Activation of cerebral sodium-glucose transporter type 1 function mediated by post-ischemic hyperglycemia exacerbates the development of cerebral ischemia

Yamazaki, Yoji; Ogihara, Saki; Harada, Shinichi; Tokuyama, Shogo

doi:10.1016/j.neuroscience.2015.10.005

Cited by 32 publications

(43 citation statements)

References 67 publications

(29 reference statements)

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“…Glucose transport by SGLT is driven by sodium concentrations gradients that are maintained by sodium exporters, which produce inward currents and membrane depolarization . Inhibition of cerebral SGLT by phlorizin or cerebral SGLT‐1 knockdown reportedly suppressed the development of cerebral ischaemic neuronal damage without suppressing postischaemic hyperglycaemia . Therefore, cerebral SGLT likely exacerbates the development of cerebral ischaemia following postischaemic hyperglycaemia.…”

Section: Discussionsupporting

confidence: 93%

“…Thus, excessive influx of sodium ions via cerebral SGLT may exacerbate the development of cerebral ischaemic neuronal damage. In addition, we previously reported that cerebral SGLT‐1 exacerbates the development of cerebral ischaemia . Taken together with present data, there is a high possibility that cerebral SGLT‐1‐mediated excessive sodium ions inflow induces the exacerbation of cerebral ischaemia.…”

Section: Discussionmentioning

confidence: 99%

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Sodium transport through the cerebral sodium–glucose transporter exacerbates neuron damage during cerebral ischaemia

Yamazaki

Harada

Wada

et al. 2016

Journal of Pharmacy and Pharmacology

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Sodium transport through the cerebral sodium–glucose transporter exacerbates neuron damage during cerebral ischaemia

Yamazaki

Harada

Wada

et al. 2016

Journal of Pharmacy and Pharmacology

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“…However, studies have shown that postischemic hyperglycemia exacerbates cerebral ischemia, neuronal injury and death through activation of cerebral sodium-glucose transporter type 1 (SGLT1) function, which happens through AMPK activation. [70] In heart, studies have shown that SGLT1 knockout in mice with the PRKAG2 Thr400Asn mutation (implicated in the development of WPW syndrome) attenuates the structural and clinical phenotype of cardiomyopathy associated with WPW syndrome. [71] Hence, this link between SGLT1 and AMPK at brain and heart suggests the urgent need for studies to evaluate the link between SGLT2 and AMPK.…”

Section: Challenges In Classification Of Antidiabetes Medicationsmentioning

confidence: 99%

Adenosine monophosphate-activated protein kinase-based classification of diabetes pharmacotherapy

Dutta

Kalra

Sharma

2017

Journal of Postgraduate Medicine

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The current classification of both diabetes and antidiabetes medication is complex, preventing a treating physician from choosing the most appropriate treatment for an individual patient, sometimes resulting in patient-drug mismatch. We propose a novel, simple systematic classification of drugs, based on their effect on adenosine monophosphate-activated protein kinase (AMPK). AMPK is the master regular of energy metabolism, an energy sensor, activated when cellular energy levels are low, resulting in activation of catabolic process, and inactivation of anabolic process, having a beneficial effect on glycemia in diabetes. This listing of drugs makes it easier for students and practitioners to analyze drug profiles and match them with patient requirements. It also facilitates choice of rational combinations, with complementary modes of action. Drugs are classified as stimulators, inhibitors, mixed action, possible action, and no action on AMPK activity. Metformin and glitazones are pure stimulators of AMPK. Incretin-based therapies have a mixed action on AMPK. Sulfonylureas either inhibit AMPK or have no effect on AMPK. Glycemic efficacy of alpha-glucosidase inhibitors, sodium glucose co-transporter-2 inhibitor, colesevelam, and bromocriptine may also involve AMPK activation, which warrants further evaluation. Berberine, salicylates, and resveratrol are newer promising agents in the management of diabetes, having well-documented evidence of AMPK stimulation medicated glycemic efficacy. Hence, AMPK-based classification of antidiabetes medications provides a holistic unifying understanding of pharmacotherapy in diabetes. This classification is flexible with a scope for inclusion of promising agents of future.

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“…; Yamazaki et al . ). Unfortunately, the immunocytochemical localizations of SGLT1 in brain must be considered with caution because using Sglt1 −/− mice as specificity control for the immunolocalization of SGLT1 in mouse brain indicate that the so far employed antibodies do not allow a specific identification of SGLT1 (Madunic et al .…”

mentioning

confidence: 97%

“…; Yamazaki et al . , ; Koepsell ). Immunocytochemical localization and in situ‐hybridization experiments strongly suggest that SGLT1 is expressed in neurons and provide hints on additional locations of SGLT1 in glial cells and the BBB (Poppe et al .…”

mentioning

confidence: 99%

RS1 (Rsc1A1) deficiency limits cerebral SGLT1 expression and delays brain damage after experimental traumatic brain injury

Sebastiani

Greve

Gölz

et al. 2018

Journal of Neurochemistry

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Acute cerebral lesions are associated with dysregulation of brain glucose homeostasis. Previous studies showed that knockdown of Na -D-glucose cotransporter SGLT1 impaired outcome after middle cerebral artery occlusion and that widely expressed intracellular RS1 (RSC1A1) is involved in transcriptional and post-translational down-regulation of SGLT1. In the present study, we investigated whether SGLT1 is up-regulated during traumatic brain injury (TBI) and whether removal of RS1 in mice (RS1-KO) influences SGLT1 expression and outcome. Unexpectedly, brain SGLT1 mRNA in RS1-KO was similar to wild-type whereas it was increased in small intestine and decreased in kidney. One day after TBI, SGLT1 mRNA in the ipsilateral cortex was increased 160% in wild-type and 40% in RS1-KO. After RS1 removal lesion volume 1 day after TBI was reduced by 12%, brain edema was reduced by 28%, and motoric disability determined by a beam walking test was improved. In contrast, RS1 removal did neither influence glucose and glycogen accumulation 1 day after TBI nor up-regulation of inflammatory cytokines TNF-α, IL-1β and IL-6 or microglia activation 1 or 5 days after TBI. The data provide proof of principle that inhibition or down-regulation of SGLT1 by targeting RS1 in brain could be beneficial for early treatment of TBI.

show abstract

Activation of cerebral sodium-glucose transporter type 1 function mediated by post-ischemic hyperglycemia exacerbates the development of cerebral ischemia

Cited by 32 publications

References 67 publications

Sodium transport through the cerebral sodium–glucose transporter exacerbates neuron damage during cerebral ischaemia

Sodium transport through the cerebral sodium–glucose transporter exacerbates neuron damage during cerebral ischaemia

Adenosine monophosphate-activated protein kinase-based classification of diabetes pharmacotherapy

RS1 (Rsc1A1) deficiency limits cerebral SGLT1 expression and delays brain damage after experimental traumatic brain injury

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