Metabolic correlates of the meal onset in the free food intake of rats

Abstract

By recording the free feeding pattern of rats, a linear relationship between meal sizes and the time elapsed until the onset of a new meal had been previously found. This fact suggested that the onset of each meal and therefore the meal frequency were directly dependent on critical metabolic events. In order to test the new possibility so offered to elucidate further the nature of metabolic signals involved in the regulation of food intake, respiratory exchanges and free feeding patterns of rats were simultaneously recorded and analysed. In thirteen 24 hr cycles of ten rats metabolic rate, lipogenesis or lipolysis rates were compared to the concomitant rate of food intake in various fractions of time of the nycthemeral D-L cycles. It was found that habituated rats exhibited a cycle of nocturnal fat synthesis and diurnal fat mobilization. The rate of calories used for lipogenesis or supplied by lipolysis respectively added to or subtracted from the metabolic rate accounted for the high rate of food intake during the dark and its low rate during the light period. Some indications existed that in the nocturnal phase, a true and measured hyperphagia of normal rats was a primary cause of the concomitant lipogenesis and that in this period, the control of food intake either escapes entirely from metabolic influences or is affected, at a low threshold, by a relative shortage of the glucose availability for cell oxidation. In the light period, the onset of each meal occurred at a maximal rate of lipolysis and at a minimal rate of the contribution of other metabolites (essentially of glucose derived from ingested foods) to the metabolic rate. The pharmacological or hormonal inhibition of this diurnal lipolysis induced an immediate increase of the food intake through shortening of meal to meal intervals. These two facts, among others, provide evidence that, in the light period and by contrast to the night, the low rate of food intake results from the concomitant lipolysis and, that, in this period, the control system of food intake is responsive at a high threshold to a critical deficit of the availability of glucose for cell oxidation. Thus this availability of glucose is confirmed as a plausible stimulus to eat.