SLC2A4 (Solute Carrier Family 2 Member 4)

In summary, our study demonstrated that long-term exposure to olanzapine increases circulating plasma levels of TNF-α, thus leading to increased expression of FABP4 protein in white adipose tissue and subsequently inhibiting Dhhc7expression, which correspondingly leads to reduced membrane translocation of GLUT4 and consequent insulin resistance. In conclusion, this study elucidated the signalling pathway through which olanzapine inhibits GLUT4 membrane transport via the TNF-α/FABP4/Dhhc7 axis, thus ultimately leading to insulin resistance.

Furthermore, apigenin and Salvia coccinea promote hypoglycemic effect by attenuating α-amylase activity, cholesterol levels, insulin resistance, DRP1 expression by improving GLUT4, GSK-3β, AMPK/PI3K/Nrf2, and Akt pathways. Moreover, Salvia coccinea regulates wound healing after infection, injury, or surgery, in addition to improving agricultural productivity by reducing rodent attacks.

Additionally, the tracking of miRNA-103 expression reveals that metformin (Met) could relieve the ovarian IR by modulating the IRS1/PI3K/AKT/GLUT4 signaling pathway. The LT-DP nanoprobes demonstrate clinical potential and provide a strategy to reveal the disease mechanisms.

AKG supplementation attenuated the decrease in peroxisome proliferator-activated receptor γ coactivator 1 alpha and GLUT4 protein levels in inguinal and epididymal adipose tissues in diabetic condition. In conclusion, the study findings suggested that AKG supplementation increased protein levels related to mitochondrial biogenesis and glucose transporters in adipocyte tissue accompanied with improved whole-body glucose metabolism in STZ and high-fat diet-induced diabetic mice.

It also examines the current status of the anti-oxidant and anti-inflammatory applications of silybin formulations in global liver disease treatments. However, more high-quality, detailed experimental studies are needed to explore its exact efficacy and safety so as to provide a stronger scientific basis for the widespread application of silybin in liver disease treatment.

EA can ameliorate energy metabolism disorders in T2DM rats, reduce ectopic lipid accumulation in skeletal muscle, and alleviate inflammatory responses, which may be related to the regulation of the PPAR-γ/NF-κB signaling pathway.

Human biomarker research is limited but indicates positive changes following interventions that increase UA. Future priorities include biomarker-driven, dose-finding trials stratified by metabotype, developing colon-targeted vs. systemic formulations, and testing combinations with chemotherapy and immunotherapy to determine safety and effectiveness.

Our results demonstrate that DIA-based proteomic analysis of tissue washings enables the identification of potential biomarkers for endometrial cancer (EC). Moreover, this study highlights tissue washings as a promising biological fluid for biomarker discovery in EC.

CDN inhibits GA by functionally modulating c-Myc/GLUT4/PGC-1α axis mediated glucose uptake and energy metabolism reprogramming, implicating its potential for GA chemotherapy.

EA ameliorated myocardial IR in a rat model of T2DM and positively impacted TNNT2 and BNP levels, as well as phosphorylation status and mRNA expression of several genes involved in the insulin signaling pathway. Our findings underscore the potential of EA to modulate multiple therapeutic targets in the treatment of myocardial IR. If these effects can be replicated clinically, EA may represent a promising non-pharmacological option for the management of cardiometabolic risks associated with diabetes.

This study shows that BSHT dose-dependently activates the PI3K/Akt pathway, inhibits GSDMD-mediated pyroptosis, and improves mitochondrial dysfunction in PCOS. Its regulation of inflammation, oxidative stress, metabolism, and ovarian function suggests a promising multi-target therapeutic strategy and provides insights for future clinical applications.

EV cargo mechanistically impairs insulin signaling (IRS-1 → PI3K-AKT → GLUT4) and cardiomyocyte pre-injury (loss of Δpsm, antioxidant repression, apoptosis), increasing the toxicity of doxorubicin. Should this framework be valid, it describes the clustering of sarcopenic patients with metabolic dysfunction and disproportional cardiotoxic incidents throughout cancer therapy and places circulating EV cargo as an indicator of outcomes and therapeutic interventions.