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The article focuses on exploring the relationship between C-peptide levels and low muscle mass in patients with type 2 diabetes mellitus (T2DM), highlighting the potential of C-peptide as a biomarker for identifying low muscle mass. Topics include the methodology of the study, the prevalence of low muscle mass among patients with varying C-peptide levels, and the association between serum C-peptide levels and low muscle mass after adjusting for potential confounders.

Background: Uncontrolled hyperglycemia, hypercholesterolemia, and hypertension are common in persons with diabetes.Objective: To compare the effectiveness of team-based care with and without a clinical decision support system (CDSS) in controlling glycemia, lipids, and blood pressure (BP) among patients with type 2 diabetes.Design: Cluster randomized trial. (ClinicalTrials.gov: NCT02835287).Setting: 38 community health centers in Xiamen, China.Patients: 11 132 persons aged 50 years or older with uncontrolled diabetes and comorbid conditions, 5475 receiving team-based care with a CDSS and 5657 receiving team-based care alone.Intervention: Team-based care was delivered by primary care physicians, health coaches, and diabetes specialists in all centers. In addition, a computerized CDSS, which generated individualized treatment recommendations based on clinical guidelines, was implemented in 19 centers delivering team-based care with a CDSS.Measurements: Coprimary outcomes were mean reductions in hemoglobin A1c (HbA1c) level, low-density lipoprotein cholesterol (LDL-C) level, and systolic BP over 18 months and the proportion of participants with all 3 risk factors controlled at 18 months.Results: During the 18-month intervention, HbA1c levels, LDL-C levels, and systolic BP significantly decreased by -0.9 percentage point (95% CI, -0.9 to -0.8 percentage point), -0.49 mmol/L (CI, -0.53 to -0.45 mmol/L) (-19.0 mg/dL [CI, -20.4 to -17.5 mg/dL]), and -9.1 mm Hg (CI, -9.9 to -8.3 mm Hg), respectively, in team-based care with a CDSS and by -0.6 percentage point (CI, -0.7 to -0.5 percentage point), -0.32 mmol/L (CI, -0.35 to -0.29 mmol/L) (-12.5 mg/dL [CI, -13.6 to -11.3 mg/dL]), and -7.5 mm Hg (CI, -8.4 to -6.6 mm Hg), respectively, in team-based care alone. Net differences were -0.2 percentage point (CI, -0.3 to -0.1 percentage point) for HbA1c level, -0.17 mmol/L (CI, -0.21 to -0.12 mmol/L) (-6.5 mg/dL [CI, -8.3 to -4.6 mg/dL]) for LDL-C level, and -1.5 mm Hg (CI, -2.8 to -0.3 mm Hg) for systolic BP. The proportion of patients with controlled HbA1c, LDL-C, and systolic BP was 16.9% (CI, 15.7% to 18.2%) in team-based care with a CDSS and 13.0% (CI, 11.7% to 14.3%) in team-based care alone.Limitation: There was no usual care control, and clinical outcome assessors were unblinded; the analysis did not account for multiple comparisons.Conclusion: Compared with team-based care alone, team-based care with a CDSS significantly reduced cardiovascular risk factors in patients with diabetes, but the effect was modest.Primary Funding Source: Xiamen Municipal Health Commission. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease is likely to be associated with increased circulating branched-chain amino acids. We investigated the relationship between changes in branched-chain amino acids levels in the serum and improvement in liver fat content caused by exercise intervention in individuals with nonalcoholic fatty liver disease. The exploratory study included 208 central obesity and nonalcoholic fatty liver disease individuals from an exercise intervention randomized clinical trial for nonalcoholic fatty liver disease. The participants were randomly assigned to control, moderate, and vigorous-moderate exercise groups for 12 months. Changes in total branched-chain amino acids, leucine, isoleucine, and valine levels from baseline to 6 months were calculated. Liver fat content was determined by proton magnetic resonance spectroscopy. Reductions in circulating levels of total branched-chain amino acids, leucine, and valine levels from baseline to 6 months were significantly associated with the improvement of liver fat content at 6 months and 12 months (p < 0.01 for all) after adjustments for age, sex, total energy intake, protein intake, intervention groups, HOMA-IR, BMI, liver fat content, total branched-chain amino acids, leucine, and valine at baseline, respectively. These associations were still significant after further adjustments for changes in HOMA-IR and BMI from baseline to 6 months (p < 0.05 for all). Our findings indicated that reductions in circulating branched-chain amino acids levels were associated with an improvement in liver fat content by exercise intervention among patients with nonalcoholic fatty liver disease, which was independent of changes in BMI or HOMA-IR. [ABSTRACT FROM AUTHOR]

Background: Tricho-rhino-phalangeal syndrome (TRPS) is a rare autosomal dominant genetic disorder characterized by distinctive craniofacial and skeletal abnormalities, while non-ossifying fibroma (NOF) is a common benign bone tumour in children and adolescents. To date, no case of TRPS coexisting with NOF has been reported. This report presents a 12-year-old girl who had the characteristic features of tricho-rhino-phalangeal syndrome and non-ossifying fibroma with a fibula fracture. Case presentation: A 12-year-old girl was admitted to the Department of Endocrinology and Diabetes for evaluation of brachydactyly and a right fibula fracture. Clinical examination revealed sparse scalp hair, a characteristic bulbous pear-shaped nose, and brachydactyly with significant shortening of the fourth metatarsal. Neither intellectual disability nor multiple exostoses were observed. Radiography of both hands showed brachydactyly and cone-shaped epiphyses of the middle phalanges of the digits of both hands with deviation of the phalangeal axis. Genetic analysis of TRPS1 identified a heterozygous germline sequence variant (p.Ala932Thr) in exon 6 in the girl and her father. Approximately 1 month before being admitted to our department, the girl experienced a minor fall and suffered a fracture of the proximal fibula in the right lower limb. The pathological cytological diagnosis of the osteolytic lesion was NOF. Ten months following the surgery, the lesion on the proximal fibula of the girl disappeared. Conclusions: In conclusion, the present study is the first to report a rare case of NOF with a pathologic fracture in the fibula of a girl with TRPS. The identification of a missense mutation, (p.Ala932Thr), in exon 6 of TRPS1 in this kindred further suggested that the patient had type I TRPS and indicated that mutations in this exon may be correlated with more pronounced features of the syndrome. Radiological techniques and genetic analysis played key roles in the definitive diagnosis. [ABSTRACT FROM AUTHOR]

Background: There are emerging studies suggesting that non-alcoholic fatty liver disease (NAFLD) is a heterogeneous disease with multiple etiologies and molecular phenotypes. Fibrosis is the key process in NAFLD progression. In this study, we aimed to explore molecular phenotypes of NAFLD with a particular focus on the fibrosis phenotype and also aimed to explore the changes of macrophage subsets in the fibrosis subset of NAFLD. Methods: To assess the transcriptomic alterations of key factors in NAFLD and fibrosis progression, we included 14 different transcriptomic datasets of liver tissues. In addition, two single-cell RNA sequencing (scRNA-seq) datasets were included to construct transcriptomic signatures that could represent specific cells. To explore the molecular subsets of fibrosis in NAFLD based on the transcriptomic features, we used a high-quality RNA-sequencing (RNA-seq) dataset of liver tissues from patients with NAFLD. Non-negative matrix factorization (NMF) was used to analyze the molecular subsets of NAFLD based on the gene set variation analysis (GSVA) enrichment scores of key molecule features in liver tissues. Results: The key transcriptomic signatures on NAFLD including non-alcoholic steatohepatitis (NASH) signature, fibrosis signature, non-alcoholic fatty liver (NAFL) signature, liver aging signature and TGF-β signature were constructed by liver transcriptome datasets. We analyzed two liver scRNA-seq datasets and constructed cell type-specific transcriptomic signatures based on the genes that were highly expressed in each cell subset. We analyzed the molecular subsets of NAFLD by NMF and categorized four main subsets of NAFLD. Cluster 4 subset is mainly characterized by liver fibrosis. Patients with Cluster 4 subset have more advanced liver fibrosis than patients with other subsets, or may have a high risk of liver fibrosis progression. Furthermore, we identified two key monocyte-macrophage subsets which were both significantly correlated with the progression of liver fibrosis in NAFLD patients. Conclusion: Our study revealed the molecular subtypes of NAFLD by integrating key information from transcriptomic expression profiling and liver microenvironment, and identified a novel and distinct fibrosis subset of NAFLD. The fibrosis subset is significantly correlated with the profibrotic macrophages and M2 macrophage subset. These two liver macrophage subsets may be important players in the progression of liver fibrosis of NAFLD patients. [ABSTRACT FROM AUTHOR]

Nuclear magnetic resonance (NMR)-based metabolomics study usually involves spectral preprocessing, identification of biomarkers and interpretation of biological processes and pathogenesis, however, the traditional procedure is bound to inborn defects. In this study, a new analytical frame was proposed to assist spectral alignment and dimensionality reduction, screen the differential metabolites and get biological explanation of the metabolic network by combing weighted gene co-expression network analysis (WGCNA) and recoupled statistical total correlation spectroscopy (RSTOCSY). The performance of RSTOCSY-based WGCNA method was evaluated by the NMR dataset of serum from coronary heart disease with diabetes mellitus (CHDDM) patients. The statistical recoupling of variables (SRV) was successfully used to categorize the whole dataset into a number of superclusters of signals and served to spectral alignment, and its effectiveness was confirmed by the wine dataset with a larger spectral drift. Three phenotype-driven metabolite modules related to CHDDM were identified from the dataset by WGCNA, and 22 metabolites were further identified from the three modules according to the metabolic correlations within or between modules, and 40 significant metabolic correlations were observed from the intra- and inter-metabolites in the 2D pseudospectrum. These modules involve amino acid metabolism, microbial metabolism and glucose metabolism, and their analysis of metabolite network diffusion revealed a new discovery that the ferroptosis pathway is related to CHDDM. This RSTOCSY-based WGCNA approach provides an effective analysis workflow for information recovery and structure identification of metabolites and improving interpretability and understanding of the disease pathogenesis. [Display omitted] ● A new frame of metabolomic analysis was proposed by combing RSTOCSY with WGCNA ● Three phenotype-driven metabolite modules were identified from CHDDM dataset ● The metabolite modules related to CHDDM involve amino acid, microbial and glucose metabolisms ● The network diffusion analysis revealed a new pathway, ferroptosis, related to CHDDM [ABSTRACT FROM AUTHOR]

Irisin, a recently identified novel myokine, drives brown-fat-like conversion of white adipose tissues and has been proposed to mediate beneficial effects of exercise on metabolism. Circulating irisin was significantly reduced in type 2 diabetes patients; however, no evidence is available about its association with metabolic syndrome (MetS) and effects of adiposity and muscle mass on circulating irisin have been controversial. Cross-sectional data on socio-demographic, lifestyle, clinical characteristics and serum irisin were collected for 1,115 community-living Chinese adults with central obesity. Associations of serum irisin with MetS (central obesity plus any two of the following four factors (raised blood pressure (BP), raised fasting plasma glucose (FPG), raised triglyceride (TG), and reduced HDL cholesterol) and each component of MetS were analyzed using multivariable logistic regression. Among the 1,115 obese Chinese adults with a mean age of 53.2(±7.2) years, serum irisin levels (log-transformed) were significantly reduced in subjects with MetS and raised FPG than their control groups (p = 0.034 and 0.041, respectively). After adjustment for potential confounders, serum irisin was significantly associated with reduced risks of MetS and raised FPG, with odds ratios (ORs) (95% CI) per standard deviation of log-transformed irisin of 0.796 (0.505–0.959, p = 0.027) and 0.873 (0.764–0.998, p = 0.046), respectively. Associations of irisin with raised BP, raised TG and reduced HDL were not statistically significant ((ORs) (95% CI): 0.733(0.454–1.182, p = 0.202), 0.954(0.838–1.086, p = 0.478) and 1.130(0.980–1.302, p = 0.092), respectively). Stepwise multivariable linear regression analysis showed that fasting insulin, HbA1c and albumin/globulin ratio were negatively associated with serum irisin level with statistical significance (all p-values <0.05) and waist circumference was negatively associated with serum risin with marginally statistical significance (p = 0.055). These results imply that irisin may play an important role in insulin resistance and MetS and should be confirmed in future prospective studies. [ABSTRACT FROM AUTHOR]

The elucidation of metabolic perturbations and gender-age-specific metabolic characteristics associated with acute myocardial infarction (AMI) is essential for clinical risk stratification and disease management. A comprehensive cross-comparative metabolomics analysis was performed on the sera from 445 healthy controls, 347 AMI patients without cardiovascular disease (CVD), 79 AMI with CVD (AMICVD) patients including 27 deaths. Machine-learning-based integrated biomarker profiling and global network analysis were used to create a multi-biomarker for distinguishing the different AMI outcomes. The changes of most metabolites were dependent on AMI, but gender and age also give additional contributions to the changes of histidine, malonate, O-acetyl-glycoprotein and trimethylamine N-oxide. The altered metabolic pathways included gut dysbiosis, increased amino acid metabolism, glucose metabolism and ketone metabolism, and inactivation of tricarboxylic acid cycle. Enhanced histidine metabolism and microbiota dysbiosis may be one of the key factors during the developing of AMI into AMICVD. For the differential diagnosis of AMI events, three sets of specific multi-biomarkers provided relatively high accuracy with the areas under the curve more than 0.8 and hazard ratio more than 1 in the discovery set, and the results were reproduced and confirmed by the validation set. First use of cross-comparative metabolomics and machine-learning-based integrated biomarker analysis gives great capability to discriminate the different AMI outcomes. Also, the multi-biomarkers seem to be a valid and accurate auxiliary diagnosis biomarker in addition to standard stratification based on clinical parameters. [Display omitted] • Gender and age make special contributions to metabolite changes of AMI. • Machine learning-based multi-biomarker serve to distinguish different AMI outcomes. • Enhanced histidine metabolism and microbiota dysbiosis may be one key factor of AMICVD developed from AMI. [ABSTRACT FROM AUTHOR]

Background: The severity of liver fibrosis is an important predictor of death in patients with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). However, there is still no definite conclusion on the relationship between triiodothyronine (T3) and the severity of liver fibrosis. Thus, the aim of this study was to analyze the correlation between T3 level and the severity of liver fibrosis. Methods: We performed a cross-sectional study of 2072 T2DM patients with normal thyroid function from January 2017 to January 2020. NAFLD fibrosis score (NFS), Fibrosis index based on the 4 factors (FIB-4) and BARD score (BARD) were used to assess the severity of fibrosis in T2DM patients, and linear regression analyses were used to determine the factors independently associated with liver fibrosis. Further experiments were performed to assess the impact of low T3 on fibrosis progression in mice model and explore possible mechanisms. Results: Free triiodothyronine (fT3) levels had significantly inverse correlations with NFS and FIB-4, and BARD in T2DM patients (P < 0.05). In multiple linear regression analyses, decreased fT3 level was an independent risk factor for the severity of liver fibrosis of T2DM patients (P < 0.01). Findings from in-vivo experiment using mice model proved that hypothyroidism mice had more severe of liver fibrosis than those mice with normal thyroid function. We also found that T3 could inhibit the profibrotic TREM2+CD9+ macrophage, which had been identified an important player in the progression of liver fibrosis. Conclusion: The findings from this study proved an inverse correlation between T3 level and the severity of liver fibrosis, and lower fT3 level within the normal range was an independent risk factor for severe liver fibrosis. [ABSTRACT FROM AUTHOR]

Background: Patients with diabetes are prone to asymptomatic hypoglycemia (AH) due to diminished ability to perceive the onset of hypoglycemia. However, the actual prevalence and influencing factors of AH in outpatients with type 2 diabetes (T2DM) have not been well investigated. Methods: A total of 351 outpatients with T2DM underwent glucose monitoring by continuous glucose monitoring system (CGMS) for consecutive 72 h without changing their lifestyle and treatment regimens. Hypoglycemia is defined as a blood glucose level less than 3.9 mmol/L, which was further divided into Level 1 hypoglycemia (blood glucose 3.0–3.9 mmol/L) and Level 2 hypoglycemia (blood glucose < 3.0 mmol/L). Univariate and multivariate logistic regression analyses were used to determine the possible risk factors of AH. Results: In all 351 subjects studied, 137 outpatients (39.0%) were captured AH events, in which Level 1 AH and Level 2 AH accounted for 61.3% and 38.7%, respectively. 85 (62.0%) of the AH patients experienced nocturnal asymptomatic hypoglycemia (NAH) and 25 (18.2%) exclusively NAH. Multivariate logistic regression analysis demonstrated that patients with younger age, lower hemoglobin A1c (HbA1c), and higher systolic blood pressure (SBP) levels were associated with increased risk of AH. While after further grading of AH, male sex and Dipeptidylpeptidase-4 inhibitors (DPP4i) regime were shown to be associated with lower risk of Level 2 AH. Conclusions: Hypoglycemia unawareness could be frequently observed at either daytime or nighttime, although NAH was more common, in outpatients with T2DM. Relative relax HbA1c targets should be considered for patients who are prone to AH. [ABSTRACT FROM AUTHOR]

• Serum IL-6 levels are positively associated with visceral fat mass in aged population. • Increased serum IL-6 levels during aging process partially contribute to visceral fat accumulation in aged mice. • Serum Il-6 levels promote adipocyte hypertrophy in aged mice via inhibiting visceral fat lipolysis mediated by PKA/HSL axis. Age-related visceral obesity could contribute to the development of cardiometabolic complications. The pathogenesis of visceral fat mass accumulation during the aging process remains complex and largely unknown. Interleukin-6 (IL-6) has emerged as one of the prominent inflammaging markers which are elevated in circulation during aging. However, the precise role of IL-6 in regulating age-related visceral adipose tissue accumulation remains uncertain. A cross-sectional study including 77 older adults (≥65 years of age) was initially conducted. There was a significant positive association between serum IL-6 levels and visceral fat mass. We subsequently validated a modest but significant elevation in serum IL-6 levels in aged mice. Furthermore, we demonstrated that compared to wildtype control, IL-6 deficiency (IL-6 KO) significantly attenuated the accumulation of visceral adipose tissue during aging. Further metabolic characterization suggested that IL-6 deficiency resulted in improved lipid metabolism parameters and energy expenditure in aged mice. Moreover, histological examinations of adipose depots revealed that the absence of IL-6 ameliorated adipocyte hypertrophy in visceral adipose tissue of aged mice. Mechanically, the ablation of IL-6 could promote the PKA-mediated lipolysis and consequently mitigate lipid accumulation in adipose tissue in aged mice. Our findings identify a detrimental role of IL-6 during the aging process by promoting visceral adipose tissue accumulation through inhibition of lipolysis. Therefore, strategies aimed at preventing or reducing IL-6 levels may potentially ameliorate age-related obesity and improve metabolism during aging. [ABSTRACT FROM AUTHOR]

Obesity is an expanding global public health problem and a leading cause of metabolic disorders. The hepatokine Fetuin B participates in regulating insulin resistance, glucose metabolism and liver steatosis. However, the mechanism underlying Fetuin B activation remains unclear. Our previous population-based study demonstrated a significant association between serum Fetuin B and body fat mass in an obese population, which indicates its potential in mediating obesity-related metabolic disorders. In the present study, we further revealed a significant correlation between Fetuin B and leptin, the classic adipokine released by expanding adipose tissue, in this obese population. Consistently, elevated Fetuin B and leptin levels were confirmed in diet-induced obese mice. Furthermore, an in vitro study demonstrated that the leptin signalling pathway directly activated the transcription and expression of Fetuin B in primary hepatocytes and AML12 cells in a STAT3-dependent manner. STAT3 binds to the response elements on FetuB promoter to directly activate FetuB transcription. Finally, the mediating effect of Fetuin B in insulin resistance induced by leptin was confirmed according to mediation analysis in this obese population. Therefore, our study identifies leptin-STAT3 as an upstream signalling pathway that activates Fetuin B and provides new insights into the pathogenic mechanisms of obesity-related metabolic disorders. [ABSTRACT FROM AUTHOR]

Our aim was to assess effects of breast-feeding (BF) in the association between large-for-gestational age (LGA) and body mass index (BMI) trajectories on childhood overweight from 1 to 4 years old. A total of 1649 healthcare records of mother–child pairs had detailed records of feeding practices and were included in this retrospective cohort study. Data were available in Medical Birth Registry of Xiamen between January 2011 and March 2018. Linear and logistic regression models were used to access the difference between BF and no-BF group. For offspring were LGA and BF was significantly associated with a lower BMI Z-score from 1 to 4 years old after adjustment confounders in Model 1 to 3 [difference in BMI Z-score in Model 1: estimated β: −0.07 [95%CI: −0.13 to −0.01]; Model 2: estimated β: −0.07 (−0.13 to −0.004); Model 3: estimated β: −0.06 (−0.12 to −0.001); P = 0.0221, 0.0371, 0.0471]. A significantly lower risk of childhood overweight was observed in Model 1 [odd ratio (OR): 0.85 (95%CI, 0.73 to 1.00)], P = 0.0475) with adjustment for maternal pre-pregnancy BMI. Furthermore, Model 2 and Model 3 showed LGA-BF infants had a lower risk for childhood overweight then LGA-no-BF infants [OR: 0.87 and 0.87 (95%CI, 0.73 to 1.03; 0.74 to 1.03)], however, there was no statistical significance (P = 0.1099, and 0.1125)]. BF is inversely related to BMI Z-score and risk for overweight in children were LGA from 1 to 4 years old. Adjustment for maternal pre-pregnancy BMI, the protective association between BF and childhood overweight was more significant. [ABSTRACT FROM AUTHOR]

Our aim was to assess effects of breast-feeding (BF) in the association between large-for-gestational age (LGA) and body mass index (BMI) trajectories on childhood overweight from 1 to 4 years old. A total of 1649 healthcare records of mother–child pairs had detailed records of feeding practices and were included in this retrospective cohort study. Data were available in Medical Birth Registry of Xiamen between January 2011 and March 2018. Linear and logistic regression models were used to access the difference between BF and no-BF group. For offspring were LGA and BF was significantly associated with a lower BMI Z-score from 1 to 4 years old after adjustment confounders in Model 1 to 3 [difference in BMI Z-score in Model 1: estimated β: −0.07 [95%CI: −0.13 to −0.01]; Model 2: estimated β: −0.07 (−0.13 to −0.004); Model 3: estimated β: −0.06 (−0.12 to −0.001); P = 0.0221, 0.0371, 0.0471]. A significantly lower risk of childhood overweight was observed in Model 1 [odd ratio (OR): 0.85 (95%CI, 0.73 to 1.00)], P = 0.0475) with adjustment for maternal pre-pregnancy BMI. Furthermore, Model 2 and Model 3 showed LGA-BF infants had a lower risk for childhood overweight then LGA-no-BF infants [OR: 0.87 and 0.87 (95%CI, 0.73 to 1.03; 0.74 to 1.03)], however, there was no statistical significance (P = 0.1099, and 0.1125)]. BF is inversely related to BMI Z-score and risk for overweight in children were LGA from 1 to 4 years old. Adjustment for maternal pre-pregnancy BMI, the protective association between BF and childhood overweight was more significant. [ABSTRACT FROM AUTHOR]

Objective: For 1–4 cm differentiated thyroid cancer (DTC), current ATA guideline recommended hemithyroidectomy (HT) as an acceptable alternative initial procedure to total or near‐total thyroidectomy (TT). The aim of this study was to evaluate benefits and harms of HT, TT in 1–4 cm DTC. Design: Retrospective cohort study. Patients: DTC patients aged 18 years or older who underwent initial thyroidectomy in a tertiary medical centre were included from January 2008 to July 2018. Measurements: The structural persistent/recurrent disease, reoperation rates and surgical complications were compared using Cox proportional regression and logistic regression. Propensity score matching was performed to adjust for related clinicopathological variables. Results: Among 1824 DTC patients, 795 patients sized 1–4 cm were included. A total of 286 patients underwent HT and 509 patients underwent TT. In the matched analysis, no significant difference in disease‐free survival (DFS) between HT and TT was observed during the median follow‐up period of 56.5 months (hazard ratio [HR] 0.86; 95% CI, 0.37–2.00; p =.733). The difference in DFS between two groups was consistent regardless of age, sex, tumour size, follow‐up duration. Meanwhile, HT was associated with a decreased risk of surgical complications (odds ratio [OR] 0.47, 95% CI 0.31–0.71, p <.001), as well as lower proportion of levothyroxine replacement (p =.007). Two cases in HT group received reoperation. Further multivariate analysis showed surgical procedure was not associated with structural persistence/recurrence (HR 0.68; 95%CI, 0.29–1.58, p =.367). Conclusions: For patients with 1–4 cm DTC without clinical evidence of lymph node metastasis or extrathyroidal extension, HT was associated with lower risk of surgical complications than TT while provided similar benefits as TT. [ABSTRACT FROM AUTHOR]

Background: The prevalence of diabetes is increasing worldwide. Our study aimed to estimate the changing trends in the prevalence and incidence of diagnosed type 2 diabetes mellitus (T2DM) among Xiamen residents and the floating population using real-world data. Method: We used real-world data from the System of Xiamen Citizens Health Information from 2014 to 2019 to estimate the changing trends in the prevalence and incidence of diagnosed T2DM. The System included the diagnosis of diabetes and the prescription of hypoglycemic drugs. Prevalent cases of T2DM were individuals who were diagnosed with T2DM and/or using hypoglycemic drugs. Incident cases were individuals with diagnosed T2DM and/or using hypoglycemic drugs in 2014 or 2019 who had not been diagnosed and/or did not use hypoglycemic drugs in the past. Results: In 2014 and 2019, the prevalence of T2DM in Xiamen was 4.04 and 4.84%, respectively. In 2014 and 2019, the incidence rate of T2DM in Xiamen was 14.1 per 1000 person-year and 15.0 per 1000 person-year, respectively. There was a significant increase in both the prevalence (Prevalence difference: 0.80, 95%CI 0.76–0.83%, P < 0.001) and the incidence of T2DM (Incidence difference: 0.9, 95%CI 0.7–1.1, P < 0.001). in Xiamen. The prevalence and incidence of T2DM in people aged 18–39 increased significantly (P < 0.001), while the prevalence and incidence of T2DM in people aged 40–69 reduced significantly (P < 0.001). Conclusions: There was a significant increase in the prevalence and incidence of T2DM in Xiamen from 2014 to 2019 especially among those with younger age. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Diabetes prevalence in China has increased, but the trend in gestational diabetes mellitus prevalence is unclear. The objective of the present study was to examine the prevalence of gestational diabetes in Xiamen, China, and its association with maternal risk factors. Materials and Methods: This linked‐database cohort study used the Medical Birth Registry of Xiamen. Between 1 March 2011 and 30 March 2018, 78,572 women who were diagnosed with gestational diabetes mellitus (GDM) were enrolled in the study. Maternal factors associated with the prevalence of GDM were examined using multivariate logistic regression. Results: A total of 13,738 (17.6%) pregnant women were diagnosed with GDM according to the International Association of Diabetes and Pregnancy Study Groups criteria. GDM prevalence ranged from 15.5% (2012) to 19.9% (2017). Increasing age was associated with GDM; women aged >40 years versus those aged >25 years had an adjusted odds ratio (OR) of 5.91 (95% confidence interval [CI] 4.202–8.314). A positive correlation was observed between weight and GDM risk; obese women versus normal‐weight women had an adjusted OR of 2.508 (95% CI 2.253–2.792). Family history of diabetes and hypertension were more commonly observed among women with GDM. Multivariate analysis showed that family history of diabetes (OR 1.101, 90% CI 1.028–1.180), weight gain during early pregnancy (OR 1.087, 90% CI 1.052–1.124) and systolic blood pressure (OR 1.015, 90% CI 1.011–1.020) were risk factors associated with GDM incidence. Conclusions: GDM affects 17.6% of all pregnant women in Xiamen. Age and maternal obesity were major contributors to GDM. The trend of GDM risk remained stable during the study. [ABSTRACT FROM AUTHOR]

Background: It has been reported that earlier age at menarche is associated with a higher risk for type 2 diabetes mellitus. However, the relationship between age at menarche and gestational diabetes mellitus is inconsistent across studies. We hypothesized that an earlier age at menarche would predict the gestational diabetes mellitus risk.Methods: This was a population-based, retrospective cohort study of 70,041 women aged 18 to 53 years old, conducted between 2011 and 2018. The subjects were recruited from the Medical Birth Registry in Xiamen, China. Age at menarche was categorized as 8-12, 13, 14, 15, 16-19 years old. Logistic regression analysis and spline analysis was used to assess the risk of the menarche age group for gestational diabetes mellitus. Linear regression analysis was performed to evaluate independent associations between age at menarche and fasting plasma glucose and blood glucose 1 hour and 2 hours after a 75-g of glucose load between 24 and 28 weeks' gestation.Results: The overall prevalence of GDM was 17.6%. After adjustment for family history of diabetes, earlier age at menarche (8-12, and 13 years old) was associated with increased odds for GDM (OR, 1.08; 95% CI, 1.02-1.15, and OR, 1.07; 95% CI, 1.03-1.14, respectively) compared with average age at menarche (14 years old). With further adjustment for pre-pregnancy body mass index, blood pressure, educational level, age at delivery, and hepatitis B surface antigen status, this association was attenuated (OR, 0.93, and OR, 1.02, respectively). Multivariable-adjusted spline regression models showed a linear dose-response association between age at menarche and GDM (P for nonlinearity, 0.203; P for linearity, 0.006). On linear regression analysis, earlier age at menarche was significantly associated with increased blood glucose one and 2 hours after a glucose load but not with the fasting plasma glucose.Conclusions: As expected, early age at menarche was found to be associated with an increased risk of gestational diabetes mellitus. However, this association may be mediated by potential confounding factors other than age. An additional finding was that earlier menarche was significantly related with elevated pregnancy glucose concentrations after a glucose load. [ABSTRACT FROM AUTHOR]

Background: There is no evidence available on the association of Fetuin-B with chronic kidney disease (CKD), and mechanisms linking nonalcoholic fatty liver disease (NAFLD) to CKD are not fully understood. We aimed to explore the independent associations and potential mechanisms of Fetuin-B and NAFLD with CKD. Methods: A cross-sectional study of 1,072 Chinese adults who underwent serum Fetuin-B test and hepatic ultrasonography scanning was conducted in Xiamen, China. CKD was defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2 and/or the presence of albuminuria. Results: Subjects with CKD showed significantly higher prevalence of NAFLD (69.5 vs. 57.2%, p < 0.001) and serum Fetuin-B levels (4.32 ± 1.45 vs. 4.05 ± 1.36 µg/mL, p = 0.007) than their controls. Increased serum Fetuin-B was also significantly associated with increased levels of fasting insulin and homeostasis model assessment – insulin resistance (both p values < 0.05). NAFLD and higher serum Fetuin-B were significantly associated with increased risk of CKD, and the unadjusted ORs (95% CIs) were 1.701 (1.256–2.303, p = 0.001) and 1.213 (1.053–1.399, p = 0.008, per SD increase of Fetuin-B), respectively. With adjustment for potential confounding factors, including metabolic/insulin resistance syndrome, NAFLD but not serum Fetuin-B was still significantly associated with increased risk of CKD, and the adjusted ORs (95% CIs) were 1.820 (1.327–2.496, p < 0.001) and 1.116 (0.959–1.298, p = 0.153, per SD increase of Fetuin-B), respectively. Conclusions: Fetuin-B might link NAFLD to CKD via inducing insulin resistance, and NAFLD contributes independently to the pathogenesis of CKD via multiple mechanisms besides of metabolic/insulin resistance syndrome. [ABSTRACT FROM AUTHOR]

Background: This study explored associations of genetic variants in the fetuin B (FETUB) locus with intrahepatic triglyceride (IHTG) content. Methods: Four tagging single‐nucleotide polymorphisms (SNPs) of the FETUB locus and patatin‐like phospholipase domain containing 3 (PNPLA3) rs738409 and transmembrane 6 super family member 2 (TM6SF2) rs58542926 were genotyped in 418 obese Chinese adults in whom serum FETUB and IHTG were measured. Results: Subjects carrying the minor G allele for FETUB rs4686434 (AG/GG) had lower serum FETUB levels (mean [±SD] 3.89 ± 1.36 vs 4.22 ± 1.46 μg/mL; P = 0.021) and IHTG content (12.7 ± 9.4% vs 14.6 ± 9.8%; P = 0.045) than their controls (AA), whereas IHTG content was higher in those carrying the minor G allele for PNPLA3 rs738409 (CG/GG) than in their controls (CC; 14.5 ± 10.1% vs 12.0 ± 8.6%; P = 0.012). After adjusting for potential confounders, IHTG content was lower in carriers of the minor G allele for FETUB rs4686434 (AG/GG vs AA, β −2.27 ± 0.91, P = 0.012), but was higher in carriers of the minor G allele for PNPLA3 rs738409 (CG/GG vs CC, β 2.65 ± 0.97, P = 0.006). There was a significant joint effect between FETUB rs4686434 and PNPLA3 rs738409 on IHTG content, with increasing genetic risk score (counting the risk allele of A in rs4686434 and G in rs738409) being associated with higher IHTG content (β 1.85 ± 0.48, P <0.001). Conclusions: Carrying the minor G allele for FETUB rs4686434 was significantly associated with decreased IHTG content and may affect hepatic triglyceride accumulation in individuals at high risk of non‐alcoholic fatty liver disease. HighlightsThe minor allele G for fetuin B (FETUB) rs4686434 was significantly associated with decreased intrahepatic triglyceride (IHTG) content.There was a significant joint effect between FETUB rs4686434 and patatin‐like phospholipase domain containing 3 (PNPLA3) rs738409 on IHTG content. [ABSTRACT FROM AUTHOR]

Objective Laboratory models suggested that Fetuin-B impaired insulin action in myotubes and hepatocytes and caused glucose intolerance in mice. We aimed to explore the independent associations and pathways among serum Fetuin-B, nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D). Methods A cross-sectional study of 1318 obese adults who underwent serum Fetuin-B test and hepatic ultrasonography scanning was conducted in Xiamen, China. Multivariable logistic regression was used to calculate adjusted odds ratio (OR) and 95% confidence intervals (CI) of serum Fetuin-B level and NAFLD for T2D in different models with adjustment for potential confounders. Structural equation modeling (SEM) was used to examine the paths among NAFLD, serum Fetuin-B, metabolic/insulin resistance syndrome and T2D. Results Subjects with T2D or NAFLD showed significantly increased serum Fetuin-B levels compared to their controls (4.25 ± 1.35 vs. 4.08 ± 1.38 µg/ml for diabetes; and 4.26 ± 1.41 vs. 4.07 ± 1.33 µg/ml for NAFLD; both p-values < 0.05). NAFLD and higher serum Fetuin-B were significantly associated with higher risk of T2D with adjustment for sociodemographic and lifestyle habits; and the adjusted ORs (95%CIs) were 2.90 (2.17–3.87, p < 0.001) and 1.16 (1.01–1.32, p = 0.032), respectively. With further adjustment for metabolic/insulin resistance syndrome (BMI, systolic and diastolic BP, triglyceride, total cholesterol, HDL- and LDL-cholesterol, HOMA-IR and serum uric acid), NAFLD but not serum Fetuin-B was significantly associated with increased risk of T2D (ORs (95%CIs): 1.58 (1.12–2.21, p = 0.009) and 1.07 (0.92–1.23, p = 0.384), respectively). A one pathway model by using SEM fitted well (χ 2  = 497.92, p < 0.001; CFI = 0.965; TLI = 0.926; and RMSEA = 0.097) and showed that NAFLD increased serum Fetuin-B and elevated Fetuin-B increased fasting insulin level, which in turn induced insulin resistance and T2D. Besides, NAFLD increased the risk of T2D directly in addition to its indirect effects of inducing metabolic/insulin resistance syndrome which in turn increased the risk of T2D. Conclusions Fetuin-B links NAFLD to T2D via inducing insulin resistance, and NAFLD contributes to the pathogenesis of T2D via multiple mechanisms. [ABSTRACT FROM AUTHOR]

Abstract: Background: Fetuin‐B impairs insulin action in myotubes and hepatocytes and causes glucose intolerance in mice. This study explored the correlation between serum fetuin‐B and intrahepatic triglyceride (IHTG) content, and the association between fetuin‐B and the risk of insulin resistance in the general adult population. Methods: A cross‐sectional study of 1318 obese adults who underwent serum fetuin‐B testing and hepatic ultrasonography was conducted in Xiamen, China. The IHTG content was determined in 428 subjects by magnetic resonance spectroscopy. Results: Non‐alcoholic fatty liver disease prevalence was significantly higher in those with the highest serum fetuin‐B concentrations and the highest IHTC content (Tertile 3) than in subjects in Tertiles 1 and 2 (62.6% vs 60.7% and 54.3%, respectively [P = 0.032], and 15.3% vs 12.8% and 12.7%, respectively [P = 0.049]). There was a significant association between increasing serum fetuin‐B tertiles and both increasing fasting insulin concentrations (mean [± SD] 11.9 ± 6.8, 12.7 ± 7.6, and 13.3 ± 6.4 mIU/L in Tertiles 1, 2 and 3, respectively; P = 0.006) and prevalence of insulin resistance (54.4%, 58.9%, and 64.5% in Tertiles 1, 2 and 3, respectively; P = 0.010). In linear regression analysis, IHTG content was independently and positively correlated with serum fetuin‐B (regression coefficient 0.015; P = 0.045). With adjustment for potential confounders, serum fetuin‐B was independently associated with increased risk of insulin resistance, with an adjusted odds ratio per standard deviation increase in fetuin‐B of 1.14 (95% confidence interval 1.01–1.30; P = 0.031). Conclusions: The results demonstrate the role of fetuin‐B linking liver fat accumulation to insulin resistance in humans. [ABSTRACT FROM AUTHOR]

Background Existing evidence about the associations of non-alcoholic fatty liver disease (NAFLD) and serum uric acid (SUA) with subclinical atherosclerosis is controversial. The aim of the present study was to examine the associations of NAFLD and SUA with subclinical atherosclerosis. Methods In the present cross-sectional study, 1354 obese adults underwent hepatic ultrasonography and arteriosclerosis detection. Indices of subclinical atherosclerosis were brachial-ankle pulse wave velocity (ba-PWV) and the ankle-brachial index (ABI). Linear regression using multivariable fractional polynomial (MFP) modeling was used to examine independent associations of NAFLD and SUA with a-PWV and ABI. Results Compared with controls, mean (± SD) ba-PWV was significantly higher in subjects with NAFLD (1534 ± 292 vs 1433 ± 259 cm/s; P < 0.001) and hyperuricemia (HUA; 1519 ± 275 vs 1476 ± 287 cm/s; P = 0.007). After adjustment for sociodemographic and lifestyle factors, NAFLD and SUA were both positively related to ba-PWV (β = 0.120 and 0.064, respectively; P < 0.05 for both). With further adjustment for insulin resistance and components of metabolic syndrome (MetS), the positive correlations were no longer significant (β = 0.017 and 0.006; P > 0.05 for both). In addition, NAFLD, but not SUA, was negatively correlated with ABI (β = −0.073; P = 0.015). Using MFP modeling, the best fractional polynomial (FP) transformation model showed that non-linear transformations were appropriate for two variables in their relationship with ba-PWV, namely age and fasting insulin as first-degree FP transformations (age3 and 1/insulin0.5, respectively). Conclusions Neither NAFLD nor SUA was related to ba-PWV with increases in insulin resistance and MetS, but NAFLD was independently and negatively correlated with ABI. [ABSTRACT FROM AUTHOR]

The present study aimed to explore the independent association and potential pathways between serum uric acid (SUA) and nonalcoholic fatty liver disease (NAFLD). 1365 community-living obese Chinese adults who received hepatic ultrasonography scanning were included. The prevalence rates of NAFLD were 71.5% for men and 53.8% for women. Compared with controls, NAFLD subjects showed significantly increased SUA levels (333.3 ± 84.9 v.s. 383.4 ± 93.7 μmol/L) and prevalence rate of hyperuricemia (HUA) (25.7% v.s. 47.3%, p < 0.001). After adjustment for insulin resistance (IR), components of metabolic syndrome (MetS) and other potential confounders, elevated SUA is independently associated with increased risk of NAFLD, with the adjusted OR of 1.528-2.031 (p < 0.001). By using multivariable fractional polynomial (MFP) modeling, the best FP transformation model shows that SUA was independently and linearly associated with risk of NAFLD. The one-pathway model by using structural equation modeling (SEM) about the relationships among SUA, IR, components of metabolic syndrome and NAFLD fits well (χ2 = 57.367, p < 0.001; CFI = 0.998; TLI = 0.992; and RMSEA = 0.048) and shows SUA might increase the risk of NAFLD directly besides of the indirect effects through increasing fasting insulin, blood pressure, triglyceride and decreasing HDL-C levels. Our results imply that elevated SUA may play an important role in NAFLD pathogenesis. [ABSTRACT FROM AUTHOR]