ACACa ELISA kit
- Known as:
- ACACa Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ACACa-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ACACa ELISA kit
Related genes to: ACACa ELISA kit
- 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
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- Obesity and associated metabolic disorders remain major public health challenges worldwide. The regulation of lipid synthesis represents a promising therapeutic target, yet the precise mechanisms remain elusive. - Source: PubMed
Publication date: 2026/05/07
Fu HuaLi YuqinLi PengzhouZhu LiyongZhu ShaihongWang Guohui - The anticipated increase in the global population and dyslipidemia will need available food resources, such as edible insects, to meet nutritional and pharmaceutical merits. Among edible insects, Locusta migratoria (namely, migratory locust) (ML), which contains n-3 fatty acids capable of binding to multiple lipids, phytosterols, and dietary fiber chitin, are expected to be a therapeutic resource for ameliorating dyslipidemia as well as an alternative protein resource. We hypothesized that the ML supplementation represented the beneficial effect on lipid metabolism in the plasma and liver of male rats with dyslipidemia induced by an AIN-93G based diet containing a low level of orotic acid (OA) (0.6 % in diet) for two weeks. The 0.6 % OA treatment, which was determined in a preliminary study on loading dosage suitable for evaluating food ingredients, did not affect the growth and severe lipid accumulation, but induced liver hypertrophy with low-moderate hematological observations and hypertriglyceridemia. The ML supplementation led to a reduction in plasma triacylglycerol levels in OA-treated rats, particularly in the chylomicron, very-low-density lipoprotein, and low-density lipoprotein (LDL), particularly small-dense LDL, fractions. In the liver, the ML supplementation also significantly or slightly reduced mRNA expression related to lipogenesis and LDL uptake genes, including Srebf2, Ldlr, Psck9, Hmgcr, Acaca, and Scd1. Moreover, the ratios of n-3 fatty acids, such as α-linolenic and docosapentanoic acids, were increased in the liver and the indices representing fatty acid desaturation in the plasma were suppressed following the ML supplementation. These results have agreed with our hypothesis that the ML supplementation ameliorates lipid metabolism by modulating hepatic lipogenesis, fatty acid metabolism, and LDL receptor function in OA-treated rats. Therefore, ML can serve as a functional and alternative food resource for ameliorating hypertriglyceridemia. - Source: PubMed
Ochiai MasaruYoshida TsugumiNagasao Jun - Diabetic kidney disease (DKD) remains a leading cause of end-stage renal disease despite advances in glucose-, blood pressure-, and albuminuria-lowering therapies. The glucose-responsive transcription factor carbohydrate response element-binding protein (ChREBP; encoded by ) regulates glycolytic-lipogenic programs, yet its causal contribution to renal injury is challenging to disentangle in advanced DKD, where bulk kidney transcriptomes reflect tissue remodeling and cellular compositional shifts. - Source: PubMed
Publication date: 2026/04/15
Liu MingliangChen ShihangWu ShiSun BeiChen Liming - Endothelial dysfunction is an early event in atherosclerosis development and is centrally linked with insufficient endothelial NO production. However, chronically increased NO levels, including NO from other cellular sources, may induce endothelial dysfunction. Here, we studied how chronically elevated NO production from erythrocytes, achieved by genetic deletion of ARG1 (arginase-1), impacts smooth muscle cell (SMC) lipid accumulation and atherosclerosis progression. - Source: PubMed
Publication date: 2026/05/01
Sun BeichenGogiraju RajinikanthGreulich FranziskaKumi FrankGhasemi ImanBochenek Magdalena LPagel Svenvan der Vorst Emiel P CKhuu My PhungMoiko KaterynaRenner LuisaGuliani PayalRuf WolframPorubsky StefanReinhardt ChristophFleming IngridBindila LauraLurz PhilippSchäfer Katrin - Gestational diabetes mellitus (GDM) exposes the fetus to chronic hyperglycemia and increases the risk of later metabolic disease. The mechanisms by which early hyperglycemia reprograms lipid and glucose metabolism remain unclear, largely due to maternal and placental confounders in mammalian models. To overcome these limitations, we developed a zebrafish model that isolates fetal hyperglycemia and enables direct investigation of its developmental and long-term metabolic effects. To mimic late-onset GDM, zebrafish embryos were exposed at 4 days post-fertilization to glucose concentrations comparable to those reported in umbilical cord blood from poorly controlled diabetic pregnancies. Developmental, metabolic, and molecular outcomes were assessed across the life course, including lipid accumulation, adipocyte differentiation, and expression of genes regulating lipogenesis and insulin signaling. To determine the role of acetyl-CoA carboxylase (ACC), embryos were exposed to hyperglycemia in the presence of an ACC inhibitor. Transient embryonic hyperglycemia induced persistent activation of de novo lipogenesis, increased adipocyte formation, and sustained upregulation of lipid storage pathways. These effects persisted into adulthood and were accompanied by hepatic lipid accumulation and insulin resistance. Hyperglycemic exposure reprogrammed key metabolic regulators (acaca, fasn, insr) and reduced phosphorylated AKT, indicating a stable shift toward lipogenic and insulin-desensitized states. Inhibition of ACC during glucose exposure prevented these long-term metabolic alterations. Transient fetal hyperglycemia, independent of maternal or placental influences, durably reprograms lipid metabolism and insulin responsiveness, providing direct evidence that early hyperglycemic exposure promotes lifelong susceptibility to metabolic disease. - Source: PubMed
Publication date: 2026/04/29
Konadu BridgetLogan Madelyn KCox Carol KEdwards Kristin SSpeed Joshua SGibert Yann