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Biomedical subjects

R Racotta

Publications and source records attributed to R Racotta.

27 records · Page 2Linked to original sources

Glycogenolytic substances, hepatic and systemic lactate, and food intake in rats.

Changes in hepatic lactate and glucose and systemic blood lactate produced by intraperitoneal injections of epinephrine, isoproterenol, glucagon, and insulin showed a high correlation (r = 0.9) with the changes in food intake elicited by the same substances. The changes in systemic blood glucose showed no correlation with the changes in feeding, which suggests that central glucoreceptors are not playing an important role in the observed changes in feeding. The intramuscular epinephrine had no significant effect on food intake, in spite of changes in systemic and hepatic lactate and glucose similar to those elicited by intraperitoneal epinephrine. However, intramuscular epinephrine had no hepatic glycogenolytic effect. This suggests that the changes in glucose and lactate elicited by intraperitoneal epinephrine result from hepatic glycogenolysis, whereas the changes elicited by intramuscular epinephrine result from muscular glycogenolysis and inhibition of insulin. Thus hepatic glucose and lactate are good predictors of feeding only when they are produced endogenously by hepatic glycogenolysis. It was concluded that hepatic lactate cannot be the substance sensed by hepatic metabolic receptors. However, due to a possible change in the hepatic lactate-to-pyruvate ratio elicited by intraperitoneal epinephrine, hepatic pyruvate may still be correlated with feeding during the action of both intramuscular and intraperitoneal epinephrine. Therefore the hypothesis that pyruvate is the substance monitored by hepatic metabolic receptors should be tested.

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Motor activity in decerebrate rats: spontaneous and nutrient-induced changes.

Bilateral decerebration was performed in adult Wistar rats of either sex under pentobarbital sodium anesthesia. Decerebrate rats were aphagic and adipsic and received 44 kcal/day subcutaneously by gastric intubation. Their motor activity was recorded in the morning after an 18-h fast, following various treatments: 10 ml mash (22 kcal) or 3.6 g glucose/kg; intragastric, intraperitoneal, or subcutaneous injection of glucose (3.6 g/kg) or glycerol (1.84 g/kg); or injection of epinephrine (25 micrograms/kg ip or im). These treatments were also applied to control rats previously maintained in the same conditions. Motor activity of both operated and control rats was generally reduced in a similar manner: intragastric mash greater than intraperitoneal glucose = intraperitoneal glycerol greater than or equal to intragastric glucose greater than intraperitoneal epinephrine. Subcutaneous glucose and glycerol and intramuscular epinephrine produced hyperactivity, at least for the first 30 min. Thus decerebrate rats respond like normal rats by reducing their general activity when subjected to the same satiating treatments given intragastrically or intraperitoneally. This suggests that the brain stem of rats can monitor peripheral information regarding caloric replenishment.

Animals↗

Unusual peaks of oxygen consumption under special alimentary conditions.

Oxygen consumption (VO2), carbon dioxide production (VCO2), the resulting respiratory quotient (RQ), and motor activity were recorded simultaneously by an on-line computer every ten seconds during 16-20 hours in two decerebrate male rats. Being aphagic and adipsic the rats were fed twice daily by gastric intubation with a mixture of powdered milk plus sugar or plus sunflower oil (approx. 300 KJ daily) in 10-20 ml tap water. In all seven tests performed on these rats the recordings presented very steep reductions of RQ due every time to steep increases in VO2 without increases in VCO2. Mean number of VO2 peaks in all experiments was 12.4 +/- 1.8 (SE) with mean duration of 21.3 +/- 2.8 min. Two normal male rats were fed the same diet and on the same schedule: they presented similar VO2 peaks in 8 out of 12 experiments. Mean number was 8.7 +/- 1.0 with mean duration of 13.6 +/- 2.2 min. The VO2 peak periods never occurred in rats fed ad libitum. In the two normal rats oil ingestion produced more effect than sugar. It is suggested that the phenomenon could be due to a metabolic imbalance possibly of hepatic origin, more evident in decerebrate rats. VO2 peaks could be produced by enhanced ketogenesis, gluconeogenesis and/or extra-mitochondrial (peroxisomal, microsomal) oxidation.

Animals↗