High-fat diet induces sarcopenic obesity in natural aging rats through the gut-trimethylamine N-oxide-muscle axis.

INTRODUCTION: The lack of suitable animal models for sarcopenic obesity (SO) limits in-depth research into the disease. Emerging studies have demonstrated that gut dysbiosis is involved in the development of SO. As the importance of microbial metabolites is starting to unveil, it is necessary to comprehend the specific metabolites associated with gut microbiota and SO. OBJECTIVES: We aimed to investigate whether high-fat diet (HFD) causes SO in natural aging animal models and specific microbial metabolites that are involved in linking HFD and SO. METHODS: Young rats received HFD or control diet for 80 weeks, and obesity-related metabolic disorders and sarcopenia were measured. 16S rRNA sequencing and non-targeted and targeted metabolomics methods were used to detect fecal gut microbiota and serum metabolites. Gut barrier function was evaluated by intestinal barrier integrity and intestinal permeability. Trimethylamine N-oxide (TMAO) treatment was further conducted for verification. RESULTS: HFD resulted in body weight gain, dyslipidemia, impaired glucose tolerance, insulin resistance, and systemic inflammation in natural aging rats. HFD also caused decreases in muscle mass, strength, function, and fiber cross-sectional area and increase in muscle fatty infiltration in natural aging rats. 16S rRNA sequencing and nontargeted and targeted metabolomics analysis indicated that HFD contributed to gut dysbiosis, mainly characterized by increases in deleterious bacteria and TMAO. HFD destroyed intestinal barrier integrity and increased intestinal permeability, as evaluated by reducing levels of colonic mucin-2, tight junction proteins, goblet cells and elevating serum level of fluorescein isothiocyanate-dextran 4. Correlation analysis showed a positive association between TMAO and SO. In addition, TMAO treatment aggravated the development of SO in HFD-fed aged rats through regulating the ROS-AKT/mTOR signaling pathway. CONCLUSION: HFD leads to SO in natural aging rats, partially through the gut-microbiota-TMAO-muscle axis.

Faecal microbiota transplantation from young rats attenuates age-related sarcopenia revealed by multiomics analysis.

BACKGROUND: Gut microbiota plays a key role in the development of sarcopenia via the 'gut-muscle' axis, and probiotics-based therapy might be a strategy for sarcopenia. Fecal microbiota transplantation from young donors (yFMT) has attracted much attention because of its probiotic function. However, whether or not yFMT is effective for sarcopenia in old recipients is largely unknown. Thus, we aimed to investigate the effect and mechanism of yFMT on age-related sarcopenia. METHODS: The fecal microbiota of either young (12 weeks) or old (88 weeks) donor rats was transplanted into aged recipient rats for 8 weeks. Then, muscle mass, muscle strength, muscle function, muscle atrophy, and muscle regeneration capacity were measured. Analysis of fecal 16 s rRNA, serum non-targeted metabolomic, gut barrier integrity, and muscle transcriptome was conducted to elucidate the interaction between gut microbiota and skeletal muscles. RESULTS: As evaluated by magnetic resonance imaging examination, grip strength test (P < 0.01), rotarod test (P < 0.05), and exhaustive running test (P < 0.05), we found that yFMT mitigated muscle mass loss, muscle strength weakness, and muscle function impairment in aged rats. yFMT also countered age-related atrophy and poor regeneration capacity in fast- and slow-switch muscles, which were manifested by the decrease in slow-switch myofibres (both P < 0.01) and muscle interstitial fibrosis (both P < 0.05) and the increase in the cross-section area of myofibres (both P < 0.001), fast-switch myofibres (both P < 0.01), and muscle satellite cells (both P < 0.001). In addition, yFMT ameliorated age-related dysbiosis of gut microbiota and metabolites by promoting the production of beneficial bacteria and metabolites-Akkermansia, Lactococcus, Lactobacillus, γ-glutamyltyrosine, 3R-hydroxy-butanoic acid, and methoxyacetic acid and inhibiting the production of deleterious bacteria and metabolites-Family_XIII_AD3011_group, Collinsella, indoxyl sulfate, indole-3-carboxilic acid-O-sulphate, and trimethylamine N-oxide. Also, yFMT prevented age-related destruction of gut barrier integrity by increasing the density of goblet cells (P < 0.0001) and the expression levels of mucin-2 (P < 0.0001) and tight junctional proteins (all P < 0.05). Meanwhile, yFMT attenuated age-related impairment of mitochondrial biogenesis and function in fast- and slow-switch muscles. Correlation analysis revealed that yFMT-induced alterations of gut microbiota and metabolites might be closely related to mitochondria-related genes and sarcopenia-related phenotypes. CONCLUSIONS: yFMT could reshape the dysbiosis of gut microbiota and metabolites, maintain gut barrier integrity, and improve muscle mitochondrial dysfunction, eventually alleviating sarcopenia in aged rats. yFMT might be a new therapeutic strategy for age-related sarcopenia.

Promoted catalytic hydrodechlorination for deep degradation of chlorophenols over Rh-La/SiO2 catalyst.

Deep degradation of chlorophenols (CPs) into safe and ecofriendly cyclohexanol during catalytic hydrodechlorination (HDC), shows important practical significance and attractive prospect in the treatment of wastewater containing chlorophenols. An efficient Rh-La/SiO2 catalyst was developed, by employing La as promoter. The presence of La in catalyst promoted catalytic performance of HDC significantly. Characterization results revealed that the interaction occurred between Rh and La in Rh-La/SiO2 catalyst. This interaction accompanied with the high dispersion and finely particle size of active Rh, and generation of abundant Rh sites neighboring La atom. Kinetic study illustrated that Rh-La(1:1)/SiO2 catalyst possessed the fastest kinetic constants, and minimized the apparent activation energies of 4-CP, phenol and cyclohexanone greatly. Complete degradation of 4-CP with a very high yield of cyclohexanol (> 98%) can be achieved at room temperature, making Rh-La(1:1)/SiO2 catalyst to be a promising candidate for deep degradation of CPs during HDC and other Rh catalyzed hydrogenation reactions.

Penta-therapy for severe acute hyperlipidemic pancreatitis.

INTRODUCTION: The purpose of our study is to evaluate the efficacy of penta-therapy for HL-SAP in a retrospective study. METHODS: Retrospective study between January 2007 and December 2016 in a hospital intensive care unit. HL-SAP patients were assigned to conventional treatment alone (the control group) or conventional treatment with the experimental protocol (the penta-therapy group) consists of blood purification, antihyperlipidemic agents, low-molecular weight heparin, insulin, covering the whole abdomen with Pixiao (a traditional Chinese medicine). Serum triglyceride, serum calcium, APACHE II score, SOFA score, Ranson score, and other serum biomarkers were evaluated. The hospital length of stay, local complications, systematic complications, rate of recurrence, overall mortality, and operation rate were considered clinical outcomes. RESULTS: 63 HL-SAP patients received conventional treatment alone (the control group) and 25 patients underwent penta- therapy combined with conventional treatment (the penta-therapy group). Serum amylase, serum triglyceride, white blood cell count, C-reactive protein, and blood sugar were significantly reduced, while serum calcium was significantly increased with penta-therapy. The changes in serum amylase, serum calcium were significantly different between the penta-therapy and control group on 7th day after the initiation of treatment. The reduction in serum triglyceride in the penta-therapy group on the second day and 7th day were greater than the control group. Patients in the penta-therapy group had a significantly shorter length of hospital stay. CONCLUSION: This study suggests that the addition of penta-therapy to conventional treatment for HL-SAP may be superior to conventional treatment alone for improvement of serum biomarkers and clinical outcomes.