ACADL
- Known as:
- ACADL
- Catalog number:
- 000978A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACADL
Related genes to: ACADL
- Gene:
- ACADL NIH gene
- Name:
- acyl-CoA dehydrogenase long chain
- Previous symbol:
- -
- Synonyms:
- LCAD, ACAD4
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1988-11-07
- Date modifiied:
- 2017-09-21
Related products to: ACADL
Related articles to: ACADL
- This study aimed to investigate the mechanism of total flavonoids from Smilacis Glabrae Rhizoma(SGF) against obesity-associated colorectal cancer(CRC) via regulation of fatty acid oxidation(FAO). In vivo, syngeneic subcutaneous and orthotopic xenograft models of CRC cells MC38 were established in obese mice induced by high fat diet(HFD), which was followed by the administration with SGF. The tumor volume and tumor weight were measured in the CRC subcutaneous model. The growth of CRC orthotopic tumors was monitored by a small animal in vivo imaging system. Hematoxylin-eosin(HE) staining was used to observe the pathological changes in tumors and peritumoral adipose tissues. Immunohistochemistry, TdT-mediated dUTP nick end labeling(TUNEL), and oil red O staining were separately conducted to detect Ki67 expression, apoptosis, and lipid accumulation in tumors. Western blot was used to detect the phosphorylation levels of adenosine monophosphate-activated protein kinase(AMPK) and acetyl-CoA carboxylase(ACC), as well as the expression of FAO-related proteins and cell death-related proteins in tumor tissues. In vitro, MC38 cells cultured under low-glucose and high-oleic acid conditions were taken as the research object and treated with varying concentrations of SGF for 48 h. Apoptosis rates were assessed by flow cytometry, and the expression of FAO-related and cell death-related proteins was analyzed by Western blot. Further, the prolyl hydroxylase domain-containing protein 3(PHD3) expression was subjected to RNA interference(RNAi), and the viability and apoptosis of PHD3-knockdown MC38 cells following SGF treatment were assessed by MTT assay and flow cytometry, respectively. The results showed that both high and low doses of SGF significantly inhibited tumor growth in two obese mouse xenograft models. The SGF-treated groups exhibited extensive, scattered necrotic areas within the tumor tissue, with marked destruction of tissue structure. Compared with the HFD group, the SGF-treated groups showed a significant reduction in the rate of Ki67-positive cells and a significant increase in the proportion of TUNEL-staining-positive apoptotic cells. In obese mice, subcutaneous tumors showed significantly enhanced oil red O staining, with large lipid droplets visible. The SGF-treated groups markedly reduced lipid deposition. In both models, peritumoral adipocytes were significantly enlarged after SGF treatment. The tumor tissues of obese mice exhibited significantly increased expression of FAO-related proteins cluster of differentiation 36(CD36), carnitine palmitoyltransferase 1(CPT1), and acyl-CoA dehydrogenase long chain(ACADL), as well as elevated adenosine triphosphate(ATP) content. The phosphorylation levels of upstream regulatory proteins AMPK and ACC were significantly increased, while the expression of the energy switch protein PHD3 was significantly decreased. SGF significantly reduced the protein expression of CD36, CPT1, and ACADL, decreased ATP content, inhibited AMPK and ACC phosphorylation, and increased PHD3 protein levels. This was accompanied by a significant increase in the apoptotic protein cysteine-dependent aspartate-specific protease-3(caspase-3) and significant decreases in the anti-apoptotic protein B-cell lymphoma-2(Bcl-2) and the cell cycle protein cyclin D1. In MC38 cells cultured under low-glucose and high-oleic acid conditions, SGF significantly induced apoptosis and inhibited lipid uptake. FAO-related protein expression was significantly suppressed. Caspase-3 expression was significantly increased, while Bcl-2 and cyclin D1 expression was significantly decreased. PHD3 expression was significantly elevated. In MC38 cells transfected with siPHD3, the inhibitory effect of SGF on cell viability and its pro-apoptotic effect were both significantly enhanced. In summary, SGF effectively reduces lipid transfer between adipose tissue and tumors under obese conditions, regulates the AMPK/ACC signaling pathway, and targetedly inhibits tumor FAO, thereby exerting potent antitumor effects against obesity-associated CRC. - Source: PubMed
Xu Jian-QinCai Zhao-WeiPang Zi-YaoChen Wen-JingChen Jia-YanWang De-JunTu Jue - Sertoli cells (SCs) provide essential metabolic support for spermatogenesis, including lactate production for developing germ cells. While insulin's role in SC glucose metabolism is well-established, its regulation of fatty acid (FA) uptake and oxidation-critical for germ cell support and residual body clearance-remains unknown. Insulin deficiency in diabetes mellitus (DM) impairs male fertility through mechanisms that may involve disrupted SC metabolism. - Source: PubMed
Publication date: 2026/07/14
Llavanera MarcMartins Ana DSantos CarlotaBernardino Raquel LAlves Marco GOliveira Pedro F - Metabolic dysfunction-associated steatohepatitis (MASH) presents a growing global health challenge with limited therapeutic options. Rhein, an active anthraquinone derived from the traditional medicine rhubarb (), has demonstrated potential in alleviating metabolic liver disorders, yet its precise mechanism of action against MASH remains unclear. - Source: PubMed
Publication date: 2026/06/23
Song LiyanHua ShuangZeng QinFu YingqiangSui Ziqi - Oral squamous cell carcinoma (OSCC) is a biologically heterogeneous malignancy with poor clinical outcomes. Hypoxia and lipid metabolic reprogramming are important drivers of OSCC progression and treatment adaptation, and these processes are biologically interconnected. However, prognostic studies integrating hypoxia- and lipid metabolism-related features in OSCC remain limited. Here, transcriptomic data from TCGA-HNSC-OSCC were integrated with curated hypoxia- and lipid metabolism-related genes to identify candidate genes, construct a prognostic signature, and characterize its biological relevance through enrichment analysis, immune profiling, single-cell RNA-sequencing analysis, and RT-qPCR validation. A four-gene signature consisting of STC2, CAV1, ACADL, and PLA2G2D showed stable prognostic performance in the TCGA-HNSC-OSCC cohort and the external validation cohort GSE41613. The risk signature remained significantly associated with overall survival after adjustment for clinicopathological factors and retained prognostic discrimination across stage- and nodal status-defined subgroups. The high- and low-risk groups displayed distinct pathway, immune, mutational, and predicted drug sensitivity features. Notably, PLA2G2D showed the strongest association with differential immune infiltration, whereas single-cell analysis identified endothelial cells as a major CAV1-enriched population with active intercellular communication and dynamic state transitions. These findings define a hypoxia- and lipid metabolism-related prognostic signature and support its relevance to immune remodeling and endothelial cell context in OSCC. - Source: PubMed
Publication date: 2026/05/19
Zhao LiWang JialeJiang KaiyuanWang KunZhang Linglin - Aberrant epithelial remodeling, driven by a shift from ciliated to goblet cell ratio, is central to chronic nasal inflammation. Despite the known role of metabolism in normal epithelial differentiation, the specific metabolic reprogramming patterns underlying this pathological shift of nasal epithelium induced by type 2 inflammatory milieu is poorly understood. This study aimed to delineate the key metabolic pathways involved in aberrant nasal epithelial differentiation. - Source: PubMed
Publication date: 2026/04/27
Lin YutongYe XiaoyanZhong YingqianLi LiyueHuang XianxiongChen HexinMeng QingxiangGao YifangLi JianHuang JianfengLi Chunwei