ACACA
- Known as:
- ACACA
- Catalog number:
- 000972A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACACA
Related genes to: ACACA
- 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
Related articles to: ACACA
- 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 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 - The Min pig, a representative northern Chinese indigenous breed, carries a unique ancestral background shaped by the historical phylogeography of Northeast Asia. This study aimed to dissect the population structure, temporal genetic divergence, and ancestral composition of Min pigs, trace their evolutionary origin, and identify trait-linked functional genes, providing information regarding their evolutionary history and conservation. We analyzed 61 Min pigs sampled across nearly 20 years and 701 reference pigs comprising other Chinese indigenous breeds, Western commercial lines, and Chinese wild boars, using PCA, NJ phylogenetic analysis, Admixture, TreeMix, D-statistic, f4-ratio, and combined selection signature scans (sliding-window F, XP-EHH, and π-ratio). Clear genetic stratification was observed among Min pig subpopulations, reflecting long-term divergence under natural and artificial selection. PCA and Admixture (K = 2-4) separated East Asian indigenous and Western ancestral components, verifying an admixed Northeast Asian origin with a dominant ancient East Asian component and a Western component. Compared with early-2000s Min pigs, contemporary individuals are genetically closer to Western breeds and exhibit a more scattered structure due to shifted ancestral component proportions, further confirmed by D-statistic and f4-ratio values. We identified 321 differentiated SNP loci based on the Animal QTL database, corresponding to core candidate genes (AKT3, ACACA, MAP3K5, FGFR4, C3, and SERPINC1) enriched for meat quality, growth, reproduction, immunity, energy metabolism, and MAPK/PI3K-Akt/AMPK pathways. This study reveals Min pigs' admixed origin and temporal divergence, clarifying their Northeast Asian evolution and providing molecular markers for genetic monitoring and conservation. - Source: PubMed
Jin LongDong FengyiFeng ChengyueNing JiayiZhang XiaoranLiu WuyangChen ChangyiWang DaliBie LuyaoBai ChunyanSun HaoSun Boxing - Endometriosis (EMs) is one of the most common gynecologic diseases, and the roles of ferroptosis in EMs have not been fully clarified. The induction of ferroptosis has been demonstrated to inhibit the growth of ectopic lesions in EMs. Although acetyl-CoA carboxylase 1 (ACC1), the rate-limiting enzyme for fatty acid biosynthesis, has been shown to regulate ferroptosis, the detailed mechanism involved has not been fully elucidated. In addition, the role of ACC1, encoded by ACACA, in EMs remains unclear. Thus, the present study aimed to explore the role of ACC1 in ferroptosis and the potential therapeutic effect of the ferroptosis inducer the ferroptosis inducer 56 (FIN56) in EMs. - Source: PubMed
Publication date: 2026/06/29
Zeng ChengZhu JingwenLu RuihuiWu PeiliLi XinLi FangyuanPeng ChaoZhou YingfangXue Qing