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
- 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 - Identifying physiological changes during the transition period is essential for improving the health and productivity of dairy goats. This study evaluated hematological, biochemical, hormonal, oxidative stress, and molecular alterations in Shami goats during the pre-pregnancy, late pregnancy, and early lactation periods. Eighty clinically healthy goats were examined, and blood samples were analyzed for hematological indices, metabolic and hormonal profiles, oxidative stress biomarkers, and relative expression of genes associated with energy metabolism, antioxidant defense, inflammation, and autophagy. Late pregnancy was characterized by significant ( < 0.05) increases in red blood cell count (RBCs), hemoglobin concentration (Hb), neutrophils, albumin, globulin, urea, insulin-like growth factor-1 (IGF-I), and malondialdehyde (MDA), accompanied by decreased glucose, cholesterol, total protein (TP), antioxidant markers, total leukocyte count, packed cell volume, and monocytes. Early lactation was associated with higher non-esterified fatty acid, triiodothyronine (T3), and thyroxine (T4) levels. Genes involved in lipid mobilization and oxidation, ketogenesis, inflammation, cellular stress, and autophagy; , , , , , , , , , , , , , and were significantly upregulated, whereas antioxidant- and glucose transport-related genes , , , , and were downregulated during the transition period. The results indicate well-orchestrated metabolic and molecular adaptations that can be employed as biological indicators to track the physiological status of Shami goats. These findings fulfilled the study objective and identified potential biomarkers of the transition period in Shami goats. - Source: PubMed
Publication date: 2026/08/04
Alqhtani Haifa AliAl-Hazani Tahani M ISayed Ahmed ElAteya AhmedGhonaim Ahmed HZarah Rowa KSafhi Fatmah AAlmubarak AdelBabiker HusseinElkhidr Rasha YassinEl-Deeb Wael MKhalid Ahmed MagzoubAlkuwayti Mayyadah AbdullahMarzok Mohamed - Renal cell carcinoma (RCC) is the most common malignancy of the urinary system, characterized by high incidence, mortality, and resistance to therapy. Its molecular heterogeneity presents challenges for effective precision treatment. RCC is highly heterogeneous, yet treatment guidelines rely predominantly on kidney renal clear cell carcinoma (KIRC) studies, neglecting other molecular subtypes, which limits therapy personalization for non-KIRC patients. This study aimed to explore the role of small ubiquitin-like modifier (SUMOylation)-associated genes in the progression and prognosis of RCC and its subtypes. We identified 298 SUMOylation-associated differentially expressed genes (DEGs), including 151 RCC-specific genes after excluding expression changes attributable to RCC subtype-specific variation. Ten core genes (, , , , , , , , , and ) were identified, with expression not only discriminates tumor from normal tissue but also separates KIRC from KICH/KIRP, proposing as a potential second-step biomarker for KIRC identification on top of traditional histology. Inter-subtype RCC heterogeneity represented a key factor limiting predictive performance of the six prognostic signature genes (, , , , and ). Its 5-year AUC exceeded 0.7 for every individual RCC subtype in the TCGA training cohort, with pooled 5-year AUCs of 0.61 (TCGA training cohort) and 0.67 (independent PCAWG validation cohort). The prognostic risk model demonstrated strong predictive performance, with a C-index of 0.791 before calibration and 0.774 after calibration. Importantly, the C-index remained above 0.75 throughout the 60-month follow-up period, indicating stable and robust long-term prognostic accuracy. High-risk patients exhibited greater immune cell infiltration, indicating potential for immunotherapy. Following secondary screening, three RCC cell lines (BFTC909, CAKI1, and CAL54) and five target genes (, , , and ) were identified as optimal candidates for subsequent mechanistic investigations. This study uncovers the prognostic and functional relevance of SUMOylation in RCC and offers a novel framework for biomarker development, therapeutic targeting, and immunotherapeutic stratification. - Source: PubMed
Publication date: 2026/07/23
Zhang XiaoboLi ZhimingLin RuoxinYang SupingSun XiaohuiChen Shicheng - This research aimed to elucidate the potential therapeutic efficacy of evodiamine (Evo) in alleviating IR associated with T2DM, and to further explain its underlying mechanism. The candidate bioactive components and targets of EVO were identified by using biomedical databases. Targets associated with IR were acquired from various databases. Intersectional analysis of Evo-related and IR-specific targets facilitated the construction of a PPI network. Cytoscape software was employed for the visualization of the "compound-target-disease" interactions, enabling the identification of key proteins. GO and KEGG analyses were then carried out to clarify the biological roles of the core Evo targets. MD analysis further confirmed the interactions between Evo and these key proteins. Additionally, the CCK-8 assay evaluated the influence of Evo on cell viability. The effects of Evo on glucose uptake and release were quantified, while Western blotting (WB) was employed to identify changes in protein expression driving the IRS-1/PI3K/AKT/GLUT4 signaling pathway. Furthermore, immunofluorescence techniques were implemented to visualize and quantify the expression levels of IRS-1, phosphorylated IRS-1 (p-IRS-1), and GLUT4 in insulin-resistant HepG2 cells. A total of 122 Evo-associated targets were obtained, among which 37 intersected with IR-related targets. Notably, AKT1, STAT3, SRC, and PTGS2 were identified as crucial proteins within this network. KEGG pathway analysis revealed enrichment of 126 significant pathways, among which the PI3K/AKT signaling pathway was particularly critical in mediating the therapeutic effects of Evo on IR. HepG2 cells in the model group showed lower glucose consumption and higher glucose production than controls, whereas Evo administration enhanced glucose consumption and reduced glucose production. Using metformin as a positive control, statistically significant differences in glucose consumption and production were found between HepG2 cells treated with Evo and metformin. Additionally, the model group exhibited significantly lower p-AKT and p-PI3K expression versus controls. In IR-HepG2 cells, Evo treatment dose-dependently restored diminished p-AKT and p-PI3K levels, mirroring metformin's action. Relative to controls, the model group exhibited elevated p-IRS-1, which was downregulated by Evo in IR-HepG2 cells; metformin, however, failed to reduce p-IRS-1 significantly. The results of our study indicate that Evo's ability to function as a therapy for IR might be linked to its role in modulating the IRS-1/PI3K/AKT signaling pathway and increasing the GLUT4 expression. - Source: PubMed
Publication date: 2026/08/24
Wang XinZhang NaWang MingshanLiu JiayiTong LeLiang XurongLi AilinGu YumingSong BailinXie XinxingChen Jiamei