Ask about this productRelated genes to: ACADM Blocking Peptide
- Gene:
- ACADM NIH gene
- Name:
- acyl-CoA dehydrogenase medium chain
- Previous symbol:
- -
- Synonyms:
- MCAD, MCADH, ACAD1
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ACADM Blocking Peptide
Related articles to: ACADM Blocking Peptide
- Cutaneous involvement is a common manifestation of systemic lupus erythematosus (SLE), and dyslipidemia has emerged as a metabolic factor that aggravates lupus-associated skin injury. - Source: PubMed
Publication date: 2026/04/23
Hua YingWu ZhenyuLi YingPan YuleiXin XingpanZhou ShihuiZhao ShihanFan YongshengWen ChengpingJi JinjunXu Li - Intramuscular fat (IMF) is a key determinant of beef sensory quality. In this study, 60 24-month-old Yanbian yellow cattle (n = 30 per group), reared under standardized environmental and dietary conditions, were categorized into high-IMF (HM) and low-IMF (LM) groups. HM beef exhibited significantly higher IMF (P < 0.05), increased monounsaturated fatty acids, and reduced saturated fatty acids compared to LM. Integrated transcriptomics and non-targeted metabolomics (n = 8 per group) revealed that IMF deposition is associated with a dual-layered regulatory framework: an upstream signaling layer (comprising PPAR, PI3K-Akt, and mTOR pathways) and a downstream metabolic execution layer (lysine degradation and cholesterol metabolism). Weighted Gene Co-expression Network Analysis (WGCNA) identified Acadm and Elovl6 as candidate hub genes within these networks. Furthermore, 9-hydroxyoctadecanoic acid (9-HODE) was identified as a differentially abundant metabolite; 100-ns molecular dynamics simulations suggested its high-affinity binding to the Thyrotropin-releasing hormone receptor (TRHR) receptor as a potential mechanism for lipid accumulation. These findings provide important biological insights and a mechanistic basis for understanding the molecular regulation of marbling in Yanbian yellow cattle. - Source: PubMed
Publication date: 2026/04/17
Sun BinWang HaowenYu JiaXin XuanyingPark SungkwonChoi Seong-HoYan ChangguoLi Xiangzi - Inborn errors of metabolism (IEM) are frequently underdiagnosed in low-resource settings due to limited diagnostic infrastructure. We hypothesized that an integrated clinical-genomic approach could improve diagnosis and management of these conditions. Nineteen Pakistani families with clinically suspected IEM underwent systematic clinical assessment, available biochemical testing, and whole-exome sequencing (WES). Variants were classified according to ACMG/AMP guidelines using evidence from population databases, in silico prediction tools, segregation analysis, and genotype-phenotype correlation. Clinical diagnoses and management strategies were reassessed based on molecular findings. WES provided a molecular diagnosis in 90% (17/19) of families and enabled targeted therapeutic interventions in 70% (13/19). However, clinical outcomes were variable due to advanced disease in some cases and limited follow-up. Seven novel variants were identified in CYP27B1, DYM, MTTP, ALDH3A2, USP53, BRAF, and JAG1, while twelve recurrent mutations were detected in PIGN, GCDH, CLCN7, RNASEH2C, ABCB11, MPV17, IDUA, SMPD1, FBP1, SLC37A4, ACADM, and UGT1A1. Integrating genomic findings with clinical reassessment improved diagnostic precision. An integrated clinical-genomic approach enabled accurate diagnosis of pediatric IEM in resource-limited settings, with particular utility in children with metabolic disorders in a consanguineous population. Identification of both novel and recurrent variants expanded the genotypic and phenotypic spectrum of these disorders and highlighted the clinical utility of genomic diagnostics in optimizing patient care. - Source: PubMed
Publication date: 2026/04/13
Mansoor SumreenaAbid SabeenImran MuhammadMalik Munir IqbalAli QamarHussain ShanawazAli Hafiz AsimMasood YasserChoudhry ShehlaQamar RaheelAzam Maleeha - Fatty liver hemorrhagic syndrome (FLHS) is a nutrition-related metabolic disorder in laying hens characterized by excessive hepatic lipid accumulation and hemorrhagic lesions, leading to reduced productivity and increased mortality. However, the regulatory mechanisms linking mitochondrial dysfunction to hepatic lipid metabolism remain unclear. This study investigated the role of SIRT3 in modulating mitochondrial fatty acid oxidation during FLHS progression. An in vivo FLHS model was established by feeding laying hens with a high-energy, low-protein (HELP) diet, and an in vitro hepatic steatosis model was induced by free fatty acid (FFA) treatment in primary hepatocytes. Both models exhibited pronounced lipid accumulation in hepatic cells and altered hepatocellular injury-related parameters, which were associated with mitochondrial dysfunction and impaired fatty acid oxidation. Mechanistically, hepatic tissues and hepatocytes showed suppression of the SIRT3-AMPKα-PGC-1α signaling cascade, accompanied by reduced expression of mitochondrial biogenesis markers (NRF1, TFAM), impaired respiratory chain components (NDUFA9, SDHA, UQCRC1, COX4I1, ATP5B), and decreased transcription of fatty acid oxidation-related genes (PPARα, ACOX1, CPT1A, CPT2, ACADL, ACADM). Pharmacological activation of SIRT3 with AR-C17 restored AMPKα-PGC-1α signaling, enhanced mitochondrial biogenesis and respiratory function, and promoted fatty acid oxidation, thereby alleviating lipid accumulation in hepatocytes in both models. Collectively, these results demonstrate that SIRT3 is a key metabolic regulator maintaining mitochondrial oxidative function and lipid homeostasis in laying hens. Targeted activation of SIRT3 may provide a novel nutritional strategy for preventing or ameliorating FLHS and related metabolic disturbances in poultry production. - Source: PubMed
Publication date: 2026/04/07
Cao PanpanChen JinyanZeng ChunHu YangYuan JianyunGuo XiaoquanCao HuabinZhang CaiyingZhuang YuHu Guoliang - () has attracted interest in recent research regarding its possible involvement in metabolic dysfunction-associated steatotic liver disease (MASLD). However, their causal relationship is still unclear. - Source: PubMed
Publication date: 2026/03/12
Chen HanWang YanSu WeiLiu YichengLi ShuoLiu YunZhou Xiaoying