. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of chronic liver disease ranging from simple steatosis (NAFL) to nonalcoholic steatohepatitis (NASH). However, the molecular mechanisms of NASH progression remain incompletely understood. White adipose tissue (WAT) has emerged as an important endocrine organ and contributes not only to the initial stage of NAFLD, but also to its severity. In the current study, through transcriptomic analysis we identified increased expression of Sparcl1, a secreted glycoprotein, in the WAT from NASH mice. Plasma Sparcl1 levels were similarly elevated and positively correlated with hepatic pathological features in NASH patients. Functional studies showed that both chronic injection of recombinant Sparcl1 protein and overexpression of Sparcl1 exaggerated hepatic inflammation and liver injury in mice. In contrast, genetic ablation of Sparcl1, knockdown of Sparcl1 in WAT, and treatment with a Sparcl1-neutralizing antibody dramatically alleviated diet-induced NASH pathogenesis. Mechanistically, Sparcl1 promoted the expression of C-C motif chemokine ligand 2 (CCL2) in hepatocytes through binding to Toll-like receptor 4 (TLR4) and activation of the NF-[kappa]B/p65 signaling pathway. Genetically or pharmacologically blocking the CCL2/CCR2 pathway attenuated the hepatic inflammatory response evoked by Sparcl1. Thus, our results demonstrated an important role for Sparcl1 in NASH progression, suggesting a potential target for therapeutic intervention., Introduction In the past decade, the prevalence of obesity has substantially increased in both the adults and children (1) due to rapid changes in lifestyle. Obesity is associated with high [...]

Poly(vinyl alcohol) (P)/alginate (A)/MMT (M) (PAM) composite aerogels was modified through interpenetrating cross-linking of methyltriethoxysilane (Ms) or γ-aminopropyltriethoxysilane (K) and calcium ion (Ca2+) as a cross-linking agent, respectively. The compressive moduli of the cross-linked PAM/MsCa and PAM/KCa aerogels greatly increased to 17.4 and 22.1 MPa, approximately 10.5- and 8.2-fold of that of PAM aerogel, respectively. The limited oxygen index (LOI) values for PAM/MsCa and PAM/KCa composite aerogels increased from 27.0% of PAM aerogel to 40.5% and 56.8%. Compared with non-cross-linked PAM aerogel, the peak heat release rate (PHRR) of PAM/MsCa and PAM/KCa composite aerogels dramatically decreased by 34% and 74%, respectively, whereas the PAM/KCa aerogel presented better flame retardancy and lower smoke toxicity than the PAM/MsCa aerogel because of the release of more inert gases and the barrier action of more compact char layer during the combustion. The highly efficient flame-retardant PAM-based composite aerogels with excellent mechanical properties are promising as a sustainable alternative to traditional petroleum-based foams. [ABSTRACT FROM AUTHOR]

Aims: The study aimed to develop a novel noninvasive model to detect advanced fibrosis based on routinely available clinical and laboratory tests. Materials and Methods: A total of 309 patients who underwent liver biopsy were randomly divided into the estimation group (n = 201) and validation group (n = 108). The model was developed using multiple regression analysis in the estimation group and further verified in the validation group. Diagnostic accuracy was evaluated using the receiver operating characteristic (ROC) curve. Results: The model was named NAFLD Fibrosis Index (NFI): −10.844 + 0.046 × age − 0.01 × platelet count + 0.19 × 2h postprandial plasma glucose (PG) + 0.294 × conjugated bilirubin − 0.015 × ALT + 0.039 × AST + 0.109 × total iron binding capacity −0.033 × parathyroid hormone (PTH). The area under the ROC curve (AUC) of NFI was 0.86 (95% CI: 0.79–0.93, p < 0.001) in the estimation group and 0.80 (95% CI: 0.69–0.91, p < 0.001) in the validation group, higher than NFS, FIB4, APRI, and BARD, and similar to FibroScan (NFI AUC = 0.77, 95% CI: 0.66–0.89, p = 0.001 vs. FibroScan AUC = 0.76, 95% CI: 0.62–0.90, p = 0.002). By applying the low cut‐off value (−2.756), advanced fibrosis could be excluded among 49.3% and 48% of patients in the estimation group (sensitivity: 93.1%, NPV: 97.9%, specificity: 55.2%, and PPV: 26.0%) and validation group (sensitivity: 81.3%, NPV: 94.2%, specificity: 53.3%, and PPV: 23.2%), respectively, allowing them to avoid liver biopsy. Conclusions: The study has established a novel model for advanced fibrosis, the diagnostic accuracy of which is superior to the current clinical scoring systems and is similar to FibroScan. [ABSTRACT FROM AUTHOR]

Background and Purpose: Salvianolic acid B (SalB) is effective for treating cardiovascular diseases. However, the molecular mechanisms underlying its therapeutic effects remain unclear. Mechanosensitive Piezo1 channels play important roles in vascular biology, although their pharmacological properties are poorly defined. Here, we aimed to identify novel Piezo1 inhibitors and gain insights into their mechanisms of action. Experimental Approach Intracellular Ca2+ ions were measured in HUVECs, murine liver endothelial cells (MLECs), THP‐1 and RAW264.7 cell lines and bone marrow‐derived macrophages (BMDMs). Isometric tensions in mouse thoracic aorta were recorded. Shear‐stress assays with HUVECs were conducted. Patch‐clamp recordings with mechanical stimulation were performed with HUVECs in whole‐cell mode. Foam cell formation was induced by treating BMDMs with oxidised LDL (oxLDL). Atherosclerotic plaque assays were performed with Ldlr−/− and Piezo1 genetically depleted mice on a high‐fat diet. Key Results: Salvianolic acid B inhibited Yoda1‐induced Ca2+ influx in HUVECs and MLECs. Similar results were observed in macrophage cell lines and BMDMs. Furthermore, we demonstrated that salvianolic acid B inhibited Yoda1‐ and mechanically activated currents. Salvianolic acid B suppressed Yoda1‐induced aortic ring relaxation and inhibited HUVECs alignment in the direction of shear stress. Additionally, Yoda1 enhanced the formation of foam cells, which was reversed by salvianolic acid B. Salvianolic acid B also inhibited formation of atherosclerotic plaques and was insensitive to Piezo1 genetic depletion. Conclusion and Implications: Our study provides novel mechanistic insights into the inhibitory role of salvianolic acid B against Piezo1 channels and improves our understanding of salvianolic acid B in preventing atherosclerotic lesions. [ABSTRACT FROM AUTHOR]

Nanocellulose has lately emerged as one of the most promising "green" materials due to its unique properties. Nanocellulose can be mainly divided into three types, i.e., cellulose nanocrystals (CNCs), cellulose nanofibrils (CNFs), and bacterial cellulose (BC). With the rapid development of technology, nanocellulose has been designed into multidimensional structures, including 1D (nanofibers, microparticles), 2D (films), and 3D (hydrogels, aerogels) materials. Due to its adaptable surface chemistry, high surface area, biocompatibility, and biodegradability, nanocellulose-based composite materials can be further transformed as drug delivery carriers. Herein, nanocellulose-based composite material used for drug delivery was reviewed. The typical drug release behaviors and the drug release mechanisms of nanocellulose-based composite materials were further summarized, and the potential application of nanocellulose-based composite materials was prospected as well. [ABSTRACT FROM AUTHOR]

Summary: Background: The PNPLA3 and TM6SF2 gene variants have been found to cause NAFLD with a favourable cardiovascular risk profile. Aims: To investigate the effects of the NAFLD risk alleles on the all‐cause and cause‐specific mortality in 5581 Chinese adults. Methods: The genome‐wide genotypes were detected using a genotyping array and serum lipoprotein profiles were examined using 1H NMR platform. Liver fat content (LFC) was measured using a quantitative ultrasound method. The vital status was determined using official registration data. Results: Genome‐wide association analysis showed that a series of variants in PNPLA3 were associated with LFC, including rs738409 C>G variant (P = 8.6 × 10−7). Further analyses validated the associations of TM6SF2 rs58542926 C>T and MBOAT7 rs641738 C>T variants with NAFLD. During 29 425.1 person‐years of follow‐up, the overall mortality was 816 per 100 000 person‐years, where 299 deaths were attributable to cardiovascular disease and 85 to liver disease. The PNPLA3 rs738409 C>G variant was independently associated with increased liver‐specific mortality (P for trend = 0.034) but reduced cardiovascular mortality (P for trend = 0.047). A composite genetic‐predisposition score of PNPLA3, TM6SF2, and MBOAT7 risk alleles presented similar opposite effects on liver‐specific and cardiovascular mortality. Moreover, interactions of the NAFLD risk alleles with adiposity for liver‐specific mortality were found (Pinteraction < 0.05). The reduced serum VLDL1 concentration was responsible for the increased liver‐specific mortality related to NAFLD risk alleles. Conclusion: The PNPLA3 rs738409 C>G variant and its combination with TM6SF2 rs58542926 C>T and MBOAT7 rs641738 C>T variants increase liver‐specific mortality but reduce cardiovascular mortality in overweight/obese Chinese. [ABSTRACT FROM AUTHOR]

Recent advances indicate that bone and energy metabolism are closely related. However, little direct evidence on causality has been provided in humans. We aimed to assess the association of three bone‐related biomarkers—25 hydroxyvitamin D (25OHD), parathyroid hormone (PTH), and osteocalcin (OCN)—with several metabolic phenotypes and investigate any causal relevance to the associations using a Mendelian randomization (MR) study. Serum 25OHD, PTH, and total OCN were measured at baseline in 5169 eligible Chinese participants in Changfeng study. Partial correlation and bivariate GREML analysis were used to estimate phenotypic and genetic correlations, respectively. Multiple linear regression and logistic regression were used to assess linear associations. Genomewide association analysis (GWAS) was performed. Bidirectional two‐sample MR analyses were conducted to examine causal relationships between OCN and body mass index (BMI), diastolic blood pressure (DBP), triglyceride (TG), high‐density lipoprotein cholesterol (HDL‐C), glycated hemoglobin A1c (HbA1c), and type 2 diabetes (T2DM), using our GWAS result of OCN and GWAS statistics from Biobank Japan project (BBJ) and the largest meta‐analysis of T2DM GWAS in East Asian population. Circulating OCN was significantly associated with higher DBP and HDL‐C and decreased TG, blood glucose level, insulin resistance, liver fat content, bone mineral density, BMI, and a favorable body fat distribution pattern. GWAS identified one novel serum PTH locus and two novel serum OCN loci, explaining 0.81% and 1.98% of variances of PTH and OCN levels, respectively. MR analysis suggested a causal effect of T2DM on lower circulating OCN concentration (causal effect: −0.03; −0.05 to −0.01; p = 0.006 for T2DM_BBJ and −0.03; −0.05 to −0.01; p = 0.001 for T2DM_EAS). These findings indicate that T2DM might impact bone remodeling and provide a resource for understanding complex relationships between osteocalcin and metabolic (and related) traits in humans. © 2021 American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]

Osteocalcin regulates energy metabolism in an active undercarboxylated/uncarboxylated form. However, its role on the development of non‐alcoholic fatty liver disease (NAFLD) is still controversial. In the current study, we investigated the causal relationship of circulating osteocalcin with NAFLD in two human cohorts and studied the effect of uncarboxylated osteocalcin on liver lipid metabolism through animal models. We analyzed the correlations of serum total/uncarboxylated osteocalcin with liver steatosis/fibrosis in a liver biopsy cohort of 196 participants, and the causal relationship between serum osteocalcin and the incidence/remission of NAFLD in a prospective community cohort of 2055 subjects from Shanghai Changfeng Study. Serum total osteocalcin was positively correlated with uncarboxylated osteocalcin (r = 0.528, p <.001). Total and uncarboxylated osteocalcin quartiles were inversely associated with liver steatosis, inflammation, ballooning, and fibrosis grades in both male and female participants (all p for trend <.05). After adjustment for confounding glucose, lipid, and bone metabolism parameters, the male and female participants with lowest quartile of osteocalcin still had more severe liver steatosis, with multivariate‐adjusted odds ratios (ORs) of 7.25 (1.07–49.30) and 4.44 (1.01–19.41), respectively. In the prospective community cohort, after a median of 4.2‐year follow‐up, the female but not male participants with lowest quartile of osteocalcin at baseline had higher risk to develop NAFLD (hazard ratio [HR] = 1.90; 95% confidence interval [CI] 1.14–3.16) and lower chance to achieve NAFLD remission (HR = 0.56; 95% CI 0.31–1.00). In wild‐type mice fed a Western diet, osteocalcin treatment alleviated hepatic steatosis and reduced hepatic SREBP‐1 and its downstream proteins expression. In mice treated with osteocalcin for a short term, hepatic SREBP‐1 expression was decreased without changes of glucose level or insulin sensitivity. When SREBP‐1c was stably expressed in a human SREBP‐1c transgenic rat model, the reduction of lipogenesis induced by osteocalcin treatment was abolished. In conclusion, circulating osteocalcin was inversely associated with NAFLD. Osteocalcin reduces liver lipogenesis via decreasing SREBP‐1c expression. © 2020 American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]

Objective: We investigated the relationship between fasting serum fructose levels and the risk of incident type 2 diabetes in a prospective Chinese cohort.Research Design and Methods: Among 949 community-based participants aged ≥40 years without diabetes at baseline, fasting serum fructose levels were measured using liquid chromatography-tandem mass spectrometry. The participants were followed up for the occurrence of diabetes. Cox regression models were performed to analyze the effect of fasting serum fructose levels on risk of incident diabetes.Results: During a median of 3.5 years' follow-up, 179 of 949 (18.9%) participants developed type 2 diabetes. Elevated fasting serum fructose levels were associated with an increased risk of incident diabetes in a dose-response manner. After adjustment for age, sex, BMI, lipid profiles, blood pressure, liver function, smoking and drinking status, baseline glucose level, and sugar-sweetened beverage consumption, a 1-SD increased fasting fructose level was associated with a 35% (95% CI 1.08-1.67) increased risk of developing diabetes. After further adjustment for serum uric acid and estimated glomerular filtration rate, the association was partially attenuated (hazard ratio 1.33 [95% CI 1.07-1.65]). The association was similar by age, prediabetes status, BMI, and family history of diabetes but attenuated in women (P for heterogeneity = 0.037).Conclusions: Elevated fasting serum fructose levels were independently associated with increased risk of incident type 2 diabetes in a middle-aged and older Chinese population. Our data suggest that higher fasting serum fructose levels might serve as a biomarker and/or a contributor to incident diabetes. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to investigate the efficacy of exenatide and insulin glargine in patients with newly diagnosed type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD).Methods: We performed a 24-week randomized controlled multicentre clinical trial. Seventy-six patients were randomly assigned 1:1 to receive exenatide or insulin glargine treatment. The endpoints included changes in liver fat content (LFC), visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) measured by magnetic resonance spectroscopy, blood glucose, liver enzymes, lipid profile, body weight, and Fibrosis-4 index (FIB-4).Results: LFC, VAT, SAT, and FIB-4 were significantly reduced after exenatide treatment (ΔLFC, -17.55 ± 12.93%; ΔVAT, -43.57 ± 68.20 cm2 ; ΔSAT, -28.44 ± 51.48 cm2 ; ΔFIB-4, -0.10 ± 0.26; all P < .05). In comparison, only LFC (ΔLFC, -10.49 ± 11.38%; P < .05), and not VAT, SAT, or FIB-4 index (all P > .05), was reduced after insulin glargine treatment. Moreover, exenatide treatment resulted in greater reductions in alanine transaminase (ALT), aspartate transaminase (AST), and gamma glutamyl transpeptidase (GGT) than insulin glargine (P < 0.05). The body weight, waist circumference, postprandial plasma glucose, and low-density lipoprotein cholesterol (LDL-C) in the exenatide group also presented greater reductions than the insulin glargine group (P < .05). The proportion of adverse events were comparable between the two groups.Conclusion: Both exenatide and insulin glargine reduced LFC in patients with drug-naive T2DM and NAFLD; however, exenatide showed greater reductions in body weight, visceral fat area, liver enzymes, FIB-4, postprandial plasma glucose, and LDL-C. [ABSTRACT FROM AUTHOR]

Background and aims: Glycated hemoglobin A1c (HbA1c) ≥6.5% (or 48mmol/mol) has been recommended as a new diagnostic criterion for diabetes; however, limited literature is available regarding the effect of age on the HbA1c for diagnosing diabetes and the causes for this age effect remain unknown. In this study, we investigated whether and why age affects the diagnostic efficiency of HbA1c for diabetes in a community-based Chinese population. Methods: In total, 4325 participants without previously known diabetes were enrolled in this study. Participants were stratified by age. Receiver operating characteristic curve (ROC) was plotted for each age group and the area under the curve (AUC) represented the diagnostic efficiency of HbA1c for diabetes defined by the plasma glucose criteria. The area under the ROC curve in each one-year age group was defined as AUCage. Multiple regression analyses were performed to identify factors inducing the association between age and AUCage based on the changes in the β and P values of age. Results: The current threshold of HbA1c (≥6.5% or 48mmol/mol) showed low sensitivity (35.6%) and high specificity (98.9%) in diagnosing diabetes. ROC curve analyses showed that the diagnostic efficiency of HbA1c in the ≥75 years age group was significantly lower than that in the 45–54 years age group (AUC: 0.755 vs. 0.878; P<0.001). Pearson correlation analysis showed that the AUCage of HbA1c was negatively correlated with age (r = -0.557, P = 0.001). When adjusting the red blood cell (RBC) count in the multiple regression model, the negative association between age and AUCage disappeared, with the regression coefficient of age reversed to 0.001 and the P value increased to 0.856. Conclusions: The diagnostic efficiency of HbA1c for diabetes decreased with aging, and this age effect was induced by the decreasing RBC count with age. HbA1c is unsuitable for diagnosing diabetes in elderly individuals because of their physiologically decreased RBC count. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Xia et al papers. To view these articles, visit https://doi.org/10.1111/apt.16772 and https://doi.org/10.1111/apt.16818 [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the association of serum betatrophin with the status and progression of nonalcoholic fatty liver disease (NAFLD). Methods: A total of 249 subjects who received ultrasonic examination of liver fat content (LFC) were recruited. Anthropometric and biochemical examinations were performed. Serum betatrophin was measured by ELISA. Results: Compared with control group, serum betatrophin significantly increased in NAFLD group (P < 0.05). There was significant difference in serum betatrophin among control, low liver fat content (LLFC), and high liver fat content (HLFC) groups (P < 0.01). After adjustment for gender, age, BMI, FPG and HbA1c, the betatrophin positively correlated with LFC (r = 0.185, P < 0.01) and TG (r = 0.195, P < 0.01). Stepwise multiple regression analysis indicated serum betatrophin was independently related to LFC (P < 0.05). Multivariate logistic regression analysis revealed subjects in the highest tertile of serum betatrophin had higher odds of having NAFLD after adjustment for traditional NAFLD risk factors (OR = 2.88, 95%CI: 1.15–7.19) (P<0.05). Conclusion: Serum betatrophin is an independent risk factor for NAFLD and potential non-invasive marker for its progression. Serum betatrophin may be helpful for the early diagnosis of NAFLD and improvement of its prognosis. [ABSTRACT FROM AUTHOR]

Background: We recently demonstrated a positive effect of berberine on nonalcoholic fatty liver disease patients after 16 weeks of treatment by comparing mere lifestyle intervention in type 2 diabetes patients with berberine treatment, which decreased the content of hepatic fat. However, the potential mechanisms of the clinical effects are unclear. We used a lipidomic approach to characterize the state of lipid metabolism as reflected in the circulation of subjects with nonalcoholic fatty liver disease (NAFLD) before and after berberine treatment.Methods: Liquid chromatography-mass spectrometry evaluated the various lipid metabolites in serum samples obtained from the participants (41 patients in the berberine group and 39 patients in the mere lifestyle intervention group) before and after treatment.Results: A total of 256 serum lipid molecular species were identified and quantified. Both treatments regulated various types of lipids in metabolic pathways, such as free fatty acids, phosphoglycerides and glycerides, in metabolic pathways, but berberine induced a substantially greater change in serum lipid species compared with mere lifestyle intervention after treatment. Berberine also caused obvious differences on ceramides. Berberine treatment markedly decreased serum levels of ceramide and ceramide-1-phosphate.Conclusions: Berberine altered circulating ceramides, which may underlie the improvement in fatty liver disease. ClinicalTrials.gov NCT00633282, Registered March 3, 2008. [ABSTRACT FROM AUTHOR]

Background/Objectives: Vitamin D exerts metabolic activities. We investigated whether the 25-hydroxy vitamin D [25(OH)D] is associated with liver fat content (LFC) and non-alcoholic fatty liver disease (NAFLD) in a middle-aged, elderly Chinese population. Subject/Methods: A total of 2,960 participants (954 men and 2,006 women) aged over 45 years old were enrolled. Each participant underwent a standard interview, anthropometric measurements and laboratory examinations. Vitamin D deficiency and insufficiency was diagnosed when serum 25(OH) D level was < 50 and 50–75nmol/L. An ultrasound quantitative method was used to assess the LFC. Results: Among the 2,960 participants, 1,982 (67.0%) subjects had vitamin D deficiency, 769 (26.0%) had vitamin D insufficiency, and 209 (7%) had normal vitamin D. Male subjects with vitamin D deficiency and insufficiency had significantly higher LFC than those with normal 25(OH)D (P = 0.034), while the LFC values showed no significant difference among the female subjects with vitamin D sufficiency, insufficiency and deficiency (P = 0.396). Univariate correlation analysis showed that 25(OH)D had a significantly negative association with LFC in men (r = -0.085, P = 0.009), but not in women. After adjusting for age, cigarette smoking, examination season, serum calcium, PTH and all possible confounders that displayed significant associations with LFC in univariate correlation analysis, serum 25(OH)D remained associated with LFC in middle-aged and elderly Chinese men. Conclusion: Serum 25(OH)D level was inversely associated with LFC in middle-aged and elderly Chinese men. [ABSTRACT FROM AUTHOR]

Background and Aims: Although many studies have indicated a relationship between nonalcoholic fatty liver disease (NAFLD) and hyperuricemia, a few studies specifically examining the effects of the severity of liver fat content (LFC) on serum uric acid (SUA) and the presence of hyperuricemia because of the limitation of the examination methods for NAFLD. In this study, we investigate the relationship between the NAFLD and SUA levels in the Chinese population using standardized quantitative ultrasound. Methods: A community-based study was conducted from May 2010 to December 2012. A total of 4,305 people aged 45 years and above without excessive drinking were enrolled. A standard interview and anthropometric and laboratory blood parameters were collected for each person. The standardized ultrasound hepatic/renal ratio and hepatic attenuation rate was used to quantify LFC. Results: The prevalence of NAFLD and hyperuricemia was 33.1% and 17.1%, respectively. A total of 23.5% of the NAFLD subjects had hyperuricemia, and their SUA was higher than that of non-NAFLD subjects (327.2±76.8 vs 301.9±77.4 μmol/L, P<0.001). The LFC was positively correlated with SUA (r = 0.130, P<0.001) and an independent factor for SUA (standardized β = 0.054, P<0.001). The OR for the presence of hypreuricemia was 1.175 (95% CI 1.048–1.318; P<0.001) with a 1 SD increase in the log LFC. LFC greater than 10% was related to elevated SUA and an increased presence of hyperuricemia. Conclusions: LFC accumulation was associated with an increase in the prevalence of hyperuricemia and elevated SUA in our community-based population. LFC greater than 10% is related to the risk for hyperuricemia. [ABSTRACT FROM AUTHOR]

Objective To evaluate the new DXA VAT method on an Asian Chinese population by comparing to a reference method, computed tomography (CT). Design and Methods In total, 145 adult men and women volunteers, representing a wide range of ages (19-83 years) and BMI values (18.5-39.3 kg/m2) were studied with both DXA and CT. Results The coefficient of determination ( r2) for regression of CT on DXA values was 0.947 for females, 0.891 for males and 0.915 combined. The 95% confidence interval for r was 0.940-0.969 for the combined data. The Bland-Altman test showed a VAT bias (CT as standard method) of 143 cm3 for females and 379 cm3 for males. Combined, the bias was 262 cm3 with 95% limits of agreement of −232 to 755 cm3. While the current DXA method moderately overestimates the VAT volume for the study subjects, a further analysis suggested that the overestimation could be largely contributed to VAT movement due to breath-holding status. Conclusions For Asian Chinese, VAT measured with DXA is highly correlated to VAT measured with CT. Validation of the DXA VAT tool using a reference method (e.g., CT) needs to carefully control the breath-holding protocol. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is closely associated with type 2 diabetes mellitus. We investigated whether the deposition of fat in the liver is associated with glycemic abnormalities and evaluated the contribution of the liver fat content (LFC) to the impaired glucose regulation. We conducted a community-based study among 2836 residents (1018 males and 1818 females) without prior known diabetes mellitus from the Changfeng Study who were at least 45 years old. A standard interview, anthropometrics and laboratory parameters were performed for each participant. The standardised ultrasound hepatic-renal echo-intensity and hepatic echo-intensity attenuation rate were used to assess the LFC. The cohort was stratified according to the quintiles for LFC. Two-hour glucose and fasting blood glucose increased across the LFC quintiles after adjustment for age and gender. LFC increased continuously among glucose categories after adjustment for age and gender (NGT: 7.7±0.3%, IFG: 10.0±0.8%, IGT: 11.8±0.5%, IFG+IGT: 11.7±0.9%, new- DM: 12.4±0.6%, P<0.001). By logistic regression analysis, 1% LFC increment independently predicted prediabetes and diabetes (OR 1.032, 1.019–1.045, P<0.001; 1.021, 1.005–1.037, P = 0.012, respectively) after adjustment for all potential confounders. Furthermore, participants with LFC higher than 10% had higher odds ratios of impaired glucose regulation as compared with those with LFC below 10% in fully adjusted logistic models. These results suggest that the LFC is strongly associated with impaired glucose regulation in the Chinese population, and that an even slightly elevated LFC is associated with increased glucose dysregulation. [ABSTRACT FROM AUTHOR]

Abstract: Background: Nonalcoholic fatty liver disease is closely associated with metabolic syndrome and cardiovascular disease (CVD). We investigated whether the liver fat content (LFC) is independently associated with carotid artery intima-media thickness (CIMT) and evaluated the contribution of the LFC to the increased CIMT. Methods: We conducted a community-based study among 1809 participants (682 males and 1127 females) from the Changfeng Study who were at least 45 years old. A standard interview, anthropometrics and laboratory parameters were performed for each participant. The CIMT was determined by ultrasonography. A large CIMT value was defined as 75th percentile of the maximum CIMT. A standardised ultrasonographic hepatic-renal ratio was used to assess the LFC. Results: The median LFC value was 6% (interquartile range, 3–14%), and 34% of the subjects had hepatic steatosis based on the criteria for diagnosis of steatosis by quantitative ultrasound. The maximum CIMT, average CIMT and plaque score were strongly associated with the LFC (β = 0.319, 0.324 and 1.361, respectively; all P < 0.05) after adjustment for age, gender, smoking history, low-density lipoprotein cholesterol and metabolic syndrome. The multiple logistic regression analysis showed that a 1 SD increase in the LFC, the OR for having a large CIMT was 1.350 (95% CI 1.180–1.545; P < 0.001) after adjustment for all potential confounders. Conclusions: These results suggest that the LFC is independently associated with carotid atherosclerosis in the Chinese population, and that the risk of atherosclerosis is proportional to the degree of hepatic steatosis. [Copyright &y& Elsevier]

A series of different contents of glycidyl methacrylate (GMA)-grafted natural rubber (GNR) copolymers were fabricated via green bulk melt-grafting reactions, and super-tough bio-based poly (lactic acid) (PLA)/GNR thermoplastic vulcanizates (TPVs) were achieved by in-situ dynamic vulcanization. Increasing the graft yield, gel fraction, and crosslinking density of GNR vulcanizates effectively improved the ductility of the PLA/GNR TPVs, while prolonging the dynamic vulcanization time and increasing the GMA graft yield led to a notable enhancement in the impact toughness of the PLA/GNR TPVs. PLA/30 wt % GNR TPVs exhibited a significantly increased elongation (410%) and notched impact strength (73.2 kJ/m2), which were 40 and 15 times higher than those of the PLA/30 wt % NR TPVs, respectively. The new bio-based PLA/GNR TPVs offer promise as replacements for petroleum-based polymers in the automotive, 3D printing, and packaging fields. [ABSTRACT FROM AUTHOR]