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Biomedical subjects

J Danguir

Publications and source records attributed to J Danguir.

At least 19 recordsLinked to original sources
PubMed1995

Increased fat oxidation during Ramadan fasting in healthy women: an adaptative mechanism for body-weight maintenance.

Possible effects of Ramadan fasting on anthropometric and metabolic variables were investigated in healthy Tunisian Moslem women. Total daily energy intake remained unchanged whereas the qualitative components of nutrients were markedly affected. Neither body weight nor body composition were influenced by Ramadan fasting. Results also indicate the concomitant decrease of plasma insulin concentrations with respiratory and energy expenditure during Ramadan. The circadian evolution of nutrient oxidation rates was modified. Fat oxidation was increased and carbohydrate oxidation was decreased during the light span of the nycthemeron. Qualitative and quantitative circadian changes in feeding associated with Ramadan might be counterbalanced by specific metabolic changes in order to preserve normal body weight and composition.

Adaptation, Physiological↗
PubMed1989

Reversal of desipramine-induced suppression of paradoxical sleep by a long-acting somatostatin analogue (octreotide) in rats.

EEG sleep recordings were performed in rats under intraperitoneal injections of saline, desipramine (DMI, 4 mg/kg) an inhibitor of noradrenaline reuptake, and DMI plus the octapeptide somatostatin analogue (octreotide, 0.2 mg/kg). As already reported, DMI resulted in selective suppression of paradoxical sleep (PS) and increased slow wave sleep (SWS). The administration of the octapeptide somatostatin analogue totally reversed the DMI-induced suppression of PS, but had no effect on SWS. This finding confirms previous results demonstrating a role of somatostatin in the generation of PS. In addition, it suggests that the suppression of PS by DMI may be due to an inhibitory effect on somatostatin release, rather than to an alteration of brain noradrenaline.

Animals↗
PubMed1989

Dextrofenfluramine, but not 8-OH-DPAT affects the decrease in food consumed by rats submitted to physical exercise.

The effects of physical exercise (1 hr of treadmill running) on nocturnal food consumption were investigated in trained rats. On the basis of previous reports which indicated that exercise increases central 5-HT synthesis, we also measured the consequences of 5-HT (indirect or direct) agonist administration. Noncumulative food intake data revealed that exercise diminished food consumption during the late postexercise periods whereas that of the first 4 hr of analysis remained unaltered. Treatment with dextrofenfluramine (d-FEN) at the end of the exercise session promoted hypophagia in both groups of rats; however, the anorexigenic effect of the 5-HT releaser and 5-HT uptake inhibitor d-FEN was found to be more pronounced in the runners. Lastly, an attempt was made to modify the feeding consequences of exercise by administering at the end of running an orexigenic compound, namely the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). At the two doses used, 8-OH-DPAT proved to be inactive on the respective amounts of food consumed by the controls and the runners. The data obtained herein suggest that (a) moderate exercise promotes late hypophagia, (b) 8-OH-DPAT is devoid of hyperphagic property when administered at the onset of the dark cycle, i.e., when the rats normally begin their gross daily food intake. The data obtained from the d-FEN study suggest that exercise-induced alterations in central serotonergic system could participate in the consequences of exercise on feeding behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Sleep patterns in the genetically obese Zucker rat: effect of acarbose treatment.

Sleep patterns were continuously recorded in the genetically obese Zucker rat. Under normal feeding conditions, Zucker rats showed large amounts of slow-wave sleep (SWS) and normal amounts of pardoxical sleep (PS). In addition, both SWS and PS were equally distributed throughout the nychthemeron. When acarbose (an alpha-glucosidase inhibitor that slows absorption of glucose, reduces plasma insulin, and increases plasma somatostatin) was added to food pellets, the daily duration of SWS was markedly decreased, whereas PS was significantly increased. These results clearly show that sleep in the Zucker rat differs substantially from that classically observed in normal lean rats. In addition, they suggest that anomalies of insulin and somatostatin production and/or levels may cause the sleep disturbances observed in Zucker rats.

Acarbose↗
PubMed1988

Scopolamine-induced suppression of paradoxical sleep is reversed by the somatostatin analogue SMS 201-995 in rats.

The intraperitoneal administration of the octapeptide somatostatin analogue SMS 201-995 produced a significant increase in paradoxical sleep (PS) in rats. The suppression of PS by the muscarinic receptor blocker scopolamine was reversed by SMS 201-995. These findings confirm previous results demonstrating a role of somatostatin in the generation of PS. In addition they suggest that the suppression of PS by scopolamine may be due to an inhibitory effect on somatostatin release, rather than to an alteration of cholinergic function alone.

Animals↗
PubMed1988

Somatostatin antiserum blocks carbachol-induced increase of paradoxical sleep in the rat.

Injection of carbachol into the nucleus tractus solitarius (NTS) produced an increase of paradoxical sleep (PS). When somatostatin antiserum (SRIF-AS) was infused continuously following carbachol injection, the increase in PS was blocked. These results suggest that carbachol-induced increase in PS is mediated by somatostatin. In addition, they confirm the role of somatostatin in the generation of PS.

Animals↗
PubMed1987

Cafeteria diet promotes sleep in rats.

Sleep patterns were continuously recorded in male Wistar rats receiving a palatable, mixed, high-energy diet with chow for ten consecutive days. Results were compared with sleep data obtained from the same rats when offered only normal laboratory chow. The "cafeteria" choice of diets resulted in a significant increase of the daily duration of both slow wave sleep (SWS) and paradoxical sleep (PS). SWS was increased during the light and dark phases of the day-night cycle, whereas PS was augmented only during the light phase. The increased sleep duration was mainly due to a significant lengthening of the respective episodes. When the cafeteria-diet was withdrawn, SWS and PS remained elevated for 3 days and 1 day, respectively before returning to normal levels. The present findings are discussed with regard to present knowledge of sleep mechanisms. A possible role of increased sleep in the development of obesity is also suggested.

Animals↗
PubMed1987

Pulsatile secretion of growth hormone and insulin in relation to feeding in rats.

In unrestrained male Wistar rats chronically implanted with intracardiac catheters, blood samples were taken every 20 min throughout the 24 h of the diurnal cycle. Plasma concentrations of growth hormone (GH), insulin, and glucose were measured. The pattern of food intake was continuously monitored. The existence of 3-h pulsatile cycles of GH secretion was confirmed. In addition, short bursts of insulin secretion were observed in the middle of every second GH peak-to-peak interval. Food intake appeared to be enhanced during short periods that corresponded with GH release into the blood and was reduced during the GH peak-to-peak periods in which the bursts of insulin secretion were observed. From these observations this study draws a schematic relationship between the rhythmicity of the secretion of GH and insulin and the probability of occurrence of feeding. We speculate that the rhythmic endocrine activity may be causally related to feeding.

Animals↗
PubMed1986

Intracerebroventricular infusion of somatostatin selectively increases paradoxical sleep in rats.

Chronic intracerebroventricular (i.c.v.) infusion of somatostatin (SRIF) elicited a specific increase of the daily duration of paradoxical sleep (PS) in rats. I.c.v. administration of cysteamine, a selective SRIF depletor, brought about a dose-dependent reduction of PS. Slow wave sleep (SWS) remained unaffected in both cases. These results suggest that SRIF may be involved in the regulation of PS.

Animals↗
PubMed1986

Apomorphine and haloperidol effects on striatal 3H-dopamine release in anesthetized, awake restrained and freely moving rats.

The ability of apomorphine (APO) and haloperidol (HAL) to affect the spontaneous release of newly synthesized 3H-DA in the striatum was studied in halothane anesthetized, gallamine paralyzed, awake restrained and freely moving rats. The striatum was continuously superfused through a push-pull cannula with a physiological medium enriched in 3H-tyrosine. Basal levels of 3H-DA release were different in the four experimental models: highest in halothane anesthetized rats, intermediate in awake restrained and gallamine treated rats and lowest in freely moving rats. In all experimental models IV or SC injection of APO (1 mg/kg) inhibited the release of 3H-DA (30-50%) from 15 to 90 min following its administration. In awake restrained and freely moving rats, stereotyped behaviour was observed for one hour following the APO injection. In halothane anesthetized rats the inhibitory effect of APO on 3H-DA release was prevented by pretreatment with HAL (2 mg/kg IV). Injection of HAL (2 mg/kg IV or SC) failed to enhance the release of 3H-DA in anesthetized and awake restrained rats, whilst a long-lasting increase in 3H-DA release was observed in gallamine treated and freely moving animals (55% and 120% respectively). However, catalepsy was observed in both restrained and freely moving rats. It is concluded that the modifications of 3H-DA release produced by HAL but not those produced by APO are dependent on the experimental model used, a fact possibly related to the different sites of action of these two drugs.

Anesthesia, General↗
PubMed1985

Superfusion of clomipramine within the ventromedial hypothalamus selectively suppresses paradoxical sleep in freely moving rats.

Sleep patterns were continuously recorded in rats which received during 2 hours and a half a push-pull superfusion of clomipramine at 10(-6) mol/l or 10(-8) mol/l concentrations, within the ventromedial hypothalamus. The superfusion of 10(-6) mol/l clomipramine resulted in a suppression of paradoxical sleep (PS) and a reduction of slow wave sleep (SWS), whereas lower concentrations of this drug (10(-8) mol/l) suppressed PS but did not affect SWS. In both cases, a secondary rebound of PS was observed. These findings are discussed with regard to the present knowledge of the role of the hypothalamus in sleep.

Animals↗
PubMed1984

Chronic intracerebroventricular infusion of insulin causes selective increase of slow wave sleep in rats.

Sleep patterns were continuously recorded in rats receiving chronic intracerebroventricular (i.c.v.) infusions of insulin. The i.c.v. administration of insulin resulted in a selective increase (25%) of the daily duration of slow wave sleep (SWS), whereas the duration of paradoxical sleep (PS) remained unchanged. The neutralization of peripheral and/or central insulin by means of continuous intravenous or i.c.v. infusions of anti-insulin serum brought about a selective decrease of SWS, whereas PS remained unchanged. The present findings are discussed with regard to the present knowledge of the origin and the role of brain insulin.

Animals↗
PubMed1984

Sleep deficits in diabetic rats: restoration following chronic intravenous or intracerebroventricular infusions of insulin.

The role of insulin in sleep was investigated in the present study by using streptozotocin-induced insulin deficiency in rats. Our previous studies showed a selective increase in the daily duration of slow wave sleep following either peripheral or central administration of insulin in normal rats. We now report sleep deficits following the pharmacological destruction of pancreatic B insulin-producing cells. The daily duration of both slow wave sleep (SWS) and paradoxical sleep (PS) were decreased on the third day following the injection of streptozotocin. However, only SWS remained lower than the control levels two weeks after the treatment whereas PS returned to normal values. The continuous intravenous infusion of exogenous insulin (2 IU per 24 hr) brought about a selective restoration of SWS in insulin-deficient and hyposomniac rats. A dose-dependent restoration of SWS was also observed when exogenous insulin was continuously administered intracerebroventricularly in streptozotocin-treated diabetic rats. Although the mechanism of the induction of sleep by insulin remains to be elucidated, these results clearly support its hypnogenic properties. A possible direct action of insulin on brain cells is suggested.

Animals↗
PubMed1984

Brain amine metabolism is reflected in cerebral ventricular CSF.

The choroid plexuses are suspended within the ventricles and account for approximately 75% of CSF production. The sodium-potassium ATPase operates within the choroidal epithelial cells and moves sodium ions towards the ventricular surface and potassium ions in the direction of the stroma. Water flows into CSF along osmotic gradient produced by sodium pump. The existence of extracellular channels by which brain metabolites could passively diffuse into the ventriculosubarachnoid space suggests an excretory role for CSF. Removal of solutes from the CSF could occur across the choroidal epithelium or arachnoid membrane into the blood. Systematically administered monoamine metabolites do not cross the blood-brain or the blood-CSF barrier. The regional concentrations of amine metabolites in the CSF is in part a reflection of the concentration of catecholamines and indoleamines in the immediately adjacent neuronal parenchyma. In order to illustrate the validity of monoamine metabolite determinations in cerebral ventricular CSF we developed a device which allowed for a continuous third ventricular CSF withdrawal in freely moving (or anesthetized) rats at a constant flow of 1 microliter/min. The elevation of biogenic amine metabolites in CSF by probenecid or their decline by monoamine oxidase inhibition was used to assess the rate of turnover of amines. Pharmacological manipulations (yohimbine, haloperidol, ouabain) resulted in mono-amine metabolite fluctuations in CSF similar to those previously described in brain tissue. Insulin administration caused an abrupt decrease in CSF glucose and elevated dopamine and serotonin metabolites in rats which had no access to food. These studies demonstrate the adaptation of in vivo analysis of CSF in rats but also exemplify the usefulness of monoamine metabolite determination in the CSF as indicators of brain function.

Amines↗
PubMed1982

LCEC monitoring of 5-hydroxyindolic compounds in the cerebrospinal fluid of the rat related to sleep and feeding.

A new technique which allows for both the chronic withdrawal of CSF and continuous recording of EEG sleep patterns and food intake in the freely moving rat is described. Liquid chromatography with electrochemical detection (LCEC) was used for the direct assay of tryptophan metabolites in the CSF. Both 5-hydroxyindolacetic acid (5-HIAA) and 5-hydroxytryptophan (5-HTP) were easily detectable. However, serotonin (5-HT) levels were relatively low and 5-hydroxytryptophol (5-HTPhol) and N-methylserotonin (N-Me-5HT) were undetectable in several cases. The continuous monitoring of 5-HIAA and 5-HTP indicated stable values throughout the 3-hr experiments during which no food or small meals were consumed. In the rat which consumed a large meal, both 5-HIAA and 5-HTP significantly increased following that meal. This increase in metabolites may be the result of an increased availability of tryptophan to the brain as a result of the meal. Although this study is preliminary, the described technique can provide further information about the possible relationship between behavioral (sleep and/or feeding) changes and the concomitant neurochemical fluctuations.

5-Hydroxytryptophan↗
PubMed1980

Cortical activity and sleep in the rat lateral hypothalamic syndrome.

Continuous EEG recordings were performed in lateral hypothalamic (LH) damaged rats from day 1 post-lesion when totally aphagic and adipsic until complete recovery of their feeding and drinking. During the early post-operative stage (days 1--3 post-lesion), LH rats showed a complete disorganization of their basal EEG which was characterized by two superimposed activities, a constant rapid low voltage activity modulated by high voltage low frequency waves. Except in the case of intense illumination, several arousing stimuli did not affect this activity. By day 4 post-lesion, the two overlapping activities were replaced by less abnormal waves on top of which the first normal sleep spindles appeared. Sleep increased gradually and normal amounts of both slow-wave and paradoxical sleep were observed during 'stage 4' of recovery when rats again ate food and drank water. During this stage, and contrary to normal rats, meal size was correlated only with sleep events occurring within the intermeal interval following the next meal, when most of the ingested nutrients reached the systemic compartment. The effect of sleep of intragastric or intravenous caloric repletion was, at least in part, in agreement with the view of indirect effect of LH lesions on sleep through metabolic impairment. Whatever the mechanism underlying sleep deficits, these are one of the major symptoms of the lateral hypothalamic syndrome.

Animals↗