Intermittent fasting, exercise, and dietary modification induce unique transcriptomic signatures of multiple tissues governing metabolic homeostasis during weight loss and rebound weight gain.

Obesity and its related metabolic diseases bring great challenges to public health. In-depth understanding on the efficacy of weight-loss interventions is critical for long-term weight control. Our study demonstrated the comparable efficacy of exercise (EX), intermittent fasting (IF), or the change of daily diet from an unhealthy to a normal chow (DR) for weight reduction, but largely divergently affected metabolic status and transcriptome of subcutaneous fat, scapular brown fat, skeletal muscles and liver in high-fat-high-fructose diet (HFHF) induced obese mice. EX and IF reduced systematic inflammation, improved glucose and lipid metabolism in liver and muscle, and amino acid metabolism and thermogenesis in adipose tissues. EX exhibited broad regulatory effects on TCA cycle, carbon metabolism, thermogenesis, propanoate-, fatty acid and amino acid metabolism across multiple tissues. IF prominently affected genes involved in mitophagy and autophagy in adipose tissues and core genes involved in butanoate metabolism in liver. DR, however, failed to improve metabolic homeostasis and biological dysfunctions in obese mice. Notably, by exploring potential inter-organ communication, we identified an obesity-resistant-like gene profile that were strongly correlated with HFHF induced metabolic derangements and could predict the degree of weight regain induced by the follow-up HFHF diet. Among them, 12 genes (e.g., Gdf15, Tfrc, Cdv3, Map2k4, and Nqo1) were causally associated with human metabolic traits, i.e., BMI, body fat mass, HbA1C, fasting glucose, and cholesterol. Our findings provide critical groundwork for improved understanding of the impacts of weight-loss interventions on host metabolism. The identified genes predicting weight regain may be considered regulatory targets for improving long-term weight control.

Heterogeneous selection dominated the temporal variation of the planktonic prokaryotic community during different seasons in the coastal waters of Bohai Bay.

To explore temporal and spatial effects on the planktonic prokaryotic community composition (PCC) in the coastal region of the Bohai Sea, surface water samples were collected from 12 to 28 regularly distributed sites in Bohai Bay across 3 months from different seasons to characterize the PCC using high-throughput sequencing of the 16S rRNA V4 region. Prokaryotic α- and ß-diversity showed significant temporal variation during the three sampling months. VPA analysis based on both weighted and unweighted UniFrac distances exhibited a shift of environmental and spatial effects on PCC variation with temporal variation. Quantification analysis of assembly processes on community turn over showed that "heterogeneous selection" dominated for PCC temporal variation, with basic abiotic parameters such as temperature, pH, ammonia nitrogen as the driving factors. Analysis of seasonal features showed that seasonal specific OTUs (ssOTUs) exhibited different seasonal attributions under the same phylum; meanwhile, the ssOTUs showed significant correlations with the driving environmental factors, which suggested that finer-level analysis was needed to more strictly reflect the temporal variation. Moreover, predicted nitrogen and sulfur metabolism were significantly shifted during the temporal variation. Our results clearly showed that seasonally varied environmental factors drive the "heterogeneous selection" process for PCC assembly in seawaters of Bohai Bay during different sampling seasons.

Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction.

Pathological remodeling is the main detrimental complication after myocardial infarction (MI). Overproduction of reactive oxygen species (ROS) in infarcted myocardium may contribute to this process. Adequate exercise training after MI may reduce oxidative stress-induced cardiac tissue damage and remodeling. SET and MYND domain containing 1 (Smyd1) is a muscle-specific histone methyltransferase which is upregulated by resistance training, may strengthen sarcomere assembly and myofiber folding, and may promote skeletal muscles growth and hypertrophy. However, it remains elusive if Smyd1 has similar functions in post-MI cardiac muscle and participates in exercise-induced cardioprotection. Accordingly, we investigated the effects of interval treadmill exercise on cardiac function, ROS generation, Smyd1 expression, and sarcomere assembly of F-actin in normal and infarcted hearts. Adult male rats were randomly divided into five groups (n = 10/group): control (C), exercise alone (EX), sham-operated (S), MI induced by permanent ligation of left anterior descending coronary artery (MI), and MI with interval exercise training (MI + EX). Exercise training significantly improved post-MI cardiac function and sarcomere assembly of F-actin. The cardioprotective effects were associated with increased Smyd1, Trx1, cTnI, and α-actinin expression as well as upregulated ratio of phosphorylated AMP-activated protein kinase (AMPK)/AMPK, whereas Hsp90, MuRF1, brain natriuretic peptide (BNP) expression, ROS generation, and myocardial fibrosis were attenuated. The improved post-MI cardiac function was associated with increased Smyd1 expression. In cultured H9C2 cardiomyoblasts, in vitro treatment with H2O2 (50 µmol/L) or AMP-activated protein kinase (AMPK) agonist (AICAR, 1 mmol/L) or their combination for 4 h simulated the effects of exercise on levels of ROS and Smyd1. In conclusion, we demonstrated a novel role of Smyd1 in association with post-MI exercise-induced cardioprotection. The moderate level of ROS-induced upregulation of Smyd1 may be an important target for modulating post-MI cardiac function and remodeling.

Aerobic exercise alleviates oxidative stress-induced apoptosis in kidneys of myocardial infarction mice by inhibiting ALCAT1 and activating FNDC5/Irisin signaling pathway.

Aerobic exercise involves in ameliorating kidney injury, but the underlying mechanisms are not fully clarified. In this study, we elucidated the potential mechanisms of aerobic exercise in ameliorating kidney injury following myocardial infarction (MI). In vivo, wildtype and alcat1 knockout mice were used to establish the MI model, and subjected to six-week moderate-intensity aerobic exercise. In vitro, Normal Rat Kidney (NRK) cells treated with H2O2 and recombinant human Irisin (rhIrisin) were used for exploring potential mechanisms. Our results showed that Irisin expression was up-regulated by aerobic exercise in kidneys after MI, while ALCAT1 was reduced. In alcat1 knockout mice, we found that ALCAT1 involved in the progressions of oxidative stress and apoptosis in impaired kidney tissues of MI mice, but aerobic exercise reversed these changes. Furthermore, in vitro, we observed that Irisin inhibited both H2O2-treatment or overexpression of alcat1-induced oxidative stress and apoptosis in NRK cells, partially via AMPK-Sirt1-PGC-1α pathway. These findings reveal that aerobic exercise participates in alleviating the levels of oxidative stress and apoptosis in impaired kidney tissues following MI, partially via activating FNDC5/Irisin-AMPK-Sirt1-PGC-1α signaling pathway and inhibiting ALCAT1 expression.

A Vibrio owensii strain as the causative agent of AHPND in cultured shrimp, Litopenaeus vannamei.

The causative agent of shrimp AHPND was identified as specific Vibrio parahaemolyticus strains, which harbor a virulent plasmid that contains the toxic genes pirA and B (pirAB). Herein, a Vibrio bacterium was isolated from shrimp in Shanghai. This bacterium was identified as Vibrio owensii using 16S rRNA gene phylogeny, whole genome sequencing and comparative analysis. The V. owensii cells are rod-shape (1.86 ±â€¯0.15 µm) with a single polar flagellum (4 µm). In addition, V. owensii form mauve colonies with jagged edges on CHROMagar plates. The pirAB genes on the plasmid revealed 100% sequence similarity to that of AHPND V. parahaemolyticus, and the encoded proteins were detected in the culture media. Subculture of V. owensii showed that the pirAB genes are unstable, and their loss rate is approximately 22% and reaches a dynamic equilibrium after the fifth generation. Upon immersion bioassay, the cumulative mortality of V. owensii (pirAB+)-infected shrimp was up to 100% within 4 days, and typical AHPND clinical signs were observed. Approximately 105 CFU/hepatopancreas of V. owensii cells were observed in the pirAB+-infected shrimp based on both culture-dependent and -independent assay. Our results indicate that the expression of pirAB in the V. owensii strain is responsible for AHPND.