ATGL _ Desnutrin
- Known as:
- ATGL _ Desnutrin
- Catalog number:
- Y213643
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATGL _ Desnutrin
Related genes to: ATGL _ Desnutrin
- Gene:
- PNPLA2 NIH gene
- Name:
- patatin like phospholipase domain containing 2
- Previous symbol:
- -
- Synonyms:
- desnutrin, TTS-2.2, ATGL, FP17548, iPLA2zeta
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-06
- Date modifiied:
- 2015-11-23
Related products to: ATGL _ Desnutrin
Adipose Triglyceride Lipase (ATGL) Elisa kit RatAdipose triglyceride lipase,ATGL,Bos taurus,Bovine,Patatin-like phospholipase domain-containing protein 2,PNPLA2Adipose triglyceride lipase,ATGL,Calcium-independent phospholipase A2,Desnutrin,FP17548,Homo sapiens,Human,IPLA2-zeta,Patatin-like phospholipase domain-containing protein 2,Pigment epithelium-derivedAdipose triglyceride lipase,Atgl,Desnutrin,Mouse,Mus musculus,Patatin-like phospholipase domain-containing protein 2,Pnpla2Adipose triglyceride lipase,Atgl,Patatin-like phospholipase domain-containing protein 2,Pnpla2,Rat,Rattus norvegicusAdipose Triglyceride Lipase（ATGL）ELISA Kit PorcineAnti- ATGL pnpla2 (mouse) AntibodyAnti-ATGL(adipose triglyceride lipase)-(C-terminal) Antibodyanti-PNPLA2 / ATGL (Internal)Antibodies: ATGL _ Desnutrin HOST: Goat Clonality: pAbAntibodies: PNPLA2 _ ATGL HOST: Goat Clonality: pAbAntibodies: PNPLA2 _ Desnutrin HOST: Goat Clonality: pAbATGL pnpla2 (mouse) Immunizing PeptideATGL antibodyATGL Antibody Related articles to: ATGL _ Desnutrin
- Triglyceride (TG) deposit cardiomyovasculopathy (TGCV) was first identified in Japanese patients with homozygous mutations in PNPLA2 encoding adipose triglyceride lipase. TGs and fatty acids released by lipolytic action are major energy substrates in a normal heart. In TGCV, the defective intracellular lipolysis of long-chain TGs causes cellular steatosis and energy failure mainly in cardiomyocytes and vascular smooth muscle cells. One of the major characteristics is diffuse narrowing TG-deposited coronary atherosclerosis which is distinct from classic cholesterol-induced focal lesions. TGCV comprises primary and idiopathic subtypes with and without homozygous PNPLA2 mutations, respectively. Genetic causes or backgrounds of idiopathic TGCV (I-TGCV) remain undetermined. We established the diagnostic criteria without requirement of genetic tests, including the reduced washout rate (<10%) of iodine-123-β-methyl-p-iodophenyl-pentadecanoic acid in myocardial single-photon emission computed tomography, which reflects defective lipolysis, as an essential item. Serum TG level and body mass index are irrelevant to the diagnosis. As of October 2024, 15 primary TGCV (P-TGCV) and 976 I-TGCV cases were diagnosed across all Japanese prefectures. The cardiac symptoms of P-TGCV and I-TGCV occurred in patients aged in their 30s and 50s, respectively. The patients exhibited heart failure (HF), diffuse coronary artery disease including vasospastic angina, and ventricular arrhythmia. The prognosis was very severe in patients with P-TGCV manifesting HF with reduced ejection fraction unless receiving cardiac transplantation. In I-TGCV, the 5-year-overall and cardiovascular event-free survival rates were 71.8% and 54.0%, respectively, with standard remedies. Tricaprin/trisdecanoin, a medium-chain TG that facilitates myocardial lipolysis, is being developed as a first-in-class orphan drug for TGCV. TGCV is a novel class of adult-onset cardiovascular disease caused by the defective lipolysis of long-chain TGs. Many patients with TGCV exhibiting high cardiovascular risk remain undiagnosed; thus, increased awareness of this emerging disease is required among cardiologists of all subspecialties. - Source: PubMed
Publication date: 2026/04/13
Mori TatsuyaHirano Ken-IchiMiyauchi HideyukiIkeda YoshihikoHigashi MasahiroNakano YusukeKanda TakahiroNagasawa YasuyukiInaba TohruOkumura TakahiroZaima NobuhiroKobayashi KunihisaMatsumoto NaoyaYamada TomomiAmano TetsuyaFujimoto Shinichiro - Bone formation requires a substantial energy supply to sustain extracellular matrix production and mineralization, yet the temporal contribution of lipid metabolism during osteoblast maturation remains incompletely characterized. This study investigated the molecular and transcriptional remodeling of lipid metabolism. Intracellular lipid distribution was analyzed by confocal microscopy using Nile Red staining. Transcriptional modulation of lipid synthesis, storage, lipolysis, genes associated with mitochondrial fatty acid oxidation, and osteogenic markers were assessed by quantitative real-time PCR, and the biochemical composition was evaluated by Raman spectroscopy. Early stages of spheroid development showed higher expression of genes involved in lipid synthesis and storage (FASN, DGAT2, and PLIN2) together with intracellular lipid accumulation, whereas later stages displayed increased expression of lipolytic and β-oxidation markers (PNPLA2/ATGL, CPT1A, and HADHA), accompanied by the redistribution of lipid droplets. The Raman analysis revealed a time-dependent variation of lipid-associated CH/CH bands and modulation of protein-related Amide I-III signals, consistent with biochemical remodeling during maturation. Overall, the data indicate a coordinated transcriptional shift from lipid accumulation-associated pathways toward lipid mobilization during osteogenic progression in a 3D culture. This model provides a controlled experimental platform for investigating metabolic regulation during bone formation and for studying metabolic alterations associated with skeletal disorders. - Source: PubMed
Publication date: 2026/04/07
Rizzo Maria GiovannaMorganti DarioSciuto Emanuele LuigiSmeriglio AntonellaCannatà GiorgiaFazio BarbaraGuglielmino Salvatore P PTrombetta DomenicoFaggio CaterinaConoci Sabrina - Beef flavor is a trait difficult to evaluate since different senses (taste, touch, and smell) are involved in its perception. In the last 20 years, 102 Quantitative Trait Loci (QTLs), associated with the variability of different beef flavor notes, have been reported. These QTLs are spread on all chromosomes, including BTA X. In these QTL regions, 2509 genes are located and, among them, 594 are involved in the metabolic processes of lipids, proteins, and carbohydrates, the main meat components for the production of volatile substances responsible for flavor. Only 19 of these genes (, , , , , , , , , , , , , , , , , , and ) are also present in the QTL regions affecting pork flavor. The applied approach allowed us to strongly restrict the number of candidate genes to affect the variability of both beef and pork flavor. - Source: PubMed
Publication date: 2026/03/25
Rando AndreaGrassi GiuliaPerna Anna MariaDi Gregorio Paola - Up to a third of the global population is afflicted by metabolic dysfunction-associated steatotic liver disease with excessive triglyceride accumulation in the liver. Prolonged fasting rapidly causes hepatic steatosis via excessive influx of free fatty acids from adipose tissue. However, it is unclear whether skeletal muscle is involved in the etiology of hepatic steatosis during starvation. Here, we demonstrate a critical connection between the liver and skeletal muscle via FoxO transcription factors. During prolonged fasting, hepatic steatosis was exacerbated in skeletal muscle-specific FoxO-deficient mice (mFoxO1,3,4) despite preventing skeletal muscle wasting, suggesting that skeletal muscle FoxOs prevent hepatic steatosis during energy deprivation. FoxO deficiency in skeletal muscle weakened fatty acid oxidation and induced abnormal glycogen accumulation in skeletal muscle during fasting. Mechanistically, the starvation-induced transcriptional regulation of triglyceride lipase was attenuated in skeletal muscle of FoxO-deficient mice. Conversely, skeletal muscle-specific FOXO1 overexpression was sufficient to increase triglyceride lipase in vivo and protected the liver from Western diet-induced metabolic dysfunction-associated steatohepatitis-like phenotype. Taken together, our results demonstrate the physiological importance of skeletal muscle FoxO signaling on the liver pathophysiology. - Source: PubMed
Publication date: 2026/04/08
Oyabu MamoruSakaue ManatoKubo AtsushiYoshioka KiyoshiKawaguchi RunaYamamoto HarukiKinjo YuzukaKwon JunginNishi HirokiYamanaka DaisukeSato TomokiMori DaikiEguchi TakahiroIto NaokiFukada So-IchiroSuganami TakayoshiMiura ShinjiOno YusukeHakuno FumihikoTakahashi Shin-IchiroGoto TsuyoshiKamei Yasutomi - Cell senescence, a state of cell cycle arrest induced by intrinsic or extrinsic stress, is linked to aging and aging-associated diseases. Senescence markers are elevated in adipose tissue with age and in obesity. Recently, it was shown that human mature adipocytes can undergo senescence in response to hyperinsulinemia. However, the functional consequences of adipocyte cell senescence remain poorly understood. - Source: PubMed
Publication date: 2026/03/17
Alexandersson IdaPalmgren HenrikUhrbom MartinOscarsson JanBoucher Jeremie