The earliest demonstration of direct in vivo effects of ketone bodies was made by Keith in the early 1930’s, when he determined that acetoacetate, when administered intraperitoneally in rabbits, prevented seizures induced by thujone (1933), a convulsant constituent found in many essential oils and an antagonist of GABAA receptors (Höld et al., 2000). This seminal observation was later confirmed in an audiogenic seizure-susceptible mouse model (Rho et al., 2002). More intriguingly, however, Likhodii and colleagues (2003) established the broad anticonvulsant properties of acetone in four different animal models, and when injected intraperitoneally, produced plasma and cerebrospinal fluid (CSF) concentrations consistent with those used to suppress seizures. These results confirmed and extended historical observations supporting an anticonvulsant action for acetone, through as yet undetermined mechanisms (Likhodii & Burnham, 2002). And in further support of this, other investigators found that acetone was detectable (up to a concentration of 0.7 mM) in the brains of fully controlled KD-treated patients with epilepsy using proton magnetic resonance spectroscopy (Seymour et al, 1999).
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Polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, C22: 6ω-3), arachidonic acid (AA, C20: 4ω-3), or eicosapentaenoic acid (EPA, C20: 5ω-3) have been reported to suppress voltage-gated sodium channels and L-type calcium channels in seizure-prone structures such as the hippocampus (Vreugdenhil et al., 1996). The KD produces elevations of both AA and DHA in serum (Fraser et al., 2003; Cunnane et al., 2002) and brain (Taha et al., 2005) of patients and animals, respectively, suggesting that these substrates might exert anticonvulsant effects by inhibiting sodium and calcium channels, like many anticonvulsant drugs (Xiao et al., 1997, 1998).
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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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Baur JA, Pearson KJ, Price NL, Jamieson HA, Lerin C, Kalra A, Prabhu VV, Allard JS, Lopez-Lluch G, Lewis K, Pistell PJ, Poosala S, Becker KG, Boss O, Gwinn D, Wang M, Ramaswamy S, Fishbein KW, Spencer RG, Lakatta EG, Le Couteur D, Shaw RJ, Navas P, Puigserver P, Ingram DK, de Cabo R, Sinclair DA. Resveratrol improves health and survival of mice on a high-calorie diet. Nature. 2006;444:337–342. [PMC free article] [PubMed] [Google Scholar]
Chicken egg roll ala Hokben ini saya buat untuk anak-anak dan mereka suka. Ternyata memasaknya tidak sesulit yang dibayangkan. Cukup dengan menggulung daging ayam giling yang sudah dibumbui dengan telur dadar dan dikukus sampai matang kemudian dipotong-potong dan digoreng kering. Siapkan plastik tahan panas atau aluminium foil untuk menggulung. Disini saya share resep chicken egg …