Abstract
To maintain its functional abilities, the mature brain obtains energy from glucose produced in carbohydrate metabolism. When carbohydrates are eliminated from the diet, the energy comes from the oxidation of fatty acids. In this metabolic state called ketosis, ketone bodies are formed: β-hydroxybutyric acid (bHb), acetone, and acetoacetate as alternative source of energy passing through the blood–brain barrier easily. The ketosis state can be achieved through various strategies like caloric restriction, supplementation with medium-chain triglycerides, intense physical training, or ketogenic diet (KD). Using KD, drug-resistant epilepsy has been successfully treated in children and adults. It can also exert neuroprotective influences in cases of brain damage, glioblastoma multiforme, and Alzheimer's or Parkinson's diseases. Although many possible mechanisms of KD activity have been proposed, newer hypotheses appear with the research progress, mostly characterizing the brain under pathological but not normal conditions. Since different pathological conditions may affect the mechanism of KD action differently, additional research on the normal brain appears reasonable. For this purpose, young adult rats were treated with 4-month-lasting KD. Then, MRI structural measurements, spectroscopy, and tractography were performed. The procedures revealed significant increases in the concentration of glutamine, glutamate, glutathione and NAA, accompanied by changes in the pattern of neuronal connections of the striatum and hippocampal formation. This implies a possible involvement of these structures in the functional changes occurring in the brain after KD application. Thus, the investigations on the normal brain add important details concerning mechanisms underlying KD effects without their possible modification by a pathological status.
Highlights
IntroductionEnergy required for proper brain functioning in adults derives from glucose generated in carbohydrate metabolism (Vannucci and Vannucci 2000)
Under normal circumstances, energy required for proper brain functioning in adults derives from glucose generated in carbohydrate metabolism (Vannucci and Vannucci 2000)
Measurements of food consumption per one animal showed that the average daily food intake was 20.0 g of normal (ND) and 10.5 g ketogenic diet (KD), providing 61.1 and 87.5 kcal/day, respectively
Summary
Energy required for proper brain functioning in adults derives from glucose generated in carbohydrate metabolism (Vannucci and Vannucci 2000). When carbohydrates are eliminated from the diet, energy can be obtained from fatty acid oxidation This process generates the amount of acetyl-co molecules sufficient for the synthesis of acetylacetic acid in the liver. It can be either spontaneously transformed into acetone or enzymatically transformed into beta-hydroxybutyric acid (ketone bodies, bHb). Ketone bodies are transported to the circulation and to extrahepatic tissues where they are used as ATP precursors They can reach the brain crossing the blood–brain barrier; acetone via simple diffusion, beta-hydroxybutyric acid and acetylacetic acid through transporters, the expression of which is connected with ketosis level (Bailey et al 2005). Upon crossing the blood brain barrier, ketones are transported across cell plasma membranes via monocarboxylate transporters 1 and 2 in astrocytes and neurons, respectively (Vijay and Morris 2014)
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