內容: Introduction: Diet intervention, especially supplementation with high-quality protein, is considered to be a critical strategy in sarcopenia. However, different sources and types of protein have different health impacts. Objectives: The aim of this study is to explore the differences in the ameliorative effects and mechanisms of different sources and types of proteins on sarcopenia, providing an optimal path for the prevention and treatment of sarcopenia. Methods: A sarcopenia model was established by intraperitoneal injection of dexamethasone (5 mg/kg). Sixty male C57BL/6 mice (8 months old) were randomly divided into the normal control, sarcopenia, goat whey protein, goat milk casein, bovine whey protein, and bovine milk casein groups. Animals were treated for 8 consecutive weeks. Organism-level and molecular phenotypes, 16S rRNA gene sequencing, and untargeted metabolomics profiling based on GC-TOF/MS were employed to investigate the correlation between host metabolism, microbial metabolism, autophagy and inflammation and their influence on sarcopenia in C57BL/6 male mice. Results: All 4 proteins increased muscle mass, and goat whey protein improved muscle strength in sarcopenic mice. Goat and bovine milk proteins promoted muscle regeneration by increasing MyoD1 and MyoG expression, and the former had a more distinct effect in inducing autophagy and decreasing inflammation than the latter. In addition, goat whey protein and casein could modulate host-microbial arginine co-metabolism. Notably, goat milk proteins responded well to sarcopenia comorbidities, including sarcopenic obesity, osteosarcopenia, and osteoarthritis. Conclusion: The study confirmed that goat milk proteins were more effective than bovine milk proteins for the control of sarcopenia. Moreover, we found that whey protein and casein could modulate host-microbial arginine co-metabolism, which shows their potential as precision nutritional supplements for the management of sarcopenia. Our study provides theoretical support for the prevention and control of sarcopenia.

內容: Background: Fructose may induce non-alcoholic fatty acids (NAFLD) due to the gut-liver axis interactions. The mechanism of fructose impairing colon barrier is unrevealed. Methods: Normal and dextran sulfate sodium (DSS)-induced Sprague-Dawley rats fed by 35% fructose diets were used to evaluate colon barrier functions. Microbiome and metabolome were applied to screen potential biomarker bacteria and metabolites induced by fructose. HT-29 cells were applied to validate metabolite biomarker indoleacrylic acid (IAA) and indole-3-carboxaldehyde (I3A) function in colon barrier which impaired by fructose. Results: Fructose induced colon barrier dysfunction, aggravated colon impairment in DSS-induced rats. With fructose intake, the colon length shortened, goblet numbers declined, inflammation infiltration induced, inflammatory cytokines increased, and apoptosis signals upregulated in colon tissue. Moreover, fructose induced dysbiosis of microbiota and their metabolites. Adlercreutzia and Holdemania were screened out as potential bacteria biomarkers, IAA and I3A as tryptophan metabolites were selected as metabolite biomarkers inhibited by fructose. IAA and I3A treatment alleviated the impairment induced by fructose by increasing trans epithelial electric resistance value, tight junction proteins, and Aryl hydrocarbon receptor (AhR) activity in HT-29 cell. Conclusion: Fructose stimulated inflammation, apoptosis, gut bacteria alteration, and induced the reduction of IAA and I3A. Since fructose inhibited production of IAA and I3A, AhR remained inactivated and consequently induced colon barrier dysfunction.

內容: Theaflavins from black tea effectively improve insulin secretion in obesity and diabetes, but the molecular mechanisms are unclear. Here, the palmitic acid (PA)-induced pancreatic β-TC-6 cells and high fat-/high glucose-induced zebrafish were used. The effects of theaflavin-3,3’-digallate (TF3) on glucolipotoxicity-induced insulin secretion dysfunction, ferroptosis and endoplasmic reticulum (ER) stress were investigated by a variety of molecular biological approaches, inductively coupled plasma-mass spectrometry (ICP-MS), transmission electron microscopy (TEM) and widely targeted metabolomics analysis. TF3 was found to potently inhibit glucolipotoxicity-induced insulin secretion dysfunction and ferroptosis in β-TC-6 cells and zebrafish, with increasing glutathione peroxidase 4 (GPX4) expression, suppressing lipid peroxidation and iron accumulation and protecting mitochondria. Additionally, TF3 attenuated ER stress by regulating 3 unfolded protein response (UPR) pathways in β-TC-6 cells, and significantly modulated linoleic acid metabolism and L-kynurenine signalling in zebrafish. The expression of sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) was obviously enhanced by TF3. Thapsigargin, a SERCA2 inhibitor, remarkably reversed the effects of TF3 on insulin production, ferroptosis, ER stress and the kynurenine signalling. Together, this work revealed the critical role of SERCA2 in ferroptosis regulation, and demonstrated TF3 targeted SERCA2 to inhibit ER stress and ferroptosis, thereby protecting β-cell secretory function from glucolipotoxicity.

內容: Some research have shown that the combination of plant extracts and probiotics may be a better way to treat type 2 diabetes mellitus (T2DM) than a single intervention. However, there are still relatively few relevant reports in this aspect. Therefore, this study aims to investigate whether the treatment of Polygonatum sibiricum saponin (PSS) and lactic acid bacteria (LAB) combination can better manage T2DM. And the anti-diabetes mechanism of the combination was studied from the perspectives of glucose metabolism, microbiome and metabolome. The results showed that PSS + LAB could better improve fasting blood glucose level, insulin sensitivity, lipid metabolism disorder, and liver function. Protein analysis showed that PSS + LAB treatment significantly increased the expression of phosphorylated-phosphatidylinositol 3 kinase (p-PI3K)/PI3K, phosphorylated-protein kinase B (p-AKT)/AKT, glucose transporter 2 (GLUT2), insulin receptor substrate 2 (IRS2), and glycogen synthase kinase 3β (GSK-3β) in the liver of T2DM mice, while inhibiting the expression of forkhead box protein O1 (FoxO1). This combination positively regulated the composition and abundance of the gut microbiota. Metabolomic analysis showed that the combination treatment exhibited more changes in gut microbiota metabolites compared to PSS treatment alone. The alteration of gut microbiota by LAB + PSS led to significant changes in alanine, aspartate and glucose metabolism pathways. This study may provide a theoretical basis for the combined application of plant extracts and probiotics for the management of T2DM.

內容: Hyperlipidemia constitutes a critical factor in the pathogenesis of vascular disease and gut microbiota dysbiosis. This study aims to investigate the role of sea buckthorn fruit oil (SBFO) in ameliorating hyperlipidemia, modulating gut microbiota, and elucidating the underlying mechanisms of its lipid-lowering effects. SBFO intervention in hyperlipidemic mice significantly reduced body weight and visceral adiposity index while mitigating symptoms associated with hyperlipidemia, including dyslipidemia, inflammation, liver damage, and endothelial dysfunction. Real-time quantitative PCR and Western blot analyses revealed that SBFO enhanced the response of free fatty acid oxidation and breakdown (adenosine 5’-monophosphate-activated protein kinase α, carnitine palmitoyltransferase1a, peroxisome proliferator-activated receptor α, and peroxisome proliferator-activated receptor γ) while suppressing the synthesis of triglycerides and fatty acids (sterol-regulatory element binding protein 1, fatty acid synthase, and acetyl CoA carboxylase) at the gene and protein expression levels. Moreover, SBFO intervention enriched the gut microbiota of hyperlipidemic mice by increasing the relative abundances of Lactobacillus, Faecalibaculum, and Allobaculum, while decreasing the Firmicutes/Bacteroidetes ratio. These findings suggest that SBFO exhibits promising therapeutic potential in attenuating hyperlipidemia in mice through the regulation of lipid metabolism and modulation of gut microbiota.

內容: The perception of salty taste is crucial for individuals to make healthy food choices. Yet, the brain electrophysiological signals underlying salty taste perception have been poorly described. In this study, electroencephalography (EEG) was used to record brain activity induced by NaCl solution as a salty taste stimulus. A combination of a custom delivery device and stimulation paradigm was employed to preserve the salty taste signal clearly. A stimulus-response capture method was proposed that could adapt to individual differences in brain responses to salty taste and accurately segment salty taste response signals. Applying this method to the EEG processing workflow can form a complete data processing framework. The results showed that the neural response induced by salty taste reached a high activity level in the initial stage within a short period (0.2 s), and there was a sustained periodic response within 0.75 s after the stimulation. Moreover, the salty taste information in the EEG signal was decoded, and discrimination of 2 similar concentrations of salty taste solutions was achieved far above the chance level (average identification rate: 89.66%). This study demonstrated experimental paradigms and research methods for understanding salty taste perception, which could provide references for research on other basic tastes.

內容: This work aims to compare the chemical composition and anti-inflammatory effects on RAW264.7 macrophages of Keemun black tea stems and leaves. A total of 50 volatile compounds were identified in tea stems and leaves, and aldehydes, alcohols, and esters were the main volatile compound categories. There were 11 key volatile compounds, including geraniol, benzeneacetaldehyde, methyl salicylate, linalool, etc. contributed to distinguishing the tea stems from the tea leaves. In the quantitative and liquid chromatography-mass spectrometry (LC-MS)-based metabolomics analysis, higher contents of amino acids, monosaccharides, and quinic acids were found in stems than those in leaves. Inversely, higher contents of tea pigments, flavan-3-ols, gallic acid, purine alkaloids, and flavonol glycosides were present in tea leaves than in stems. LC-MS-based metabolomics also revealed that organic acids were the most critical non-volatile compounds responsible for the differences between tea stems and leaves. Furthermore, tea stems had better inhibiting effects of pro-inflammatory cytokines (interleukin (IL)-1β and IL-6) in lipopolysaccharide-challenged RAW264.7 macrophages than tea leaves, while no significant differences exist between leaves and stems for inhibiting the secretion of tumor necrosis factor α (TNF-α) and NO. In conclusion, our results support using Keemun black tea stems as a novel source of anti-inflammatory compounds.

內容: Whole-grain foods have attracted emerging attention due to their health benefits. Whole grains are rich in bound polyphenols (BPs) linked with dietary fibers, which is largely underestimated compared with free polyphenols. In this study, in vitro simulated gastrointestinal digestion and colonic fermentation models were used to study the release profile and metabolism of BPs of oat bran. Significantly higher level of BPs was released during in vitro colon fermentation (3.05 mg GAE/g) than in gastrointestinal digestion (0.54 mg GAE/g). Five polyphenols were detected via LC-MS and their possible conversion pathways were speculated. Released BPs exhibited chemical antioxidant capacity. 16S rRNA sequencing further revealed that Clostridium butyricum, Enterococcus faecalis, Bacteroides acidifaciens were the key bacteria involved in the release of BPs, and this was verified by whole-cell transformation. Our results helped to explain the possible mechanism of the health benefits of BPs in whole grains.

內容: In order to save manpower and time costs, and to achieve simultaneous detection of multiple animal-derived components in meat and meat products, this study used multiple nucleotide polymorphism (MNP) marker technology based on the principle of high-throughput sequencing, and established a multi-locus 10 animal-derived components identification method of cattle, goat, sheep, donkey, horse, chicken, duck, goose, pigeon, quail in meat and meat products. The specific loci of each species could be detected and the species could be accurately identified, including 5 loci for cattle and duck, 3 loci for sheep, 9 loci for chicken and horse, 10 loci for goose and pigeon, 6 loci for quail and 1 locus for donkey and goat, and an adulteration model was established to simulate commercially available samples. The results showed that the method established in this study had high throughput, good repeatability and accuracy, and was able to identify 10 animal-derived components simultaneously with 100% repeatability accuracy. The detection limit was 0.1% (m/m) in simulated samples of chicken, duck and horse. Using the method established in this study to test commercially available samples, 4 samples from 14 commercially available samples were detected to be inconsistent with the labels, of which 2 did not contain the target ingredient and 2 were adulterated with small amounts of other ingredients.

內容: Maternal consumption of a high-fat diet has been linked to increased risks of obesity and impaired glucose metabolism in offspring. However, the precise epigenetic mechanisms governing these intergenerational effects, particularly during the early stages of offspring development, remain poorly understood. In this study, female C57BL/6J mice were randomly assigned to either a high-fat diet or normal chow diet throughout gestation and lactation. Methylated DNA immunoprecipitation (MeDIP) coupled with microarray analysis was employed to identify differentially methylated genes in the livers of offspring at weaning age. We found that maternal high-fat diet feeding predisposes offspring to obesity and impaired glucose metabolism as early as the weaning period. DNA methylation profile analysis unveiled a significant enrichment of differentially methylated genes within the natural killer (NK) cell-mediated cytotoxicity pathway. MeDIP-PCR validated reduced methylation levels of specific genes within this pathway, including tumour necrosis factor α (TNF-α), phosphoinositide 3-kinase (PI3K), and SHC adaptor protein 1 (SHC1). Consistently, the expressions of TNF-α, PI3K, and SHC1 were significantly upregulated, accompanied by elevated serum TNF-α and interleukin-6 (IL-6) levels in offspring from dams fed with high-fat diet. Moreover, we assessed the expressions of genes associated with NK cell activities, uncovering a notable rise in hepatic granzyme B levels and a trend towards increased CD107a expression in offspring from dams fed a high-fat diet. In addition, methylation levels of TNF-α, PI3K, and SHC1 promoters were inversely correlated with glucose response during glucose tolerance testing. In conclusion, our findings underscore the critical role of the NK cell-mediated cytotoxicity signaling pathway in mediating DNA methylation patterns, thereby contributing to the programming effects of maternal high-fat diet consumption on offspring glucose metabolism as early as the weaning period.