Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Wnt Pathway and KATP Channels

Rubio, Carmen; Luna, Rudy; Rosiles, Artemio; Rubio-Osornio, Moisés

doi:10.3389/fneur.2020.584298

Cited by 16 publications

(6 citation statements)

References 162 publications

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“…The KD provides ketone bodies as a brain energy source instead of glucose, stabilizing synapses and improving brain energy reserve which leads to a neuronal function enhancement. The CR also decreases glucose sensitivity, but without producing ketone bodies [163][164]. The KD should be recommended with caution, more evidence is needed to support this type of therapy, there is a concern in patients with T1DM because of the lipid profile provided by the diet, as well as in patients with T2DM with increased cardiovascular risk, therefore, each diet should be tailored for each patient [165].…”

Section: Measures To Prevent and Treat Neuronal Changes In Diabetesmentioning

confidence: 99%

A Comprehensive Review of Neuronal Changes in Diabetics

Luna¹,

Manjunatha²,

Bollu³

et al. 2021

Cureus

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Section: Measures To Prevent and Treat Neuronal Changes In Diabetesmentioning

confidence: 99%

A Comprehensive Review of Neuronal Changes in Diabetics

Luna¹,

Manjunatha²,

Bollu³

et al. 2021

Cureus

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“…The Wnt/β-catenin pathway participates not only in neuronal synchrony regulation. But also in NMDA receptor modulation, which, as previously described, plays an important role not only in epilepsy but also in epileptogenesis [25,26].…”

Section: Molecular Signaling Pathways For Epileptogenesismentioning

confidence: 74%

Neurotoxicity and Epileptogenesis

Rubio¹,

Rosiles-Abonce²,

Taddei³

et al. 2022

Neurotoxicity - New Advances

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Many neurotoxic substances produce toxic effects on the nervous system. Given the neurotoxic substances found in the human body, certain people have been regarded as having a propensity to epileptic seizures. In many situations, the neurotransmission processes of these toxins are similar to the physiopathology of epilepsy. Epileptic models have been developed to induce seizures in animals, allowing researchers to study convulsive seizure mechanisms. Pentylenetetrazol, kainic acid, pilocarpine, penicillin, aluminum, bicuculline, picrotoxine, 4-aminopyridine, strictine, domoic acid, and other compounds fall under this category. However, there are some drugs used in clinical practice that can cause neurotoxicity as well. In this chapter, the predominant substances and drugs involved in epileptogenesis through neurotoxicity effects are reviewed. Throughout this chapter, we attempt to describe the mechanisms documented in the literature, in which epileptic seizures cause neurotoxicity in the brain by themselves, as shown with excitotoxicity mediated by glutamate and ions involved.

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“…Among the genes altered, the Abcc8 mRNA levels are downregulated and Kcnj11 levels tend to increase (Kundap et al, 2020). This situation is supported by the observation that epilepsy is positively modulated with diets such as the ketogenic diet or caloric restriction which produce a hyperpolarization mediated by the K ATP channels (Rubio et al, 2020). These data show the complex interaction of SUR1 proteins with ion channels and the importance of their study during brain disease.…”

Section: Reviewmentioning

confidence: 75%

The short form of the SUR1 and its functional implications in the damaged brain

et al. 2022

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Sulfonylurea receptor (SUR) belongs to the adenosine 5′-triphosphate (ATP)-binding cassette (ABC) transporter family; however, SUR is associated with ion channels and acts as a regulatory subunit determining the opening or closing of the pore. Abcc8 and Abcc9 genes code for the proteins SUR1 and SUR2, respectively. The SUR1 transcript encodes a protein of 1582 amino acids with a mass around 140–177 kDa expressed in the pancreas, brain, heart, and other tissues. It is well known that SUR1 assembles with Kir6.2 and TRPM4 to establish K ATP channels and non-selective cation channels, respectively. Abbc8 and 9 are alternatively spliced, and the resulting transcripts encode different isoforms of SUR1 and SUR2, which have been detected by different experimental strategies. Interestingly, the use of binding assays to sulfonylureas and Western blotting has allowed the detection of shorter forms of SUR (~65 kDa). Identity of the SUR1 variants has not been clarified, and some authors have suggested that the shorter forms are unspecific. However, immunoprecipitation assays have shown that SUR2 short forms are part of a functional channel even coexisting with the typical forms of the receptor in the heart. This evidence confirms that the structure of the short forms of the SURs is fully functional and does not lose the ability to interact with the channels. Since structural changes in short forms of SUR modify its affinity to ATP, regulation of its expression might represent an advantage in pathologies where ATP concentrations decrease and a therapeutic target to induce neuroprotection. Remarkably, the expression of SUR1 variants might be induced by conditions associated to the decrease of energetic substrates in the brain (e.g. during stroke and epilepsy). In this review, we want to contribute to the knowledge of SUR1 complexity by analyzing evidence that shows the existence of short SUR1 variants and its possible implications in brain function.

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Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Wnt Pathway and KATP Channels

Cited by 16 publications

References 162 publications

A Comprehensive Review of Neuronal Changes in Diabetics

A Comprehensive Review of Neuronal Changes in Diabetics

Neurotoxicity and Epileptogenesis

The short form of the SUR1 and its functional implications in the damaged brain

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