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Furthermore, if the KD increases GABA levels in the brain, then such an effect is approximated by vigabatrin, an irreversible inhibitor of the degradative enzyme GABA-transaminase, as well as by tiagabine, a GABA re-uptake blocker that interferes with presnaptic GABA transporters (White et al., 2007). Yet, the anticonvulsant profile of the KD is distinct from that of vigabatrin and tiagabine (Hartman et al., 2007). The general approach of deriving another pill that enhances brain GABA levels may not be relevant or viable, since many seizure types seem to be exacerbated by agents that contribute to enhanced tonic inhibition, and extrasynaptic GABA receptors that mediate tonic inhibition are more sensitive to elevated ambient GABA concentrations (Sazgar & Bourgeois, 2005). Indeed, increased GABAergic inhibition in the cortex appears to underlie the mechanism of synchronization and seizure generation in two mouse models of autosomal dominant nocturnal frontal lobe epilepsy (Klassen et al, 2006)

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To understand how Regal Keto works, you firstly have to be familiar with keto mechanism. The term keto comes from ketones which are compounds that are produced when fats are metabolized. There are three different types of ketones that are mainly released into the body. Ketones are very rich in energy and they also help to provide energy to the brain which is not possible for fats to do. So, Regal Keto helps the body achieve this state that is called ketosis so that fats are burnt on a fast rate and as a result of that, the excess lipids are removed from the body. This is why ketosis is very helpful in making that belly bulge go away or slimming down the thighs. Since it plays a role in removing the extra fat and slimming down the body, this process is also being incorporated into diets these days.
Diet keto atau disebut juga dengan diet ketogenik berasal dari kata keton. Keton adalah senyawa kimia yang dihasilkan dari pemecahan lemak oleh hati. Biasanya, energi diambil dari glukosa yang bersumber dari karbohidrat. Namun, dikarenakan rendah karbohidrat maka tubuh akan kekurangan glukosa. Alhasil, secara otomatis tubuh menggunakan cadangan energi dari senyawa lainnya, yaitu lemak.
Resep Tahu Sutra Rumput Laut Keto – Sewaktu bersantap di sebuah restoran China, si sulung menunjuk gambar tahu sutra rumput laut dengan saus jamur yang menggugah selera. “Coba bikin kayak gini versi Keto mam”, gumamnya. Akhirnya saya mencoba membuat versi Ketonya dan senang sekali hasilnya tak jauh berbeda, saosnya sempurna! Saya menggunakan xantham gum sebagai …

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One potential explanation for the anticonvulsant action of the KD argues that increased ATP synthesis should produce a positive bioenergetic balance, allowing stabilization of the resting membrane potential via enhanced activity of Na+-K+-ATPase (Bough & Rho, 2007). Several decades ago, De Vivo and colleagues (1978) reported that the KD increased the total quantity of bioenergetic substrates (such as adenosine triphosphate, or ATP) and elevated the energy charge in rat brain. These changes were purported to stabilize the cell membrane, especially in the face of excessive excitation. Consistent with these observations, a later human study utilizing magnetic resonance spectroscopic techniques indicated that patients with epilepsy fed a KD had elevated phosphocreatine to creatine levels in the brain (Pan et al., 1999). Recently, using cDNA microarray technology, increased expression of the mitochondrial ATP synthase β,D subunit in mouse brain was reported after KD treatment (Noh et al., 2004). And in the most comprehensive study of this kind to date, the KD was found to enhance mitochondrial biogenesis and significantly increase the number of transcripts encoding energy metabolism genes in rats (Bough et al., 2006). This increase in bioenergetic capacity enabled hippocampal slices from these animals to better withstand metabolic challenge from low glucose exposure. Taken together, the prevailing notion has been that increased energy production and reserve capacity enable greater resistance to neuronal hyperexcitability and hypersynchrony.
Glucose restriction is believed to be a key mechanism of KD action. Calorie restriction in rodents reduced seizure susceptibility and the resultant low blood glucose levels correlated with inhibition of epileptogenesis in a genetic model of stimulus-induced epilepsy (Greene et al., 2001). Along related lines, Garriga-Canut et al. (2006) demonstrated that 2-deoxyglucose, which inhibits the glycolytic enzyme phosphoglucose isomerase, prevented seizure progression in the rat kindling model of temporal lobe epilepsy, and decreased the expression of brain-derived neurotrophic factor (BDNF) and its principal receptor, TrkB. More recently, Lian and colleagues (2007) demonstrated that fructose-1,6-bisphosphate (F-1,6-BP), a metabolite that shifts the metabolism of glucose from glycolysis to the pentose phosphate pathway, exhibits potent anticonvulsant activity in several rat models of acute seizures (i.e., pilocarpine, kainic acid, and pentylenetetrazole), and efficacy in these models exceeds that of 2-DG and KD treatment. Collectively, these emerging data indicate that the overall strategy of limiting glycolytic flux may be a powerful way of preventing acute seizures and perhaps epileptogenesis as well.

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