Ask about this productRelated genes to: ACADVL Blocking Peptide
- Gene:
- ACADVL NIH gene
- Name:
- acyl-CoA dehydrogenase very long chain
- Previous symbol:
- -
- Synonyms:
- VLCAD, LCACD, ACAD6
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-30
- Date modifiied:
- 2017-09-21
Related products to: ACADVL Blocking Peptide
Related articles to: ACADVL Blocking Peptide
- Improving feed efficiency in dairy cattle requires a better understanding of tissue-specific mechanisms that support energy and nutrient utilization. Skeletal muscle represents a major proportion of body mass in dairy cows and plays a major role in post-absorptive metabolism. Our previous liver proteomics study highlighted that high-efficiency (HE) cows exhibit enhanced hepatic fatty acid oxidation, supporting lower feed intake without compromising productivity. This study aimed to identify muscle-based metabolic adaptations associated with feed efficiency. Skeletal muscle samples from 8 HE (low residual feed intake, RFI) and 8 low-efficiency (LE; high-RFI) mid-lactation (119 ± 33 DIM) Holstein cows, ranked at the top and bottom 10% of RFI, were analyzed using tandem mass tag proteomics and RT-qPCR to identify differences in skeletal muscle related to feed efficiency. HE cows had significantly greater muscle glycogen content and exhibited a coordinated metabolic shift favoring lipid utilization. RT-qPCR showed increased expression of β-oxidation (PPARA, ACADS, ACADVL, ACOX1) and triglyceride mobilization (ATGL) in HE cows. In contrast, proteomics revealed lower abundance of glycolytic and glycogenolytic enzymes (e.g., ALDOA, PFKM, PGAM2, PYGM, AGL) in HE muscle, indicating reduced glucose and glycogen catabolism. Proteins involved in the SLC2A4 (GLUT4) translocation pathway (ACTG1, YWHAH, YWHAZ) were more abundant in HE cows, suggesting an increased capacity for insulin-stimulated GLUT4 translocation, which may contribute to greater glycogen storage. Proteomics also showed enhanced redox regulation in HE cows, with greater abundance of GSR, CAT, GPX1, and PRDX2, and lower abundance of mitochondrial complexes I (NDUFB8) and III (UQCRC2), major sites of reactive oxygen species formation. These results indicate that skeletal muscle in HE cows adopts a metabolic phenotype characterized by increased reliance on lipid-derived fuels, glucose sparing, and improved oxidative homeostasis. Together with previously reported hepatic adaptations, these muscle-specific responses likely contribute to whole-animal feed efficiency in lactating dairy cows. - Source: PubMed
Publication date: 2026/05/30
Daddam Jayasimha RSura MounicaSarmikasoglou EfstathiosAhmad GhayyoorNaughton SarahMills MorganWhite Heather MVandeHaar MichaelZhou Zheng - Endurance exercise (EXE) has been recognized as a cardioprotective strategy against metabolic diseases, including obesity and type 2 diabetes. However, the precise molecular mechanisms remain incompletely understood, especially in female populations. This study investigates the molecular metabolic signaling nexus in a female mouse model of obese type 2 diabetes (OT2D) induced by a high-fat diet (HFD) and a single dose of streptozotocin (STZ). - Source: PubMed
Publication date: 2026/05/27
Ko JoungboChung EunheeCosio-Lima LudmilaMahmoudian ArmaghanLee Youngil - Tinnitus is a complex auditory perceptual disorder often accompanied by neuroinflammatory responses and metabolic abnormalities. Increasing evidence suggests that persistent oxidative stress, together with its interactions with immune regulation and energy metabolism, contributes to the pathophysiology of tinnitus. However, the molecular mechanisms by which oxidative stress drives tinnitus development remain to be systematically elucidated. - Source: PubMed
Publication date: 2026/04/28
Han JingjieCao YingZhang CaiZhang QianqianLi JinyingXu HongenZhao XingleYu Changyun - Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is a rare genetic metabolic disorder involving impaired fatty acid β-oxidation. It is caused by mutations in the Acyl-CoA Dehydrogenase Very Long Chain (ACADVL) gene, which encodes the VLCAD enzyme. The clinical presentation is diverse, ranging from a severe neonatal-onset form to a milder adult-onset form. We describe the first reported case in Vietnam, which is a 20-year-old man who presented with exercise intolerance, myalgia, and recurrent rhabdomyolysis triggered by fasting and exertion. Acylcarnitine profiling suggested a fatty acid oxidation disorder, and whole-exome sequencing identified the diagnosis of VLCAD deficiency with c747G > T (p.Trp249Cys) mutation. It has not previously been reported in the Vietnamese population. This case highlights the important role of neonatal screening and genetic testing in the early diagnosis of metabolic myopathies. In addition, it raises awareness of genetic disorders among healthcare providers and the public in developing countries. - Source: PubMed
Publication date: 2026/01/06
Kieu Vinh PhucNguyen Thang Van VietVu Anh Duc - Metabolic dysfunction-associated fatty liver disease (MAFLD) remains a global health burden with limited definitive therapies, highlighting the need for safe, food-derived interventions. Salvianolic acid B (SALB), a major water-soluble bioactive component of the traditional Asian health-promoting food , exhibits lipid-lowering, anti-inflammatory, and antioxidant properties, but its therapeutic potential and mechanisms in MAFLD remain unclear. Here, we employed an integrated approach combining network pharmacology, molecular docking, surface plasmon resonance affinity assays, lipidomics, and experiments in vitro and in vivo to address this gap. Network pharmacology combined with lipidomics identified PPAR-α as a key target of SALB. Molecular docking and SPR assays confirmed direct binding between SALB and PPAR-α. In vitro, SALB reduced triglyceride levels and lipid accumulation in HepG2 cells, enhanced fatty acid oxidation (FAO), and upregulated PPAR-α, PGC-1α, and FAO-related genes (CPT1, CPT2, ACADL, ACADVL). In HFD-fed mice, SALB decreased serum total cholesterol, triglycerides, LDL-C, ALT, AST, while increasing HDL-C. Additionally, SALB upregulated hepatic PPAR-α and FAO-related gene expression and suppressed hepatic reactive oxygen species production and inflammatory responses in both models. Collectively, our findings demonstrate that SALB, a natural food-derived bioactive compound, targets PPAR-α to ameliorate MAFLD by enhancing FAO, modulating lipid metabolism, and mitigating oxidative stress and inflammation. This work supports SALB's potential as a dietary supplement for MAFLD and metabolic disease management, reinforcing the value of exploring functional components from health-promoting food. - Source: PubMed
Publication date: 2026/03/19
Huang FengyanQiu ChenWang DannaNi YuanyingFu ZhuotaoFu LinchunLiang ChaoHuang ShangyiDeng Zhitong