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R Racotta

Publications and source records attributed to R Racotta.

18 recordsLinked to original sources
PubMed1995

The role of conditioned taste aversion in the hypophagia induced by intraperitoneal epinephrine and glucose.

It has been repeatedly shown that relatively high doses of epinephrine (E) and glucose (G) injected intraperitoneally (ip) produce hypophagia in fasted rats. In the present work we used a conditioned taste aversion (CTA) paradigm in order to test whether this effect could be due to "malaise." We determined the effect on food intake and saccharin preference with the following treatments: (a) E ip 100 and 250 micrograms/kg; (b) E ip 250 micrograms/kg with or without previous alpha 1 plus beta adrenergic blockade; (c) G ip 3.5 and 4 g/kg. Both doses of E significantly reduced food intake more than 75% but only the high dose produced a significant (50%) reduction in saccharin preference. Blockade of alpha 1 and beta adrenergic receptors completely suppressed the E-induced hypophagia but attenuated only slightly the taste aversivon effect. Both doses of G decreased food intake but only the high dose reduced saccharin preference; part of these effects would appear to be due to the high osmolarity of the solution. The present results indicate that E and G may induce CTA in our experimental conditions. However, their hypophagic and aversive effects seem to be elicited by different mechanisms.

Animals↗
PubMed1995

Norepinephrine inhibition of water and food intake: comparison with vasopressin effects.

UNLABELLED: In a previous publication we showed that intraperitoneally (IP) injected norepinephrine (NE) induces hypodipsia (hD) in rats by an alpha 1-adrenergic effect which might be due to splanchnic vasoconstriction. In the present work we administered two vasoconstrictive hormones: NE 250 ug/kg and arginine vasopressin (VP) 550 mU/kg either by IP or intramuscular (IM) route to fasted rats in two different thirst-inducing conditions: (a) water-deprivation; or (b) induced hyperosmolarity. IP NE inhibited significantly food and water intake under both conditions. IM NE did not affect food intake and elicited significantly less hD and this only in (a). VP did not affect food intake but induced hD regardless of the route of administration in (a) but not in (b). NE administrated to anesthetized rats after food and water deprivation increased arterial pressure by both routes while VP effect was weaker and more variable. IN CONCLUSION: blood pressure elevation may be implicated in the hD effect but IP NE elicits a specific splanchnic action; splanchnic-induced hypophagia is not necessarily related to water intake inhibition.

Animals↗
PubMed1993

Specificity of alpha- and beta-adrenergic inhibition of water and food intake.

In previous publications from our laboratory it was shown that catecholamines (CA) injected intraperitoneally (IP) to fasted rats induce a transient inhibition of food intake. This effect seems to be both alpha- and beta-adrenergic. According to more recent data (20), IP CA also reduced water intake in water-deprived rats, and the effect is exclusively alpha-adrenergic. In order to obtain more information on the adrenergic specificity of the two inhibitory effects we measured the amount of food and water ingested during 30 min by male and female rats previously deprived of both food and water for 18 h. Three adrenergic agonists (norepinephrine, isoproterenol, and salbutamol) were injected IP after the administration (IP) of the following adrenergic antagonists: phentolamine, prazosin, yohimbine, propranolol, or metoprolol. Results showed that, under these experimental conditions, water intake inhibition was due exclusively to an alpha 1 effect, whereas food intake inhibition seemed to depend on alpha 1 and beta 1 actions plus some beta 2 participation. It is also suggested that blocking one type of receptors may enhance the responsiveness of the other type.

Adrenergic alpha-Antagonists↗
PubMed1991

Effects of catecholamines on water intake in rats.

It is known that intraperitoneally (IP) injected adrenaline (A) inhibits food intake in otherwise hungry animals. In a recent work, Hinton et al. (6) showed that IP A also inhibits water intake in thirsty rats, concluding that A's effect is unspecific. We administered A IP or intramuscularly (IM) in different doses in rats made thirsty either by 18-h water deprivation or by subcutaneous injection of hypertonic saline or polyethylene glycol. IP A reduced water intake in all experimental conditions. A dose-related inhibition was observed in water-deprived animals. On the other hand, IM A showed a small effect only at the highest dose (50 micrograms/100 g body weight). When some of these experiments were repeated using noradrenaline (NA) and isoproterenol (IS), IM administration of either substance showed no effect. IP administration reduced water intake significantly only at the highest dose of NA (50 micrograms/100 g). It is concluded that water intake inhibition by catecholamines in rats made thirsty either by osmotic or by volumetric challenges is of porto-hepatic origin and, in contrast with food intake inhibition, has no beta-adrenergic component.

Animals↗
PubMed1989

Gender differences between the effect of monosodium glutamate on food intake in rats.

Monosodium glutamate (MSG) was recently reported to increase feeding in ad lib. fed rats [Reddy et al.(4)]. In the present study the responses of male and female adult rats to subcutaneous (SC) administration of MSG were compared. In female rats MSG 3 g/kg did not significantly affect food or water intake as compared with SC NaCl 0.9%; MSG 6 g/kg significantly reduced food intake but increased water intake. On the contrary, in male rats MSG 6 g/kg significantly increased food and water intake. It is concluded that there are differences between genders of rats in what concerns the effect of glutamate on food intake.

Animals↗
PubMed1987

Anorexia elicited by different catecholamines in rats.

Adrenaline (A) produces a strong anorexic effect, possibly by acting on hepatic receptors (nerve endings on hepatocytes). To study whether this is mediated by alpha- or beta-adrenergic mechanisms, or both, the anorexigenic effects of intraperitoneal injections of A, noradrenaline (NA) and isoproterenol (I) were studied under four different experimental conditions: (I) at the beginning of the dark period in rats fed ad libitum, or (II) on a 24 h-feeding/24 h-fasting schedule; (III) during the light period, under the same feeding schedule; (IV) after an acute 24 h fast. In condition I, the three catecholamines produced a marked decrease in feeding, slightly larger for A. In condition II (dark), they elicited a decrease in food intake about double that in condition III (light), their relative potencies also differed: A greater than I greater than NA in II and A greater than I = NA in III. In IV, the same relative potencies were obtained as in III. A mixture of half-doses of NA and I had the same effect in III and IV as either NA or I alone, suggesting that the alpha and beta effects are additive. However, even a mixture of the full doses of NA and I was not as effective as A in condition IV. This suggests that A is more potent than NA or I at stimulating hepatic adrenergic receptors that cannot be classified as either alpha or beta.

Animals↗
PubMed1986

Metabolic effects of chronic infusions of epinephrine and norepinephrine in rats.

Chronic infusions of epinephrine, norepinephrine, or vehicle were performed in adult male rats by means of subcutaneous implanted osmotic minipumps (ALZET). The calculated dose was 180 ng/min during 7-8 days. Daily food intake and body weight were measured during this period and also 7 days before and 5 days after it. During the period of infusion, norepinephrine stopped body weight gain while epinephrine-infused rats gained weight at the same rate as controls. Once the infusion period was finished, epinephrine-infused rats gained more weight than controls, while norepinephrine-infused rats just returned to the slope of weight gain of the controls. In no group did food intake change. In a second experiment, similar infusions were carried out in other rats on the same schedule; body temperature, glycemia, and serum insulin and triiodothyronine were measured. Epinephrine infusion significantly elevated glycemia and triiodothyronine, whereas norepinephrine infusion increased temperature and serum insulin. The results obtained by chronic administration of the catecholamines support the concept of a disassociation of adrenomedullary and sympathetic nervous system metabolic effects.

Animals↗
PubMed1984

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.

Animals↗
PubMed1984

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↗
PubMedDate not supplied

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↗