ACACA (Human) Recombinant Protein (Q01)
- Known as:
- ACACA (Human) Recombinant Protein (Q01)
- Catalog number:
- H00000031-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ACACA (Human) Recombinant Protein (Q01)
Related genes to: ACACA (Human) Recombinant Protein (Q01)
- Gene:
- ACACA NIH gene
- Name:
- acetyl-CoA carboxylase alpha
- Previous symbol:
- ACAC, ACC
- Synonyms:
- ACC1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-09-11
- Date modifiied:
- 2018-05-03
Related products to: ACACA (Human) Recombinant Protein (Q01)
Related articles to: ACACA (Human) Recombinant Protein (Q01)
- High-fat diets (HFDs) are known to disrupt gut microbiota, contributing to obesity, inflammation, and metabolic disorders. Although sucrose is a known driver of gut dysbiosis, the microbiome alterations caused by sucrose-free fish oil and sunflower oil-based HFDs remain unclear. To investigate how sucrose-free sunflower oil-based (S-HFD) and fish oil-based (F-HFD) high-fat diets influence gut microbiota composition, metabolic health, and liver inflammation in mice. C57BL/6 mice were fed either S-HFD or F-HFD for 24 weeks. Body weight, insulin sensitivity, liver inflammation, and gene expression were assessed. Gut microbiota composition was analyzed using 16S rRNA sequencing, followed by diversity analysis and taxonomic profiling with Microbiome Analyst and MIAOME tools. Despite similar body weights between groups, the gut microbiota composition differed significantly. The S-HFD group showed a higher abundance of Firmicutes (40%) compared to the F-HFD group (3%), while Verrucomicrobia were dominant in F-HFD (26%) and nearly absent in S-HFD. Taxa such as RF39, Christensenellaceae, Mogibacteriaceae, and Yaniella were enriched in S-HFD mice and associated with metabolic and immune dysregulation. S-HFD mice also had elevated fasting glucose, increased hepatic monocyte/macrophage (F4/80+) infiltration, macrovesicular steatosis, lobular inflammation, and upregulation of genes related to fatty acid oxidation (Cpt1a), monocyte chemotaxis (Ccl2), lipogenesis (Scd1, Fasn, Acaca), and glycolysis (Pklr). Conversely, F-HFD mice showed increased expression of the insulin-sensitive gene FATP1. Sucrose-free sunflower oil- and fish oil-based high-fat diets induce distinct gut microbiota changes and metabolic responses. S-HFD is associated with gut dysbiosis and steatohepatitis-like features, highlighting the importance of fat sources in shaping microbiome-host interactions in metabolic disease. - Source: PubMed
Publication date: 2026/09/11
Bahman FatemahMalik Md ZubbairKochumon ShihabNazim RasheebaAl Madhoun AshrafSindhu SardarTuomilehto JaakkoAl-Mulla FahdAhmad Rasheed - To reconnoitre the mechanism of Abietic acid (AA) in diabetes by and experiments. Using GeneCards, diabetes gene targets were obtained. The protein-protein interaction and network topology analysis were performed using the String platform and Cytoscape 3.7.2. The enrichment analysis was done by Shiny GO. The docking was by Autodeck. Diabetes was induced by injecting STZ (55 mg/kg, i.p once) in Sprague-Dawley rats. The parameters included glucose, lipids, blood pressure, ECG, OGTT, kidney and cardiac markers, liver enzymes, AMPK, Nrf2, PPAR-γ, TLR-4, oxidative markers, LVF tests, and histopathology. AA interacts with 15 important targets (PIK3CD, MAPK1, NF-κB, mTOR, STAT3, GRIN1, ITGB3, ACACA, HSP90AB1, SERPINE1, ADRB1, ULK1, TLR4, CTSD, CDK5). The signalling pathways, like insulin, MAPK1, TLR, AMPK, JAK-STAT, are associated with these proteins. In docking, the highest affinity of AA was observed for ITGB3 (- 8.1), TLR4 (- 7.8), and ACACA (- 7.3). In rats, AA(40 and 80 mg/kg) decrease hyperglycaemia and hyperinsulinemia, improves glucose tolerance, normalize blood pressure, combat dyslipidaemia (decrease triglyceride, total cholesterol, LDL, increase HDL), preserves myocytes and ventricular function (decrease troponin-I, LDH, CK-MB, LVEDP, normal ECG), hepatoprotective (decrease AST, ALT), reno-protective (decrease creatinine, urea, uric acid) and combat oxidative stress (decrease MDA, increase SOD, catalase). Nrf2, AMPK, and PPAR γ levels were increased while TLR-4 levels were decreased after AA treatment. The study is supported by the preserved histopathological architecture of pancreatic, renal, hepatic, and cardiac cells. The present study preliminarily clarifies that AA exhibits therapeutic potential in preclinical models through multitargets and multi-pathways (Nrf/TLR4/PPAR γ), which points out a new direction for further research and clinical application. - Source: PubMed
Publication date: 2026/09/24
Mishra AkashShah Hital - Most studies on l-carnitine and hepatic lipid metabolism have focused on deficiency or HFD-associated metabolic disorders, whereas its low-dose nutritional effects under standard chow-fed conditions remain unclear. In this study, standard chow-fed C57BL/6 J mice were orally administered low doses of l-carnitine for 35 days, and hepatic responses were evaluated using phenotypic, histological, metabolomic, transcriptomic, and proteomic analyses. l-carnitine supplementation reduced liver weight and hepatic lipid accumulation in a dose-associated manner, accompanied by decreased hepatocyte area and reduced H&E-based hepatocellular vacuolation. Multi-omics integration suggests attenuation of canonical fatty acid oxidation marker activation. Instead, l-carnitine treatment was associated with attenuation of lipogenesis-related signatures, including reduced xylulose-5-phosphate abundance, decreased PPP2CB protein abundance, and lower Acaca and Fasn levels, providing evidence for a potential suppression of a Xu-5P/PP2A/ChREBP-associated lipogenic signature. Concurrent remodeling of amino acid-, carbohydrate-, pyrimidine-, and ascorbate/aldarate-related pathways further indicated coordinated regulation of substrate metabolism, nucleotide metabolism, and detoxification-associated processes. Together, these findings highlight a previously underexplored nutritional dimension of l-carnitine action, showing that low-dose supplementation can reshape hepatic lipid-associated metabolic networks even under standard chow-fed, non-HFD conditions. This study extends the current understanding of l-carnitine from a classical fatty acid transport cofactor to a dietary factor involved in the network-level regulation of hepatic lipid homeostasis. - Source: PubMed
Publication date: 2026/09/10
Zhang ZhenDing BaojunZhang LiZhang LuyaoHuang Yizhong - Interleukin-1 (IL-1) signaling is a key mediator of metabolic inflammation, yet its tissue-specific contribution to obesity-associated dysfunction remains incompletely understood. Here, we investigated the effects of pharmacological IL-1 receptor antagonism on systemic metabolism, adipose tissue dysfunction, and hepatic lipid handling under distinct nutritional conditions. Male mice fed a normal diet (ND) or high-fat diet (HFD) were treated subcutaneously with the IL-1 receptor antagonist (IL-1RA) anakinra for three weeks. IL-1RA did not significantly affect body weight or global adiposity; however, under ND conditions, it reduced fat mass and circulating leptin levels and increased the adiponectin/leptin ratio, indicating improved adipose endocrine function. In adipose tissue, IL-1RA partially restored Acaca expression and selectively modulated extracellular matrix remodeling genes, including Mmp9, without broadly suppressing inflammatory markers. In the liver, triglyceride content was altered in a diet-dependent manner without changes in the expression of key metabolic genes (Fasn, Acaca, Ppara), suggesting that IL-1 blockade does not directly reprogram intrinsic hepatic lipid metabolism. Consistent with this, analyses in complementary models, including leptin-deficient mice, showed that Il1rn expression is regulated by local inflammatory and endocrine cues rather than adiposity per se. Together, these findings identify IL-1 signaling as a context-dependent modulator of adipose tissue function and systemic lipid handling. The dissociation between adipose tissue responses and hepatic triglyceride accumulation highlights the tissue-specific effects of IL-1 receptor antagonism and underscores the need for direct metabolic flux studies to define the mechanisms underlying these effects. - Source: PubMed
Publication date: 2026/09/21
Salmón-Gómez LauraCarcaño NormanCatalán VictoriaRamírez BeatrizLanza-Argueta JuliaNeira GabrielaBecerril SaraRodríguez AmaiaFrühbeck GemaGómez-Ambrosi Javier - Tourette Syndrome (TS) and Persistent Tic Disorder (PTD) are childhood-onset neuropsychiatric conditions with high heritability. Due to current sample size limitations, identifying TS/PTD risk genes has been challenging. This study addressed this issue by conducting a meta-analysis of microarray copy number variant (CNV) studies from three TS/PTD genomics consortia, supplemented with new data from 3291 cases. This approach more than doubled the sample size of previous TS/PTD CNV studies, with CNV calls generated from 5725 TS/PTD cases and 10,982 matched controls. The results confirmed that TS/PTD cases 1) have a higher burden of ultra-rare deletions overlapping loss-of-function intolerant genes (OR = 1.68, P = 9.3×10) and 2) are more likely to carry established neurodevelopmental CNVs (OR = 1.42, P = 3.9×10) compared to controls. Additionally, a novel, genome-wide significant CNV locus for TS/PTD was discovered, involving duplications at 17q12 (hg19 chr17:34.8 - 36.2 Mb). This locus is associated with a known duplication syndrome associated with variable neuropsychiatric traits, but has not been previously linked to tic disorders. Eight cases and one control carried the canonical ~1.4 Mb duplication at chr17:34.8-36.2 Mb, while one additional case had a smaller 110 kb duplication within this known CNV that included only one gene, ACACA (acetyl-CoA carboxylase, OR = 26.7, P = 5.69×10). Overall, this study provides further evidence that rare, genic CNVs play a substantial role in the genetic architecture of TS/PTD and identifies a new genome-wide significant association with this neurodevelopmental disorder. - Source: PubMed
Publication date: 2026/09/16
Halvorsen Matthew WWang ShengMiller-Fleming Tyne WYu DongmeiTopaloudi Apostoliade Schipper EllesBäckman JuliaMataix-Cols DavidRück ChristianMahjani BehrangBuxbaum Joseph DGrice Dorothy ECavallari Larisa HAngiolillo Dominick JFranchi FrancescoDavis Lea KHan LideRuderfer Douglas M Dietrich AndreaHoekstra Pieter JMattheisen ManuelPorras Luz MGiusti-Rodriguez PaolaMathews Carol APaschou PeristeraScharf Jeremiah MWillsey A JeremyCrowley James J