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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.

Accumulating evidence indicates that acetate is increased under energy stress conditions such as those that occur in diabetes mellitus and prolonged starvation. However, how and where acetate is produced and the nature of its biological significance are largely unknown. We observed overproduction of acetate to concentrations comparable to those of ketone bodies in patients and mice with diabetes or starvation. Mechanistically, ACOT12 and ACOT8 are dramatically upregulated in the liver to convert free fatty acid-derived acetyl-CoA to acetate and CoA. This conversion not only provides a large amount of acetate, which preferentially fuels the brain rather than muscle, but also recycles CoA, which is required for sustained fatty acid oxidation and ketogenesis. We suggest that acetate is an emerging novel ‘ketone body’ that may be used as a parameter to evaluate the progression of energy stress.

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. The objective of this study was to examine recent trends in the prevalence of gestational diabetes mellitus (GDM) in Xiamen, China, and to investigate its associations with maternal risk factors. Overall, in this study, GDM affected 17.6% of all pregnant women in Xiamen, China. Maternal age and obesity were major contributors to GDM. Encouragingly, the trend of GDM risk remained stable over the course of the study.

Background Advanced maternal age (AMA; ≥35 years) is considered to be a major risk factor for adverse pregnancy outcomes. Along with the global trend of delayed childbearing, and in particular, the implementation of China’s second and third-child policy leading to a dramatic increase of AMA in recent years, the association between maternal age and pregnancy outcomes requires more investigation. Methods A population-based retrospective study was performed. Data were derived from the Medical Birth Registry of Xiamen from 2011 to 2018. Univariate and multivariate logistic regression was used to evaluate the effects of maternal age on pregnancy outcomes. Results A total of 63,137 women categorized into different age groups (< 25 years, 25–29 years, 30–34 years, and ≥ 35 years) were included in this study. Compared with the mothers aged 25–29 years, the univariate regression analysis showed that mothers aged < 25 years had lower risks of gestational diabetes mellitus (GDM) and cesarean. AMA was associated with higher risks of GDM, hypertension, cesarean, preterm birth, low-birth weight (LBW), large-for-gestational-age (LGA), macrosomia, and stillbirth (all P < 0.01). After adjustment for potential confounding factors, increased risks of GDM, hypertension, cesarean, preterm birth, and LBW remained significantly associated with AMA (all P < 0.05), whereas AMA mothers showed a lower risk of macrosomia than their younger counterparts. Additionally, no significant differences were detected in terms of Apgar score < 7. Conclusion AMA was associated with adverse pregnancy outcomes including increased risks of GDM, hypertension, cesarean, preterm birth, and LBW. This study confirmed the relationship between AMA and certain adverse maternal and fetal outcomes and emphasizes the necessity for women to be cautious about the age at which they become pregnant.

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.

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.

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.

ObjectiveAnimal studies and epidemiological studies have shown that there is potential sex-specific sensitivity to the intrauterine environment in relation to the developmental programming of obesity. The objective of this study was to assess the sex-specific association between prenatal antibiotics exposure and body mass index (BMI) in offspring from 1 to 4 years.MethodsA total of 10,163 mother–child pairs from the Medical Birth Registry in Xiamen, China, were included in this prospective cohort study. Data on prenatal antibiotics exposure were collected from the prescription database.ResultsA total of 4909 (48.3%) offspring had prenatal antibiotics exposure. The associations between prenatal antibiotics exposure and offspring’s BMI were significantly different among female offspring and male offspring (P for interaction: 0.034 at 1 year of age; 0.033 at 2 years of age; 0.020 at 3 years of age; and 0.021 at 4 years of age). In female offspring, prenatal antibiotic use was significantly associated with a higher BMI Z-score from 1 to 4 years old (difference in BMI Z-score: 0.11 [95% CI: 0.05–0.17] at 1 years of age; 0.10 [95% CI: 0.05–0.16] at 2 years of age; 0.14 [95% CI: 0.09–0.21] at 3 years of age; and 0.13 [95% CI: 0.07–0.19] at 4 years of age) after adjustment for confounder. Prenatal antibiotics use was not associated with offspring BMI Z-score from 1 to 4 years in male offspring.ConclusionsThe association of prenatal antibiotics exposure and BMI Z-score from 1 to 4 years old may differ by sex of offspring.

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.