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Biomedical subjects

J Le Magnen

Publications and source records attributed to J Le Magnen.

At least 73 records · Page 4Linked to original sources
PubMed1980

Failure of naloxone to affect initial and acquired tolerance to ethanol in rats.

The effects of naloxone on the initial sensitivity to ethanol and the subsequent changes in tolerance induced by prior ethanol treatment were studied in rats by using the drinking test for assessing behavioral effects. Naloxone (N) was administered concurrently with ethanol (E) in either 5 successive single doses spaced at 2-day intervals (Experiment 1) or during 4 days of chronic i.v. infusion (E: 9 g/kg, N: 9 mg/kg in 6 injections per day, Experiment 2). Both treatments produced an increase in nervous tolerance toward ethanol. However naloxone was found to exert no effect on either initial or acquired tolerance toward ethanol. The results are discussed in terms of possible relations between the CNS mechanisms involved in tolerance to morphine and ethanol.

Animals↗
PubMed1980

A bioassay of ethanol-dependence in rats.

A bioassay for the quantitative assessment of ethanol dependence in rat is proposed. It is based upon the alleviation by ethanol of the withdrawal syndrome in previously intoxicated animals. The conditioning by ethanol of a taste preference, linearly related to the duration of the previous chronic intoxication, provides a reliable measure of the level of ethanol dependence. In addition, the results display the neurobehavioural mechanism by which self-maintained intoxication is established in physically dependent rats and humans.

Alcoholism↗
PubMed1980

Parameters of the meal pattern in rats: their assessment and physiological significance.

Parameters of the meal pattern in rats were assessed and their physiological significance investigated through a detailed study of continuous graphic recordings over 20 consecutive days in ten rats. Both prandial and diurnal periodicities were examined. The definition of meals, by a criterion of 40 min of non-eating before and after a feeding episode, was validated statistically. The two superimposed periodicities were substantiated by studying night and daytime differences in meal sizes, meal-to-meal intervals, meal size/interval ratios, and post prandial correlations. The results provide new evidence for the role of metabolic and neuroendocrine factors in determining the relationships between meal size and post-meal intervals and their differences during the two parts of the diurnal cycle.

Animals↗
PubMed1980

Fall in blood glucose level precedes meal onset in free-feeding rats.

It has been suggested for a long time that the metabolic stimulation to eat or the hunger arousal of eating, originated from a fall in the blood glucose level induced by the periodic failure of hepatic glucose production to match the peripheral glucose uptake. However, this suggestion has not been substantiated directly by the results of periodic blood glucose evaluations performed during intermeal intervals in free-fed rats. In this experiment, a technique involving a continuous blood glucose determination over several hours was used in free-feeding, undisturbed rats. It was shown that all nocturnal and diurnal meals were preceded by a 6 to 8% fall of blood level, starting 5 to 6 min prior to meal onset. The overall consequences of these findings are discussed.

Animals↗
PubMed1980

Food deprivation induced parallel changes in blood glucose, plasma free fatty acids and feeding during two parts of the diurnal cycle in rats.

The changes in plasma glucose and free fatty acid levels and in subsequent feeding induced by 4 to 10 hr of food deprivation were investigated in rats and compared for the two parts of the diurnal cycle. It was found that increasing fast duration at night induced a more rapid fall of plasma glucose and elevation of plasma free fatty acids than in the day. However, a similar increment of the first post fast meal was elicited by an identical decrement of blood glucose level for the two periods except after a 10 hr fast during the day. The acute effect of darkness and light per se being experimentally excluded, it was concluded that the size of the first meal following short term food deprivation was dependent throughout the diurnal cycle on the fast induced glucoprivic condition.

Animals↗
PubMed1980

Changes of meal patterns induced by food deprivation: metabolic correlates.

Six hour food intake following 0 to 6 hours of food deprivation was compared during the light and dark cycle in rats. Changes in the size of the first meal and the length of the first post-meal interval, as a function of deprivation, were related to plasma glucose and free fatty acid levels immediately prior to and 90 minutes following the first meal. It was determined that at night the size of the first meal increased and the relative duration of the post-meal interval decreased as a function of previous fast duration. The shortening of post-meal satiety was associated with the food deprivation induced decrease of blood glucose level and rise of free fatty acids which were observed prior to the meal. The fast induced changes of the meal pattern observed at night and the resulting 6 hour hyperphagia support the conclusion that the duration of post-meal satiety is determined by the meal-to-meal balance between energy intake and utilization.

Animals↗
PubMed1980

Variations of meal-to-meal liver glycogen in rats.

Liver glycogen content was determined in free feeding rats sacrificed at the beginning of nocturnal meals or 60 min later. It was found that the glycogen content at the beginning of meals and 60 min later was highly correlated with the cumulative food intake since the beginning of the dark cycle, and therefore, increased from meal to meal. The comparison of these correlations between the cumulative food intake and the liver glycogen at the beginning of the meal and 60 min after ruled out the possibility that a constant decrement of glycogen might be involved in both meal onset and prandial periodicity of feeding. Rather the results are consistent with the view that the glycogen load during the night is a minute carbohydrate store which, like the fat store, is involved in the diurnal 12/12 hr feeding periodicity.

Animals↗
PubMed1980

Differential effects of 2-deoxy-D-glucose on plasma glucose, free fatty acids and feeding during the light and dark cycle in rats.

The effects of 2-deoxy-D-glucose (2-DG) combined with 0 to 6 hr of food deprivation on plasma glucose (PG), plasma free fatty acid (PFFA) levels and feeding were compared during the 2 parts of the diurnal cycle. In one group, PG and PFFA were measured prior to the injection of either 2-DG or saline and 90 min after injections without restoration of access to food. In a second group, food was reintroduced following injection and intake was measured. At night, PG and PFFA measured prior to injections decreased and increased with respect to the length of food deprivation. Ninety minutes after 2-DG, PG and PFFA were elevated above control levels as a function of previous deprivation. During the day, fasting time did not affect PG and PFFA 90 min after a saline injection; but, after 2-DG, PG increased and PFFA decreased irrespective of the previous deprivation period. At night, food intake increased after saline and 2-DG as a function of fast duration, but increases were significantly lower after 2-DG. During the day, the duration of food deprivation did not affect food intake after 2-DG and saline; but irrespective of previous food deprivation, the cumulative intake of the first 2 hr was higher after 2-DG. Results are discussed in relation to the dual activation by 2-DG of facilitatory and inhibitory mechanisms of food intake.

Animals↗
PubMed1980

Aspects of the neuroendocrine bases of the diurnal metabolic cycle in rats.

The difference between nocturnal and diurnal glucose disappearance rate, glucose stimulated insulin release and insulin sensitivity has been studied in normal adult female rats. The glucose clearance rate measured after an IV injection of glucose (1 g/kg) was found to be slower during the day than at night. However, due to the non-physiological level of hyperglycemia induced, the insulinogenic index failed to reveal a difference in glucose stimulated insulin release. On the contrary, the hypoglycemic response to an IV injection of 0.5 IU/kg of insulin indicated a higher insulin sensitivity and tissue glucose uptake at night compared to the day. The results are discussed with respect to the role of the neuroendocrine diurnal pattern underlying the diurnal periodicity of feeding.

Animals↗
PubMed1980

Palatability and preabsorptive insulin release.

The purpose of these experiments was to determine whether the level of orally-triggered and vagally-mediated preabsorptive insulin release was related to the degree of food palatability as measured by the amount of food necessary to produce satiation. Rats were habituated to a feeding schedule of five meals per day. During a test meal they were presented with one of 3 forms of their regular diet: unaltered, sweetened with Sucaryl sodium or adulterated with quinine hydrochloride. From 1.5 min preceding the meal to 19.5 min later, blood was continuously drawn via a chronic intravenous catheter. Blood was collected for regular intervals and immunoreactive insulin levels were determined. During the test meals, the rats ate 3, 4.9 and 1.5 g of the three diets, respectively. Within the first 3 min following meal onset, they exhibited a peak insulin release of 47, 65 and 25 microU/ml, respectively. Since this early insulin response disappeared long before the end of the meal, it was suggested that the palatability-dependent amount eaten could be affected by the palatability-modulated preabsorptive insulin release.

Animals↗
PubMed1980

Recovery of body weight following starvation or food restriction in rats.

Recovery of body weight and food intake have been studied and compared after a 25% weight loss produced by total starvation in one group of rats or by food restriction in a second group. It was shown that rats in both groups returned to their initial body weight within the same time on the average, but the hyperphagia observed during the recovery phase was significantly higher in restricted than in starved rats. In the former, the increase of food intake fully accounted for the weight gain. On the contrary, the recovery of body weight in previously starved rats involved both hyperphagia and a long lasting persistence of the fasting hypometabolism. In addition, it was shown that in those rats the higher the contribution of hypometabolism the longer the recovery. Starvation diabetes was higher in starved than in restricted rats and might be one factor which impairs weight regulation through hyperphagia after a weight loss induced by food deprivation.

Animals↗
PubMed1980

Behavioral regulation of the blood glucose level in rats.

Rats bearing one or two intravenous (IV) or one intravenous and one intragastric (IG) chronic catheters, were allowed to press one or two levers controlling the IV injection of either insulin or glucagon alone, or insulin paired with glucagon or with a glucose solution IV or IG. It was shown that rats readily learned to press for the various solutions and exhibited a sustained pattern of self-injection specific to these solutions and to their combinations. The rats self-injected insulin, glucagon and glucose preferentially during the 20 min preceding and following meals. Alone, or in combination with other solutions, glucose and glucagon were self-injected preferentially before meals and insulin after meals. Consequently, glucose or glucagon to insulin self-injection ratios were inversed from the pre-meal to the post-meal periods. In addition, rapid alternations from one lever to the other were observed in the coupled self-injections of insulin and glucose or insulin and glucagon. No effects of the self-injections on the free feeding pattern were observed. The results are interpreted as evidence for the reinforcing effects of a correction of both hypoglycemia and hyperglycemia and for a role of these systemic primary reinforcements in the normal post-ingestive modulation of oral feeding responses.

Animals↗
PubMed1980

Oral induction of the insulin hyper-responsiveness in rats with ventromedial hypothalamic lesions.

Bilateral electrolytic or sham-lesions of the ventromedial nuclei of the hypothalamus (VMH) were performed on fasting (prior to and after the lesion) ether anesthetized rats. Post-operatively (2 hours), sham-operated rats were either offered an oral glucose solution or were submitted to an intravenous glucose injection or were left undisturbed; lesioned rats were offered an oral glucose load or were submitted to an intravenous glucose injection. Three hours later, the insulin response to an intravenous glucose load was tested in all rats. No significant difference could be detected between the results obtained in the three subgroups of sham-operated rats. By contrast, the VMH lesioned rats exhibited a differential response according to the post-lesion treatment. In lesioned rats, given an intravenous glucose injection in the immediate post-lesion period, the tested insulin response was not significantly different from the response of the controls. When lesioned animals were allowed to taste and ingest as little at 0.5 g glucose, the tested insulin response was greatly enhanced. It is concluded that an oral intake is a prerequisite to the induction of the insulin hyper-responsiveness characteristic of fed VMH lesioned rats and that a 0.5 glucose oral intake is sufficient.

Administration, Oral↗
PubMed1980

Effect of liver denervation on the feeding pattern of rats.

This study was undertaken to assess the role of the hepatic innervation in the short-term regulatory mechanisms of food intake. A liver denervation was performed in male Wistar rats: the liver was entirely freed from the surrounding organs, its vessels (with the exception of the hepatic veins) and the bile ducts were stripped. Controls consisted of two groups of liver-denervated rats in which sympathectomy or vagotomy were carried out. A continuous recording of food intake was performed in a third group. The complete absence of the hyperglycemic response to trauma in adrenalectomized liver-denervated animals was taken as evidence of functional sympathectomy of the liver. The disappearance of a vagovagal reflex--heart rate variation brought about by a glucose injection into the portal vein--was taken as evidence of functional vagotomy. The analysis of the recorded feeding patterns of liver-denervated and sham-operated animals showed that, in rats, this liver denervation did not affect in any way the feeding behavior.

Afferent Pathways↗