Search Results (1,126)

Background/Objectives: Remnant cholesterol (remnant-C), derived from triglyceride-rich lipoproteins, is an important risk factor for cardiometabolic diseases. Given the metabolic link between dyslipidemia and skeletal muscle dysfunction, we aimed to evaluate the association between remnant-C and two key components of sarcopenia—low muscle mass and myosteatosis (ectopic fat deposition in skeletal muscle). Methods: This cross-sectional study included 11,570 patients who underwent abdominal computed tomography (CT) for health check-ups. Remnant-C was calculated as total cholesterol minus low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. We conducted multivariable logistic and linear analyses to assess the association between remnant-C and low muscle mass, defined as appendicular skeletal muscle mass divided by body mass index. Additional analysis examined the relationship between remnant-C and myosteatosis, defined using the NAMA (normal attenuation muscle area) divided by TAMA (total abdominal muscle area) index, a novel index derived from muscle quality mapping of abdominal CT scans. Results: Low muscle mass was observed in 244 males (3.9%) and 74 females (1.4%). Myosteatosis affected 950 males (15.0%) and 800 females (15.3%). There was an increasing prevalence of both low muscle mass and myosteatosis across remnant-C quartiles. The multivariate-adjusted odds ratios (ORs) for low muscle mass in the highest remnant-C quartile compared with the lowest quartile were 2.17 (95% confidence interval [CI] 1.45–3.26) for males and 1.37 (95% CI 0.68–2.76) for females. The corresponding ORs for myosteatosis were 1.37 (95% CI 1.11–1.69) for males and 1.24 (95% CI 0.96–1.59) for females. Conclusions: Elevated remnant-C level is associated with low muscle mass and myosteatosis, especially in male patients. Individuals with higher remnant-C levels may warrant comprehensive evaluation for skeletal muscle health. Full article

This study examined the effects of dietary crude protein (CP) level and starch: fat ratio (SFR) on glucose and lipid metabolism in geese. A total of 360 male Jiangnan White geese were allocated to a 3 × 2 factorial arrangement with two CP levels (14.5% and 16.5%) and three SFRs (SFR_20:1, SFR_11:1, and SFR_5:1) from 28 to 63 days of age. Under the low-protein condition, Both the SFR_11:1 and SFR_5:1 group enhanced body weight of geese at 63 d, but SFR _5:1 increased subcutaneous and abdominal fat deposition. Dietary SFR changed liver cholesterol metabolism and glycogen content, while CP levels mainly affected the activity of enzymes related to liver glucose and lipid metabolism: 14.5% CP increased AMPK and ACC activity, but decreased FAS, CS and G6PC activity. Both CP level and SFR altered muscle fatty acid composition, but the effect of SFR was usually more significant. An SFR of 11:1 was beneficial for improving the muscle fatty acid profile. Gene expression analysis further revealed that low protein compensatorily regulated liver energy metabolism, while excessive fat in low SFR diets led to lipid metabolism disorders. In conclusion, optimizing the energy structure of low-protein diets, especially by maintaining a medium SFR (11:1), could improve glucose and lipid metabolism in geese while increasing body weight. Full article

Aims: Coronary heart disease (CHD) associated with rheumatoid arthritis (RA) is a primary driver of mortality in RA patients. In this study, we sought to establish a combined rat model of CHD and RA by integrating cardiac ischemia/reperfusion (I/R), high-fat diet (HFD), and intradermal administration of bovine type II collagen emulsified in complete Freund’s adjuvant. The aim of constructing this model is to investigate and analyze the pathogenesis of RA-induced CHD under the modulation of HFD and cardiac I/R exposure. Methods and Results: Sixty-four male Sprague–Dawley rats were randomly categorized into eight groups (n = 8 per group): control, I/R, HFD, collagen-induced arthritis (CIA), I/R + CIA, HFD + CIA, I/R + HFD, and I/R + HFD + CIA groups (n = 8 per group). We applied Synchrotron radiation-based X-ray micro-computed tomography (micro-CT) to observe the structural changes within the model over time. To further elucidate molecular mechanisms, transcriptome RNA-seq analysis was carried out to identify key signaling pathways, with particular emphasis on the homeostasis of Toll-like receptor 4 (TLR4)/Myd88 signaling in the ischemic myocardium. Furthermore, we conducted in vivo shRNA-mediated knockdown of polymerase I and transcription release factor (PTRF) and evaluated the co-localization of PTRF and TLR4 through immunofluorescence experiments. It is worth mentioning that our rat model of RA-induced (CHD) under a high-fat diet effectively manifested the relevant pathological features that align with the Traditional Chinese Medicine (TCM) definition of “bi” syndrome. The results indicate that the combined stimulation of HFD and CIA significantly elevated cardiac injury markers (CK-MB, LDH, CRP, and c-TNT) and was accompanied by a more severe expansion of the infarct area and increased cardiomyocyte apoptosis compared to the I/R group alone. In addition, the histopathological evaluation revealed significantly aggravated myocardial inflammation and fibrosis deposition, accompanied by extensive areas of tissue damage, further indicating a state of heightened inflammation and severe cardiac degenerative changes. Consistently, myocardial tissues from rats in the I/R + CIA + HFD group exhibited robust activation of the TLR4/MyD88 signaling pathway and a pronounced elevation in the p-JNK/JNK ratio. Moreover, pronounced co-localization between PTRF and TLR4 was evident in small vessels surrounding the infarcted myocardium. Importantly, AAV-mediated knockdown of PTRF attenuated the HFD- and CIA-induced exacerbation of myocardial injury in I/R rats. Conclusions: We successfully established a rat model of CHD with rheumatic syndrome using I/R in combination with RA and HFD. The present findings suggest that the PTRF-related TLR4/MyD88-JNK signaling pathway may act as an important regulatory mechanism underlying myocardial injury aggravated by combined HFD and CIA stimulation. Full article

This study evaluated the carcass characteristics and nutritional composition of duck meat from farmed (organic and conventional) and wild sources. Duck carcasses were analyzed to determine carcass traits (weight and yield of individual carcass portions) and meat quality parameters, including chemical composition and fatty acid profile. Results showed that farmed ducks (conventional and organic) had significantly higher live weight, carcass weight, and dressing percentage compared with wild ducks (p < 0.05). Conventional and organic groups exhibited comparable carcass yields; however, organic ducks demonstrated greater deposition of skin and subcutaneous fat, which may be partly attributed to their longer production period (~7 months) compared with conventional ducks (~45 days). Wild ducks had markedly lower carcass yield but a higher proportion of muscle protein in breast and thigh meat. Fatty acid analysis revealed that conventionally farmed ducks had significantly higher levels of polyunsaturated fatty acids (PUFA), particularly PUFA n-3, compared with organic and wild ducks (p < 0.05), which could be attributed to dietary basis (rapeseed-rich compound feed). Organic and wild ducks had higher levels of monounsaturated fatty acids than conventionally famed ducks. The study demonstrates that the rearing system significantly influences duck carcass traits and meat quality. Farmed ducks showed higher carcass yields, whereas wild ducks provided leaner meat with a higher protein content. These findings enhance understanding of the nutritional and technological properties of duck meat from different production systems. Full article

Intramuscular fat (IMF) is a pivotal determinant of meat quality in yaks (Bos grunniens). While nutritional factors are well-documented, the epigenetic landscape, particularly the transcriptional architecture governed by super-enhancers (SEs), remains largely unexplored in the context of IMF deposition. To investigate SE-associated genes, Chromatin immunoprecipitation sequencing (ChIP-seq) assays using H3K27ac antibodies and RNA-sequencing (RNA-Seq) were conducted on longissimus dorsi (LD) muscle tissues with high and low IMF contents. Integrated multi-omics analysis identified 82 enhancer-associated genes exhibiting significant upregulation in high-IMF samples, with 63 loci characterized as SE-associated. In particular, H3K27ac signal distribution analysis indicated that SEs were distributed across functional regions such as promoters, gene bodies, exons, and introns. Among these SE-related genes, 3-hydroxybutyrate dehydrogenase 1 (BDH1) was further investigated to understand its function and regulatory mechanisms. To address this, overexpression or knockdown experiments were conducted, followed by CCK-8, EdU, Bodipy functional assays, and Real-time quantitative PCR (RT-qPCR) analysis. Functional experiments revealed that BDH1 acts as a key positive regulator of yak preadipocyte differentiation and is a prime SE-associated candidate regulatory gene. Furthermore, dual-luciferase reporter assays were performed to identify its SE region, revealing that the activity of 4 enhancer regions was significantly upregulated. Collectively, these findings implicate SE-associated genes in IMF deposition in yaks, provide a valuable resource for future research, and underscore the functional relevance of BDH1 in this process. Full article

Background: Computed tomography-based body composition parameters are emerging prognostic markers in pancreatic cancer. While sarcopenia and myosteatosis have been widely studied, the prognostic significance of ectopic fat deposition within the psoas muscle remains unclear. We aimed to evaluate the prognostic impact of the fat ratio within the psoas muscle (FRPM) in patients with stage IV pancreatic cancer receiving first-line systemic chemotherapy. Methods: This retrospective cohort study included 99 patients with stage IV pancreatic cancer treated with first-line chemotherapy. Baseline CT images at the L3 level were analyzed, and FRPM was calculated as the proportion of intramuscular fat to total psoas muscle area. FRPM was analyzed primarily as a continuous variable. Exploratory low- and high-FRPM groups were defined using sex-specific medians for descriptive comparisons and Kaplan–Meier analyses. Overall survival (OS) and progression-free survival (PFS) were assessed using Kaplan–Meier and Cox regression analyses. Multivariable models were adjusted for age, sex, ECOG performance status, liver metastasis, and C-reactive protein (CRP). Results: Among 99 patients, 48 were categorized as having low FRPM and 51 as having high FRPM based on exploratory sex-specific median-based groups. Higher FRPM correlated with older age and higher BMI and inversely correlated with psoas muscle size and PMI. Median OS was 9.76 months in the low-FRPM group versus 5.78 months in the high-FRPM group, and median PFS was 5.29 versus 3.68 months. In the main multivariable Cox model, higher FRPM was associated with worse OS when analyzed as a continuous variable and reported per 1-standard deviation increase (adjusted HR: 1.43, 95% CI: 1.08–1.91, p = 0.014). After additional adjustment for first-line treatment-regimen category, the association remained directionally consistent but did not retain conventional statistical significance (adjusted HR: 1.32, 95% CI: 0.99–1.77, p = 0.060). Conclusions: Higher FRPM was associated with shorter OS and PFS in patients with stage IV pancreatic cancer receiving first-line systemic chemotherapy. These findings suggest that ectopic fat deposition within the psoas muscle may represent a potential CT-based muscle-quality marker associated with adverse prognosis. External validation and comparison with conventional adiposity parameters are required before clinical application. Full article

Crohn’s disease (CD) is a chronic immune-mediated inflammatory disorder characterized by transmural inflammation and a progressive course that frequently leads to structural complications such as intestinal fibrosis. Fibrostenosing disease represents a major clinical challenge, affecting up to 50% of patients over time and often requiring surgical intervention. Despite advances in anti-inflammatory therapies, no effective treatments currently exist to prevent or reverse established fibrosis. Intestinal fibrosis arises from a dysregulated tissue remodeling process driven by excessive extracellular matrix deposition and persistent activation of mesenchymal cells, particularly fibroblasts and myofibroblasts. This process is orchestrated through complex interactions between immune and non-immune cells and mediated by key signaling pathways, including transforming growth factor beta (TGF-β1) and the TL1A/DR3 axis. Genetic susceptibility, notably variants in NOD2 and other fibrosis-related genes, contributes not only to disease risk but also to phenotype progression. Epigenetic mechanisms, particularly microRNAs such as the miR-29 and miR-200 families, further modulate fibrogenesis and represent promising non-invasive biomarkers. Additionally, intestinal dysbiosis and specific microbial signatures, including reduced short-chain fatty acid-producing bacteria and the presence of adherent-invasive Escherichia coli, play a critical role in promoting fibrotic pathways. Mesenteric adipose tissue, especially creeping fat, also contributes to fibrosis through immune and metabolic signaling. Emerging biomarkers related to collagen metabolism and advances in molecular profiling are improving early detection strategies. Novel therapeutic approaches targeting fibrogenic pathways, including anti-TL1A agents, show promising preliminary results. A deeper understanding of these mechanisms is essential to develop effective antifibrotic therapies and improve long-term outcomes in CD. Full article

Objectives: Obesity precipitates excessive lipid accumulation within the kidney, culminating in ectopic lipid deposition that compromises target organ function through lipotoxicity. Given the pivotal role of GDF15 in lipid metabolism, this study aims to determine whether GDF15 can ameliorate ectopic lipid deposition and mitigate the resulting renal injury. Methods: C57BL/6J mice were used to establish a high-fat diet-induced obesity model. Based on Lee’s index, the mice were categorized into a diet-induced obesity group and an obesity-resistant group. Subsequently, the diet-induced obesity group received an injection of AAV-shGFRAL to knock down the GFRAL receptor. Results: In obesity resistant mice, ectopic lipid deposition in the kidneys was markedly reduced, accompanied by decreased expression of the renal injury marker KIM-1 and significantly elevated levels of GDF15. Modulation of the GDF15-GFRAL axis demonstrated that reduced autophagy levels led to increased lipid accumulation and exacerbated renal injury. Conversely, GDF15 activates the AMPK/SIRT1 signaling pathway to promote cellular autophagy, thereby mitigating renal damage induced by ectopic lipid deposition. Consistent with this mechanism, the suppression of autophagy results in the aggravation of renal injury caused by ectopic lipid accumulation. Conclusions: GDF15 ameliorates renal injury induced by ectopic lipid deposition in the kidney primarily through activation of autophagy via the AMPK/SIRT1 signaling pathway. Full article

Economic traits in livestock and poultry arise from the intricate interplay between genetic inheritance and environmental factors, mediated largely by epigenetic regulation. Histone modifications, particularly methylation and acetylation, serve as fundamental epigenetic mechanisms that dynamically remodel chromatin architecture and regulate gene expression in response to developmental and environmental cues. By bridging the gap between static DNA sequences and complex phenotypes, these dynamic marks offer a novel perspective for elucidating trait formation. This review examines the regulatory roles of histone modifications in shaping key economic traits, focusing on skeletal muscle development, fat deposition, and reproductive performance. Furthermore, we highlight two prospective strategies for integrating histone modification data into modern breeding programs: utilizing comprehensive epigenomic maps as novel biomarkers for precision selection, and implementing targeted nutritional regimens to program early phenotypic development. Despite substantial mechanistic advances, critical challenges persist, including high detection costs, inherent tissue specificity, and the necessity to validate transgenerational stability. Looking forward, the integration of multi-omics approaches is anticipated to propel animal breeding beyond traditional genomic selection toward an era of precise epigenomic design. Full article

Obesity development is linked to disturbances in the gut microbiota. Inonotus obliquus polysaccharides (IOPs) have potential therapeutic efficacy in alleviating metabolic disorders. However, the mechanism by which IOP prevents obesity via regulating gut microbiota remains elusive. IOP was extracted and structurally characterized by FT-IR and NMR spectroscopy, confirming typical polysaccharide structures. Structurally, IOP is a 5.4 kDa polysaccharide predominantly composed of glucose, galactose, xylose, mannose, galacturonic acid, glucuronic acid, as well as rhamnose, arabinose, and methyl-galactose. Administration of IOP to high-fat diet (HFD)-fed mice effectively curtailed weight gain and improved serum lipid parameters. Furthermore, it mitigated lipid deposition within hepatic and adipose tissues, while successfully countering HFD-triggered liver damage. Notably, IOP induced significant changes in microbial diversity and composition by selectively increasing the abundance of Streptococcaceae while suppressing Faecalibaculum rodentium at the family and species levels. These findings highlight that IOP is a promising functional food ingredient that regulates gut microbiota for obesity prevention. Full article

Previous studies have demonstrated that phloretic acid (PA), a phenolic compound, exerts beneficial effects on inflammation, oxidative stress, and aging. However, its effects on obesity and associated metabolic abnormalities, including dyslipidemia and metabolic dysfunction-associated steatotic liver disease (MASLD), remain unclear. To evaluate the effects of PA on these obesity-related metabolic alterations and explore the underlying mechanisms, male C57BL/6J mice were divided into three groups and fed for 10 weeks with a low-fat diet (10 kcal% fat), a high-fat diet (HFD, 60 kcal% fat), or an HFD containing 0.02% (w/w) PA. PA-supplemented mice showed no significant weight loss and fat loss. However, PA supplementation significantly reduced circulating levels of free fatty acid, triglyceride, and non-high-density lipoprotein cholesterol (HDL-C) while increasing HDL-C levels in HFD-fed mice. It also reduced hepatic lipid deposition and alleviated hepatocellular injury. These effects were accompanied by the coordinated modulation of hepatic lipid metabolism, including reduced lipogenesis and cholesterol esterification, enhanced fatty acid oxidation, and increased bile acid synthesis and excretion. Furthermore, PA attenuated hepatic oxidative stress and suppressed systemic and hepatic inflammation. These observations suggest that PA may counteract HFD-induced MASLD by modulating hepatic lipid metabolism, and that its anti-inflammatory and antioxidant effects may also contribute to these metabolic improvements. Full article

Background/Objectives: Although plant-derived dietary fiber and protein are favorable factors for improving host metabolic disorders, it remains unclear whether these two macronutrients exhibit synergistic health benefits. Methods: To address this gap, utilizing oat dietary fiber (GLU) and soybean protein (SBP) as representative bioactive models, we investigated the effects of 5% GLU, 20% SBP, and their combined supplementation on high-fat diet (HFD)-induced metabolic dysregulation in C57BL/6J mice. Results: Our results demonstrated that the combined GLU + SBP intervention provided comprehensive protection against HFD-induced obesity, significantly attenuating body weight gain (12.29 ± 2.02 g vs. 21.90 ± 2.86 g, p < 0.05) and adiposity (3.34 ± 1.19% vs. 10.77 ± 1.16%, p < 0.05) compared with HFD mice, without altering caloric intake. Crucially, the compound formulation exhibited synergistic superiority over individual components, as evidenced by greater reductions in serum aspartate aminotransferase (AST) activity (113.13 ± 28.50 U/L vs. 158.00 ± 30.25 U/L, p < 0.05) and improved glucose tolerance, with lower OGTT AUC values (999.09 ± 95.83 vs. 1434.66 ± 80.56 mmol/L·min, p < 0.05). Mechanistically, 16S rRNA sequencing revealed a distinct remodeling of the gut microbial community, highlighted by a substantial enrichment of Akkermansia. Functional prediction analysis specifically linked this microbial shift to the modulation of Akkermansia-associated metabolic pathways, which subsequently facilitated the activation of host metabolic networks to combat lipid deposition and systemic metabolic stress. Conclusions: Collectively, the GLU + SBP combination offers synergistic metabolic benefits driven by a distinct gut microbiota signature, supporting a feasible “soluble fiber + plant protein” strategy for developing functional foods targeting metabolic health. Full article

The fat mass and obesity-associated gene (FTO) has been shown to play a critical role in fat deposition in both humans and livestock. However, its involvement in subcutaneous and intramuscular fat deposition in chickens remains underexplored. In this study, we investigated the regulatory effects and pathways of FTO on subcutaneous and intramuscular fat deposition in chickens through functional gene verification and bioinformatics analysis. Our results demonstrated that, compared to the control group, exogenous transfection of an FTO lentiviral overexpression vector significantly inhibited cell proliferation and increased lipid accumulation in both subcutaneous and intramuscular adipocytes (p < 0.05). Furthermore, transfection of FTO siRNA markedly increased cell proliferation and reduced lipid accumulation in both subcutaneous and intramuscular adipocytes. A total of 413 and 164 differentially expressed genes were regulated by FTO in subcutaneous and intramuscular adipocytes, respectively. Pathway analysis revealed that the regulation of the actin cytoskeleton was a key process involved in FTO-mediated fat deposition in both subcutaneous and intramuscular adipocytes. Additionally, NRAS and ITGAV (subcutaneous fat), as well as FGF9, PIK3R2, FGF16, and RHOA (intramuscular fat), were identified as key genes enriched in this pathway. In conclusion, FTO differentially regulates fat deposition in chicken subcutaneous and intramuscular adipocytes by targeting distinct functional genes within the actin cytoskeleton pathway. Full article

Obesity is associated with excessive lipid deposition in adipose tissue and the liver, leading to systemic metabolic disturbances. In this study, we investigated the anti-obesity efficacy of Tisochrysis lutea (TL) powder, standardized to fucoxanthin (12.18 ± 0.21 mg/g DW) and docosahexaenoic acid (DHA) (16.03 ± 0.49 mg/g DW), in a high-fat diet (HFD)-induced obesity model in C57BL/6N mice. TL supplementation (50–150 mg/kg) over eight weeks significantly reduced body weight gain by up to 63.2%, total white adipose tissue mass by 53.4%, and liver weight by 38.2% compared to the HFD control, without affecting renal safety markers. Histological examination revealed smaller adipocytes and diminished hepatic steatosis in TL-treated groups. Serum triglycerides and leptin concentrations were significantly lowered by 38.5% and 70.1%, respectively, while HFD-induced elevations of ALT and AST were reduced by 61.7% and 38.6%, respectively. At the transcriptional level, TL downregulated adipogenic markers including PPARγ, C/EBPα, and SREBP-1c by 46~54%, as well as lipogenic regulators including FAS and ACC1 by up to 72%. Furthermore, TL treatment upregulated the mRNA levels of HSL and AMPK 2.3- and 2.1-fold, respectively, compared to the HFD control. These findings indicate that fucoxanthin- and DHA-enriched TL powder improves obesity-related metabolic alterations by modulating lipid storage and utilization pathways, supporting its development as a marine-derived functional ingredient for metabolic health management. Full article

Pancreatic steatosis is closely associated with metabolic disorders, pancreatitis, and pancreatic cancer, yet the underlying mechanisms remain incompletely understood and ideal animal models are lacking. We established and compared four mouse models based on distinct pathogenic mechanisms. In the high-fat diet (HFD)-fed model, pancreatic steatosis occurred later than hepatic steatosis. In ob/ob mice, despite severe obesity and hepatic steatosis, no significant intrapancreatic fat deposition was observed. In the caerulein combined with HFD model, caerulein markedly accelerated HFD-induced intrapancreatic fat accumulation, indicating a synergistic effect of inflammation and metabolic stress. Orthotopic injection of adipogenically differentiated 3T3-L1 cells established a focal model without altering systemic metabolism, enabling investigation of localized fat deposition. Collectively, these four models recapitulate metabolic, genetic, inflammatory, and localized mechanisms, exhibit divergent histological features, and provide a complementary platform for mechanistic studies and drug screening in pancreatic steatosis. Full article