Zinc‐α2‐glycoprotein relieved seizure‐Induced neuronal glucose uptake impairment via insulin‐like growth factor 1 receptor‐regulated glucose transporter 3 expression

Peng, Wuxue; Liu, Xi; Tan, Chong-Tin; Zhou, Wen; Jiang, Jin; Du, Juncong; Mo, Lijuan; Chen, Lifen

doi:10.1111/jnc.15254

Cited by 5 publications

(2 citation statements)

References 57 publications

(97 reference statements)

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“…GC10289, Glpbio), a glucose uptake assay was performed as described previously. 14 2‐NBDG solution was diluted to 100 μM with glucose‐free neurobasal. Cells were seeded in plates.…”

Section: Methodsmentioning

confidence: 99%

GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat

Guo,

Qi,

Luo

et al. 2024

CNS Neurosci Ther

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AimGlucose‐dependent insulinotropic polypeptide (GIP) is a ligand of glucose‐dependent insulinotropic polypeptide receptor (GIPR) that plays an important role in the digestive system. In recent years, GIP has been regarded as a hormone‐like peptide to regulate the local metabolic environment. In this study, we investigated the antioxidant role of GIP on the neuron and explored the possible mechanism.MethodsCell counting Kit‐8 (CCK‐8) was used to measure cell survival. TdT‐mediated dUTP Nick‐End Labeling (TUNEL) was used to detect apoptosis in vitro and in vivo. Reactive oxygen species (ROS) levels were probed with 2', 7'‐Dichloro dihydrofluorescein diacetate (DCFH‐DA), and glucose intake was detected with 2‐NBDG. Immunofluorescence staining and western blot were used to evaluate the protein level in cells and tissues. Hematoxylin‐eosin (HE) staining, immunofluorescence staining and tract‐tracing were used to observe the morphology of the injured spinal cord. Basso‐Beattie‐Bresnahan (BBB) assay was used to evaluate functional recovery after spinal cord injury.ResultsGIP reduced the ROS level and protected cells from apoptosis in cultured neurons and injured spinal cord. GIP facilitated wound healing and functional recovery of the injured spinal cord. GIP significantly improved the glucose uptake of cultured neurons. Meanwhile, inhibition of glucose uptake significantly attenuated the antioxidant effect of GIP. GIP increased glucose transporter 3 (GLUT3) expression via up‐regulating the level of hypoxia‐inducible factor 1α (HIF‐1α) in an Akt‐dependent manner.ConclusionGIP increases GLUT3 expression and promotes glucose intake in neurons, which exerts an antioxidant effect and protects neuronal cells from oxidative stress both in vitro and in vivo.

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“…GC10289, Glpbio), a glucose uptake assay was performed as described previously. 14 2‐NBDG solution was diluted to 100 μM with glucose‐free neurobasal. Cells were seeded in plates.…”

Section: Methodsmentioning

confidence: 99%

GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat

Guo,

Qi,

Luo

et al. 2024

CNS Neurosci Ther

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“…GLUT1 deficiency syndrome (GLUT1 DS) caused by GLUT1 deficiency indicates the types of variable focal and multiple local seizure, and electroencephalography (EEG) manifestations [ 103 ]. The 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose (2-NBDG) method and glucose uptake colorimetric method have shown that seizures could dramatically reduce neuronal glucose uptake and GLUT-3 expression [ 104 ]. However, study on hippocampal neurons from cultured primary rats and hippocampal slices from mice [ 98 ] have demonstrated that adiponectin enhances glucose uptake, glycolysis rate, and ATP production through the AMPK -dependent mechanism.…”

Section: The Effects Of Adiponectin On Epilepsymentioning

confidence: 99%

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

Shan

Chen

et al. 2023

Neurochem Res

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Epilepsy is a common and severe neurological disorder in which impaired glucose metabolism leads to changes in neuronal excitability that slow or promote the development of epilepsy. Leptin and adiponectin are important mediators regulating glucose metabolism in the peripheral and central nervous systems. Many studies have reported a strong association between epilepsy and these two adipokines involved in multiple signaling cascades and glucose metabolism. Due to the complex regulatory mechanisms between them and various signal activation networks, their role in epilepsy involves many aspects, including the release of inflammatory mediators, oxidative damage, and neuronal apoptosis. This paper aims to summarize the signaling pathways involved in leptin and adiponectin and the regulation of glucose metabolism from the perspective of the pathogenesis of epilepsy. In particular, we discuss the dual effects of leptin in epilepsy and the relationship between antiepileptic drugs and changes in the levels of these two adipokines. Clinical practitioners may need to consider these factors in evaluating clinical drugs. Through this review, we can better understand the specific involvement of leptin and adiponectin in the pathogenesis of epilepsy, provide ideas for further exploration, and bring about practical significance for the treatment of epilepsy, especially for the development of personalized treatment according to individual metabolic characteristics.

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Epileptiform Discharges Reduce Neuronal ATP Production by Inhibiting F0F1-ATP Synthase Activity via A Zinc-α2-Glycoprotein-Dependent Mechanism

et al. 2023

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Zinc‐α2‐glycoprotein relieved seizure‐Induced neuronal glucose uptake impairment via insulin‐like growth factor 1 receptor‐regulated glucose transporter 3 expression

Cited by 5 publications

References 57 publications

GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat

GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat

Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism

Epileptiform Discharges Reduce Neuronal ATP Production by Inhibiting F0F1-ATP Synthase Activity via A Zinc-α2-Glycoprotein-Dependent Mechanism

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