Methylmalonate (MMA) accumulates in the tissues of patients with methylmalonic acidaemia, who present severe neurological signs soon after birth and later mental retardation. Attempting to understand the pathophysiology of the disorder, we investigated the effects of MMA on brain glucose uptake, lactate release and CO2 production. Glucose uptake and lactate release were studied by incubating 40 microns wide brain prisms from 15-day-old rats in Krebs-Ringer bicarbonate buffer, pH 7.0, containing 5.0 mmol/L glucose and one of three concentrations of MMA (1.0, 2.5 and 5.0 mmol/L). Controls did not contain MMA in the incubation medium. MMA induced a significant increase of lactate production in a dose-dependent pattern that was proportional to glucose uptake by the brain prisms. We also studied the influence of MMA on brain CO2 production from [2-14C]glucose and [U-14C]acetate by incubating brain prisms in the same buffer in the presence of the substrates with (experimental groups) or without (controls) 5.0 mmol/L MMA. MMA significantly reduced CO2 formation from both substrates.

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Aim: the aim of this study was to induce obesity in rats using the neonatal overfeeding protocol and evaluate in adult male animals standard chow intake, sweet food intake, the preference between sweet food and standard chow, locomotor activity and anxiety-like behavior. Methodology: The neonatal overfeeding protocol consisted of reducing the litter size to 4 animals (small litters = SL) compared to 8 animals in normal litters (NL). In these experiments we used 55 offspring from 18 litters. Results: obesity was successfully induced as observed by increased body weight and

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