(1) Background: hyperlipidemia is one of the cardiovascular diseases which becomes a great threat to the health of people worldwide. Oat beta-glucan is reported to have a beneficial effect on lowering blood lipids. To probe the effect of oat beta-glucan consumption on serum lipid profiles (total cholesterol, total triglyceride, high-density lipoprotein-cholesterol, and low-density lipoprotein-cholesterol), we carried out a systematic search on randomized controlled trials of oat beta-glucan intervention on hypercholesterolemic individuals. (2) Methods: the pieces of literature were obtained from PubMed, Scopus, Cochrane Library, Web of Science, and the Embase from inception to 28 February 2022. The results were presented with the weighted mean difference (WMD) with a 95% CI. The random-effects or fixed-effects model was applied according to the heterogeneity. The subgroup analysis and meta-regression were used to identify the source of heterogeneity. (3) Results: thirteen trials with 927 participants were included in our meta-analysis. Overall, oat beta-glucan supplementation significantly reduced levels of TC (pooled WMD = −0.24 mmol/L; 95%CI: −0.28 to −0.20 mmol/L), LDL-c (pooled WMD = −0.27 mmol/L; 95%CI: −0.35 to −0.20 mmol/L). Furthermore, beta-glucan consumption did not show significant effects on TG (pooled WMD = −0.04 mmol/L; 95%CI: −0.13 to 0.05 mmol/L), HDL-c (pooled WMD = 0.00 mmol/L; 95%CI: −0.05 to 0.05 mmol/L). Subgroup analysis indicated that critical factors, such as disease severity of participants, the daily intervention of oat beta-glucan, source of oat beta-glucan, and duration of intervention had impacts on outcomes. (4) Conclusions: oat beta-glucan intake may significantly decrease the level of TC and LDL-c while no significant changes in TG and HDL-c were observed. This meta-analysis supports the health benefits of oat beta-glucan, especially for its cholesterol-lowering features, although it has some inevitable limitations.

Sarcopenia and sarcopenic obesity (SO) represent significant age-related muscular disorders. Their specific biomarkers and pathophysiological mechanisms remain insufficiently elucidated. This study aims to identify differential and shared biomarkers between these conditions to reveal distinct pathophysiological processes, providing a foundation for precision diagnostics and targeted interventions. We conducted a systematic review and meta-analysis of studies examining biomarkers related to sarcopenia and SO in adults aged 45 and older. Electronic and manual searches were performed in PubMed, Web of Science, Cochrane Library, and Embase up to December 2024. The quality of each study was assessed using the National Institutes of Health Quality Assessment Tool. Meta-analysis was performed when at least three studies investigated the same biomarkers in frailty and sarcopenia, calculating the pooled effect size based on the standard mean difference using a random effects model. In total, 80 studies (64 on sarcopenia and 16 on SO) were included, encompassing 36,680 older adults (aged 45 and above) from 16 countries with varying levels of development. Participants were categorized based on their setting, age, and gender distribution. Sarcopenia is characterized by lower serum triglycerides and stable HDL/LDL ratios, while SO presents with higher triglycerides and disrupted cholesterol correlation, indicating distinct metabolic interactions. Analysis of inflammatory profiles revealed significantly elevated CRP levels in SO, with WBC as a specific marker, while TNF-α was associated with sarcopenia, suggesting a subtype-specific role of chronic inflammation. Vitamin D deficiency is prevalent in both conditions and may represent a potential therapeutic target. Subgroup analyses indicated an increased risk of muscle function decline in high-risk communities in developing regions, underscoring the urgent need for early intervention. A set of shared metabolic, hematologic, and inflammatory biomarkers was identified in sarcopenia and SO. These findings address a knowledge gap in biomarker research and highlight the distinct mechanisms involved in the development of both conditions. Developing biomarker-based diagnostic algorithms is essential for optimizing personalized treatment. Subgroup analyses have also identified high-risk populations, underscoring the need for early intervention.

The purpose of this study was to explore the effect of omega-3 polyunsaturated fatty acids (n-3 PUFAs) supplementation on serum lipid profile and blood pressure in patients with metabolic syndrome. We searched PubMed, Web of Science, Embase, and the Cochrane library from database inception to 30 April 2022. This meta-analysis included eight trials with 387 participants. We found that supplementation of n-3 PUFAs has no significant reduction in TC level (SMD = −0.02; 95% CI: −0.22 ~ 0.18, I² = 23.7%) and LDL-c level in serum (SMD = 0.18; 95% CI: −0.18 ~ 0.53, I² = 54.9%) of patients with metabolic syndrome. Moreover, we found no significant increase in serum high-density lipoprotein cholesterol level (SMD = 0.02; 95% CI: −0.21 ~ 0.25, I² = 0%) in patients with metabolic syndrome after consuming n-3 PUFAs. In addition, we found that n-3 PUFAs can significantly decrease serum triglyceride levels (SMD= −0.39; 95% CI: −0.59 ~ −0.18, I² = 17.2%), systolic blood pressure (SMD = −0.54; 95% CI: −0.86 ~ −0.22, I² = 48.6%), and diastolic blood pressure (SMD = −0.56; 95% CI: −0.79 ~ 0.33, I² = 14.0%) in patients with metabolic syndrome. The results from the sensitivity analysis confirmed that our results were robust. These findings suggest that n-3 PUFA supplementation may serve as a potential dietary supplement for improving lipids and blood pressure in metabolic syndrome. Given the quality of the included studies, further studies are still needed to verify our findings.

Background/Objectives: This study aimed to investigate the effects of fish oil-derived omega-3 polyunsaturated fatty acids (omega-3 PUFAs) on gut microbiota and serum lipid metabolites in T2DM. Methods: In a three-month, randomized, double-blind, placebo-controlled study, 110 T2DM patients received either fish oil (n = 55) or corn oil (n = 55) capsules daily. Serum lipids, glycemic parameters, gut microbiota diversity, and lipidomics were assessed. Results: This study found that fish oil-derived omega-3 PUFAs intervention did not significantly lower the fasting plasma glucose levels when compared with the baseline level (p > 0.05). However, serum fasting blood glucose (p = 0.039), glycosylated hemoglobin levels (p = 0.048), HOMA-IR (p = 0.022), total cholesterol (p < 0.001), triglyceride (p = 0.034), LDL cholesterol (p = 0.048), and non-HDL levels (p = 0.046) were significantly lower in the fish oil group compared with the corn oil group after three months of intervention. Also, it altered glycerophospholipid metabolism and gut microbiota. After three months, the fish oil group showed a significantly lower abundance of Desulfobacterota compared with the corn oil control group (p = 0.003), with reduced levels of Colidextribacter (p = 0.002), Ralstonia (p = 0.021), and Klebsiella (p = 0.013). Conversely, the abundance of Limosilactobacillus (p = 0.017), Lactobacillus (p = 0.011), and Haemophilus (p = 0.018) increased significantly. In addition, relevant glycolipid metabolism indicators showed significant correlations with the altered profiles of serum lipid metabolites, intestinal bacteria, and fungi. Conclusions: This study highlights the impact of fish oil-derived omega-3 PUFAs on intestinal microbiota structure and function in patients with type 2 diabetes. The observed decrease in pathogenic bacterial species and the enhancement of beneficial species may have significant implications for gut health and systemic inflammation, both of which are pivotal in managing diabetes. Further research is warranted to comprehensively elucidate the long-term benefits and underlying mechanisms of these microbiota alterations.

Nonalcoholic fatty liver disease (NAFLD) is considered the most prevalent chronic liver disease, but the understanding of the mechanism of NAFLD is still limited. The aim of our study was to explore hub lncRNAs and mRNAs and pathological processes in high-fat diet (HFD)-induced and lycopene-intervened liver steatosis. We analyzed the gene profiles in the GSE146627 dataset from the Gene Expression Omnibus (GEO) database to identify differentially expressed lncRNAs and mRNAs, and we constructed coexpression networks based on weighted gene coexpression network analysis (WGCNA). The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were utilized for functional enrichment analysis. We found that the turquoise, blue, brown, yellow, green, and black modules were significantly correlated with NAFLD. Functional enrichment analysis revealed that some hub lncRNAs (Smarca2, Tacc1, Flywch1, and Mef2c) might be involved in the regulation of the inflammatory and metabolic pathways (such as TNF signaling, metabolic, mTOR signaling, MAPK signaling, and p53 signaling pathways) in NAFLD. The establishment of an NAFLD mouse model confirmed that lycopene supply attenuated hepatic steatosis in HFD-induced NAFLD. Our analysis revealed that the inflammatory and metabolic pathways may be crucially involved in the pathogenesis of NAFLD, and hub lncRNAs provide novel biomarkers, therapeutic ideas, and targets for NAFLD. Moreover, lycopene has the potential to be a phytochemical for the prevention of HFD-induced liver steatosis.