Human SLC2A4 regulator(SLC2A4RG) ELISA kit
- Known as:
- Human SLC2A4 regulator(SLC2A4RG) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- CSB-EL021558HU
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Cusabio
- Gene target:
- Human SLC2A4 regulator(SLC2A4RG) ELISA kit
Related genes to: Human SLC2A4 regulator(SLC2A4RG) ELISA kit
- 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: Human SLC2A4 regulator(SLC2A4RG) ELISA kit
Related articles to: Human SLC2A4 regulator(SLC2A4RG) ELISA kit
- Antipsychotic-associated metabolic toxicity remains one of the most persistent clinical problems in psychopharmacology. Clozapine and olanzapine are especially effective for psychosis but carry high liability for weight gain, dyslipidemia, insulin resistance, and type 2 diabetes. Current monitoring recommendations recognize this risk, yet they remain largely uniform across patients and do not incorporate ancestry-specific genetic risk or mechanistic drug-gene information. We performed a transcriptome-wide association study-informed drug-gene prioritization analysis to examine whether approved antipsychotic target genes overlap with genes whose genetically predicted expression is associated with type 2 diabetes. The analysis used ancestry-specific type 2 diabetes transcriptome-wide association study (TWAS) results derived from a multi-ancestry genome-wide association study (GWAS) and approved antipsychotic drug-gene interactions from the Drug-Gene Interaction Database (DGIdb). For each drug, target genes were matched to TWAS genes across six metabolic tissues, and a weighted risk score was calculated as the sum of the absolute TWAS z-score multiplied by the drug-gene interaction score for significant targets. Follow-up analyses decomposed signals into targets with positive and negative TWAS directions, operationally interpreted as aggravating and compensatory, while also examining curated metabolic axis genes including GLP1R, GIPR, PPARG, and SLC2A4. The analysis identified recurrent exploratory target-overlap signals for clozapine and olanzapine. Clozapine showed the most consistent cross-ancestry aggravating profile, with recurrent target overlap involving GLP1R and immune-related genes. Olanzapine showed strong mechanistic-axis overlap involving GLP1R, GIPR, and PPARG, although its simple TWAS directionality was often classified as compensatory. Trifluoperazine emerged as a notable candidate, with significant target enrichment in the European ancestry analysis and top ranking in the Hispanic analysis. Fluspirilene also met the combined enrichment false discovery rate threshold in the European ancestry analysis, although its clinical metabolic interpretation was less direct. Haloperidol decanoate showed a high burden driven partly by SLC2A4, but its directionality was frequently mixed or compensatory. These findings nominate the incretin axis as a plausible translational bridge between antipsychotic metabolic liability and existing interventions such as GLP-1 receptor agonists. They also identify a key methodological gap. Future models must incorporate the pharmacologic mode of action to distinguish receptor blockade from activation. Except for the enrichment-positive European ancestry findings for trifluoperazine and fluspirilene, the results are exploratory prioritization signals and do not establish drug-specific metabolic effects, causal mechanisms, or ancestry-specific treatment effects. Overall, this TWAS-informed analysis provides a hypothesis-generating framework for ancestry-aware metabolic monitoring and targeted validation studies. - Source: PubMed
Publication date: 2026/07/16
Cheung Ngo - The serine/threonine kinase AKT is a key regulator of glucose and energy metabolism. Prevailing dogma suggests that AKT is an obligate intermediate for glucose uptake in all metabolic tissues and that impaired AKT signalling is a major molecular driver of insulin resistance in obesity. However, whether AKT is universally required for insulin-stimulated glucose uptake across tissues in vivo has remained unresolved. - Source: PubMed
Jaiswal NatashaGavin MatthewLantier LouiseOng Olivia Yu YuWasserman David HTitchenell Paul M - Fat deposition plays an important role in yak metabolism, reproduction, and meat quality, and male yaks are often castrated to facilitate management and improve production performance. The effect of castration on the characteristics of fat deposition in male yaks and the molecular mechanisms of action was explored in this study. The subcutaneous fat thickness in castrated and common male yaks was measured, further the content of fatty acids in yak subcutaneous fat was detected using gas chromatography-mass spectrometer (GC-MS); the transcriptome, metabolome in the yak subcutaneous fat were detected using mRNA-Sequencing, ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS), respectively; the integrative analyses of differentially expressed genes (DEGs), different metabolites (DMs), fatty acids and fat thickness were carried out. The results showed that castration can strengthen the ability of fat deposition and improve the content of fatty acids, especially PUFAs, in male yaks, and both transcriptome and metabolome were significantly different between castrated male yaks and common male yaks. The effect of castration on the male yak fat deposition was closely related to the PPAR signaling pathway, citrate cycle, and insulin resistance. Data suggests that , , , , , , , and may be the crucial control genes for the fat amount in yaks, and that , , and may be the crucial control genes for the polyunsaturated fatty acids (PUFAs) content in yak adipose tissue. Further functional studies will be conducted to determine the specific role of each gene in regulating fat deposition and fatty acid composition in yaks. - Source: PubMed
Publication date: 2026/06/12
Xiong LinPei JieGe QianyunDing ZhiqiangKang YandongChen ChaoWei RuichaoGuo Xian - Imeglimin, a novel oral antidiabetic agent derived from metformin, improves insulin secretion and sensitivity in patients with type 2 diabetes. Recent clinical clamp studies have identified adipose tissue as a potential target of imeglimin; however, its direct effects on adipocytes are unclear. In this study, differentiated 3T3-L1 adipocytes were treated with imeglimin or metformin. We then examined glucose concentration in the culture medium, glucose uptake, plasma membrane glucose transporter expression, and the effects of signaling inhibitors. Imeglimin enhanced glucose uptake in a dose-dependent manner and reduced glucose concentration in the culture medium. Imeglimin was more effective than metformin at equivalent concentrations. Imeglimin also exerted an additive effect in the presence of insulin. Plasma membrane fractionation and immunoblotting revealed that imeglimin increased cell-surface glucose transporter (GLUT) 4 expression selectively, without altering total GLUT4 protein or plasma membrane GLUT1 levels. This suggests that increased GLUT4 translocation contributes to enhanced glucose uptake. Further, pharmacological inhibition studies demonstrated that imeglimin-induced glucose uptake was unaffected by AMPK inhibition but attenuated by inhibition of phosphoinositide 3-kinase, Akt, or protein kinase C. Additionally, the PI3K inhibitor Ly294002 suppressed imeglimin-induced GLUT4 accumulation at the plasma membrane. These findings identify adipocytes as a relevant cellular target of imeglimin and support, at least in part, the involvement of PI3K-dependent GLUT4 regulation in facilitating glucose transport, which may contribute to favorable effects of imeglimin on adipose tissue glucose metabolism in vivo. - Source: PubMed
Publication date: 2026/06/23
Takahashi NobuhikoKimura Atsushi PYoshizaki TakayukiOhmura Kazumasa - Insulin resistance is a key pathological feature of metabolic disorders, closely associated with impaired insulin signaling and reduced GLUT4-mediated glucose uptake in adipose tissue. Luteolin, a flavonoid from Lonicera japonica Thunb., has been reported to exhibit various metabolic regulatory effects, but its direct role in restoring GLUT4-dependent glucose uptake under insulin-resistant conditions remains insufficiently elucidated. This study aimed to investigate whether luteolin restores GLUT4-mediated glucose uptake and to elucidate the underlying PI3K/Akt-dependent mechanism in obesity-related insulin resistance. Network pharmacology and molecular docking analyses identified luteolin as a candidate compound targeting insulin resistance pathways. Differentiated 3T3-L1 adipocytes and high-fat diet-induced insulin-resistant mouse models were used and glucose uptake, insulin signaling protein phosphorylation and GLUT4 translocation were analyzed by biochemical assays, Western blotting, immunofluorescence and flow cytometry. Network analysis revealed strong associations between L. japonica-related targets and insulin resistance pathways, including PI3K/Akt signaling. In vitro and in vivo experiments demonstrated that luteolin enhanced glucose uptake and promoted GLUT4 translocation to the plasma membrane in 3T3-L1 adipocytes, accompanied by increased phosphorylation of IRS, PI3K, Akt and AS160. These effects were abolished by wortmannin, which suppressed both GLUT4 translocation and glucose uptake, indicating a PI3K-dependent mechanism. In addition, luteolin improved metabolic parameters and restored insulin signaling under insulin-resistant conditions in vivo. Collectively, these findings suggest that luteolin from L. japonica improves insulin signaling associated with GLUT4-mediated glucose uptake through a PI3K/Akt-dependent mechanism. - Source: PubMed
Publication date: 2026/06/13
Park JieunChoi You YeonChoi Yong JunHa In JinYang Woong Mo