GLUT4 _ SLC2A4
- Known as:
- GLUT4 _ SLC2A4
- Catalog number:
- BM436
- Product Quantity:
- 0.2 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GLUT4 _ SLC2A4
Related genes to: GLUT4 _ SLC2A4
- Gene:
- SLC2A4 NIH gene
- Name:
- solute carrier family 2 member 4
- Previous symbol:
- GLUT4
- Synonyms:
- -
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-06
- Date modifiied:
- 2016-10-05
Related products to: GLUT4 _ SLC2A4
Related articles to: GLUT4 _ SLC2A4
- Maternal immune activation induced by lipopolysaccharide (LPS) exposure is a critical factor in the pathogenesis of cerebral palsy (CP). This early inflammatory response predisposes the postnatal brain to hypoxic injury and metabolic dysregulation. Although hypoxic injury and metabolic dysregulation are well characterized individually, their interplay in CP and the potential role of metabolic modulators remain poorly understood. - Source: PubMed
Publication date: 2026/09/30
Silva-Araújo Eulália RebecaManhães-de-Castro RaulDos Santos Júnior Osmar HenriqueDos Santos Júnior Joaci PereiraAntônio Da Silva Araújo MarcosJosé Cavalcanti Bezerra Gouveia HenriqueDe Oliveira Rodrigues ThyagoGeneilson Silva JoséJimenez-Chillaron Josep CPadrón-Hernández EduardoToscano Ana Elisa - Insulin resistance, metabolic dysfunction, inflammation, and vascular impairment characterize Type 2 Diabetes Mellitus (T2DM). Mesenchymal stem cells (MSCs) have shown promise in preclinical studies. However, their variable efficacy in human settings warrants strategies to enhance their therapeutic potency. This study evaluates preconditioning of human umbilical cord-derived MSCs (UCMSCs) with diabetic microenvironment (serum) to improve T2DM therapeutic outcomes. - Source: PubMed
Publication date: 2026/09/19
Mante NishantUndale VaishaliSanap AvinashBhonde RameshSuryawanshi Poonam - Glucose is the primary energy substrate for the developing foetus, and placental glucose transport is a key element of pregnancy physiology. In early gestational diabetes mellitus, metabolic alterations may disrupt the expression of glucose transporters (GLUTs). This study evaluated the influence of physical activity, monitored using pedometers, on the expression of the SLC2A1 (GLUT-1), SLC2A3 (GLUT-3), and SLC2A4 (GLUT-4) genes in the placentas of women with early gestational diabetes, and analysed associations between GLUT expression and clinical parameters. - Source: PubMed
Publication date: 2026/09/21
Sochacki MateuszSibiak RafalMantaj UrszulaAdamczak LukaszBlatkiewicz MalgorzataRucinski MarcinWender-Ozegowska Ewa - Diacylglycerol acyltransferase 2 (DGAT2) codes an enzyme which synthesize triglyceride by esterifying fatty acid to last portion of diacylglycerol backbone, and contributes to intramyocellular lipid metabolism. Small interfering RNA (siRNA)-mediated knockdown of was previously shown to reduce AKT phosphorylation and glucose uptake, decrease fatty acid partitioning into triglycerides, and increase free fatty acid release and oxidation in skeletal muscle cells. The current study aimed to determine whether knockdown affects lipid and glucose metabolism in glycolytic muscle (GM) and oxidative muscle (OM) under high-fat diet conditions, consistent with our previous findings. Male C57BL/6J mice were fed high-fat diet, and treated with or control-siRNA, and the effects were compared in different muscle types. Muscle suppression reduced intramuscular triglyceride content by up to 38.2% whereas increased circulating triglyceride levels. In addition, decreased mRNA levels supported a reduction in lipid esterification capacity. suppression increased the integration of C14-tagged fatty acids into acid-soluble metabolites, and altered gene expressions related to glucose utilization; GLUT4 protein were decreased and mRNA increased in both GM and OM fibers. GM exhibited decreased AKT phosphorylation about 50%, whereas OM showed no change in AKT phosphorylation. Noticeably OM exhibited reduced and glycogen accumulation. Together, these findings suggest that muscle inhibition redirects fatty acid channeling from triglyceride storage toward oxidation , with accompanying changes in glucose metabolism-related markers. These results extend our previous cell-based findings to a more physiologically relevant setting, while highlighting distinct response patterns in GM and OM. - Source: PubMed
Publication date: 2026/09/02
Jiyun YeoPark Ju YoungKwon Min GyeongKim Eun SeongOh Rae HyeonSeo Byoung BooBu So Young - Regulation of skeletal muscle glucose uptake is an effective strategy for reducing postprandial hyperglycemia and improving whole-body glucose homeostasis in the management of type 2 diabetes. The present study investigated that cardamom enhances glucose uptake in skeletal muscle in vitro and improves glucose tolerance in vivo. Bioactivity-guided fractionation of cardamom identified an ethyl acetate fraction (Fr. A) and its subfraction (Fr. A-i) as potent stimulators of glucose uptake in L6 myotubes. Both fractions significantly promoted glucose uptake by enhancing glucose transporter type 4 (GLUT4) translocation to the plasma membrane. Mechanistic investigations revealed activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, accompanied by increased phosphorylation of Akt substrate of 160 kDa (AS160), a key regulator of GLUT4 vesicle trafficking, while no significant changes were observed in insulin receptor substrate-1 (IRS-1) or AMP-activated protein kinase (AMPK) phosphorylation. Fr. A induced a more pronounced effect on AS160 phosphorylation and was therefore selected for further evaluation. The antihyperglycemic potential of Fr. A was assessed in ICR mice using an oral glucose tolerance test. Oral administration of Fr. A (1 and 10 mg/kg body weight) significantly improved glucose tolerance and alleviated postprandial hyperglycemia. Cardamom in skeletal muscle and highlights its potential as a natural therapeutic candidate for the management of postprandial hyperglycemia. - Source: PubMed
Fang LiyuanHironao Ken-YuAshida HitoshiYamashita Yoko