Biomedical subjects

S Nicolaidis

Publications and source records attributed to S Nicolaidis.

At least 55 records · Page 3Linked to original sources

PubMed1992

Umami taste of monosodium glutamate enhances the thermic effect of food and affects the respiratory quotient in the rat.

Having previously shown that orogastric stimulation with carbohydrates or sweeteners triggers an increase in metabolic rate and in respiratory quotient, we investigated the possibility that the umami taste of monosodium glutamate (MSG) could act similarly on metabolic responses to protein ingestion. Monosodium glutamate solutions (0.01 and 0.15 M) or vehicle were infused via an intraoral tube during a standardized meal of chow taken in a metabolic device linked to a computer capable of instantaneously measuring RQ and background (resting) metabolic rate in the freely behaving rat. Monosodium glutamate added to the food resulted in a rapid enhancement of metabolic rate that lasted about 30 min, i.e., the period of the anticipatory fraction of thermogenesis. The RQ also switched towards figures indicative of protein utilization. Monosodium glutamate is ineffective when administered independently of meal taking. Taken together these data indicate that the umami taste of MSG exerts an enhancing and specific action on metabolism that obeys the rules of anticipatory reflexes in the sense that both the metabolic rate and substrate utilization adapt from the very first announcement of ingestion of an extra load of protein.

Animals↗

PubMed1992

Spontaneous feeding-related monoaminergic changes in the rostromedial hypothalamus revealed by microdialysis.

The activity of hypothalamic monoamines in response spontaneous feeding was investigated using the in vivo technique of brain microdialysis together with the instrumental recording of feeding pattern. The simultaneous variations of dopamine (DA), serotonin (5-HT), and their respective metabolites, DOPAC and 5-HIAA, were measured in the rostromedian hypothalamus, where the probe was located between the PVN and VMH. Throughout the experiment, the changes in DOPAC followed a mirror image of those in DA: DA regularly increased, reaching its zenith within the 15-min sample collected during the meal before returning to the same level as just before the meal. Following a premeal plateau, both 5-HT and 5-HIAA increased as soon as the beginning of feeding; 5-HT reached its zenith during the meal while 5-HIAA showed a more delayed and prolonged increase. When a new meal was initiated, 60 to 70 min later, a similar monoaminergic pattern was observed again. These data suggest that building up hunger is announced by an ascending slope of DA and setting up of satiation is concomitant with a descending slope of DA. Concerning serotonergic changes, the sharp 5-HT release during the meal would be a signal of satiation (transient preabsorptive fullness) while the longer-lasting increase in 5-HIAA, reflecting 5-HT synthesis, would be associated with satiety (more persistent postabsorptive state substituting satiation). These data partially confirm and extend previous pharmacological studies as well as the findings on deprivation-induced, imposed meals. They suggest a possible causal relation between monoaminergic changes and behavioral initiatives.

Animals↗

PubMed1992

The metabolic signal of hunger and satiety, and its pharmacological manipulation.

Hunger is elicited by the depletion of available macronutrients to the cells. The question is how the depletion is sensed and transduced into a biologically meaningful signal of hunger. Accumulating data show that the signal comes not from depletion of carbohydrates alone or from one of the other major macronutrients. Instead, the signal is generated by the overall cellular power production that induces hunger when it decreases and satiety when it increases. As for satiation, i.e. the state that causes the termination of a meal before nutrients cross the intestinal barrier, it is induced by early metabolic events elicited reflexly from orogastric afferences and tuning the preprandial metabolism towards the level of the postprandial metabolism. Neuronal responses from the medial hypothalamus suggest that they may integrate information on the degree of utilization of glucose and of lipids. Some of the pharmacological agents that reduce feeding seem to operate by increasing the metabolic rate in a way similar to that induced by a meal. These pharmacological agents are active because they mobilize endogenous metabolites, such as lipids, so inducing a sort of 'autocanibalic' meal.

Animals↗

PubMed1991

Organum cavum pre-lamina terminalis, an undescribed brain organ in rats: morphology and physiology.

Morphological as well as physiological findings reported here point to the existence of a previously undescribed brain organ we refer to as the organum cavum pre-lamina terminalis (OCPLT). The organ is a hollow, sagittal, forebrain structure consisting of a vertical interhemispheric horn that overlies the anterior aspect of the lamina terminalis and a horizontal horn that lies in the septum below the corpus callosum. This horizontal horn was previously referred to as the cavum septi pellucidi, a vestigial anatomic curiosity. The narrow cavities of the horizontal and vertical horns join under the genu of the corpus callosum and communicate freely. The two horns do not communicate with the cerebral ventricular system or the subarachnoid spaces. Microinjections of greater than or equal to 0.2 ng angiotensin II into all regions of the cavity resulted in significant drinking, whereas injections into areas surrounding the cavities were ineffective. These data show that the organ is a discrete brain entity and displays high sensitivity to angiotensin II. These findings suggest that the OCPLT is another brain organ with significant effects on fluid and electrolyte homeostasis and perhaps other brain functions.

Angiotensin II↗

PubMed1990

Extracellular dehydration during pregnancy increases salt appetite of offspring.

The propensity to prefer and to consume salty foods varies considerably from person to person, and excessive salt intake has been linked to a number of pathological conditions. Extracellular dehydration occurs in humans after vomiting or diarrhea and is commonly observed during pregnancy. Because the hormonal responses to extracellular dehydration are known to increase salt appetite, we tested the hypothesis that extracellular dehydration during pregnancy increases the propensity of offspring to consume salt. Pregnant rats were treated with polyethylene glycol, which is known to produce extracellular dehydration and to exaggerate sodium appetite. The offspring of these treated pregnant rats showed an increase in salt appetite as compared with the offspring of control untreated dams. These results demonstrate that extracellular dehydration during pregnancy can enhance the natriophilic propensity in offspring and suggest that gravidic vomiting may contribute to the epidemiological factors of hypertension and other pathologies.

Animals↗

PubMed1989

Increased food intake and carbohydrate preference in the rat following treatment with the serotonin antagonist metergoline.

The effect on feeding of antagonism of the serotonergic system was studied. Intraperitoneal injection of one of 8 doses of the serotonin antagonist metergoline (MET) (0.06-1.5 mg.kg-1) given prior to a 3 h food deprivation produced a significant dose-related increase in intake of a standard laboratory diet throughout a 2 h measurement period. A 1 mg/kg dose of MET administered prior to one of 3 isocaloric powdered diets a medium carbohydrate, a high carbohydrate, and a non-carbohydrate diet - produced a significant increase in the intake by rats of all 3 diets in the first hour after food presentation. However, in the second hour MET continued to increase consumption of the high carbohydrate diet, whereas intakes of the medium carbohydrate and non-carbohydrate diets were no longer affected by MET treatment. These data suggest that the serotonergic system is a tonic inhibitor of food intake and of carbohydrate preference.

Animals↗

PubMed1989

Effects of food intake and body weight on a serotonergic turnover index in rat hypothalamus.

Absolute levels and ratio of serotonergic compounds in food-related hypothalamic nuclei were determined with a chromatographic method comparing for control (C) versus lean (L) versus obese (O) rats. In all three groups, a second parameter, i.e., fasting (F) versus satiation (S) was superimposed on the body weight factor. Indoleamine levels failed to show statistical differences depending on the body weight and/or the nutritional status. A significant negative correlation between an index of the serotonin turnover, the 5-HIAA/5-HT ratio, and body weight was found for the paraventricular (PVN) nucleus in the C and L groups as well as for the lateral (LH) nucleus for the C and O groups. A positive correlation was found for the ventromedian (VMH) nucleus in the O group. These data suggest that the body weight factor is implicated in the central serotonergic regulation more than the feeding parameter.

Animals↗

PubMed1989

Metabolic rate and feeding behavior.

According to the ischymetric hypothesis, hunger is induced by the decrease of overall metabolic rate. In order to assess such a mechanism, it was necessary to monitor the muscular contraction-free metabolic rate designated "métabolisme de fond" (MF) in rats that were either resting or moving. MF was then examined in relation to either spontaneous or induced feeding patterns. A computerized open-circuit gas analysis system allowed us to monitor MF and behavior and to show that the onset of a spontaneous meal was preceded by a decrease of MF and its termination is preceded by a rebound of MF. Pharmacological blockade of utilization of both glucose and lipids enhanced feeding only to the extent that it reduced MF. These findings apply to pharmacotherapy because the anorexigenic effect of dexfenfluramine results from the enhancement of MF induced by the capacity of this drug to mobilize endogenous fat reserves and to so provide an endogenous meal that inhibits the exogenous meal. The ischymetric mechanism of hunger does not exclude important modulatory input from hormonal, circadian, and environmental factors in the control of feeding.

Animals↗

PubMed1988

Evidence for vasopressin V1 receptors of rostrodiencephalic neurons: iontophoretic studies in the in vivo rat. Responses to oxytocin and to angiotensin.

Extracellular recordings were obtained in anaesthetized rats from single neurons located in various structures around the rostral end of the third ventricle, known to harbour integrative neurons sensing deficiencies in and originating corrective responses for water-electrolyte balance. Once arginine vasopressin (AVP) responsive neurons were located, a selective antidiuretic agonist (binding to V2 receptors) and either V1 (pressor response related) or V2 (antidiuretic) antagonists were iontophoretically applied. Neurons in this region did not respond to the V2 agonist and only the V1 antagonist was able to block the response to AVP. It is assessed that the investigated region has neurons equipped only with receptors of the V1 type. Interestingly, a number of these neurons also responded to angiotensin II (AII), oxytocin and to blood pressure changes. The integrative neuronal population of parasagittal rostrodiencephalic neurons seem therefore to sense indices of haemodynamic changes including their neuro-hormonal signals within the brain such as AII and AVP which bind to V1 (pressor response related) receptors.

Action Potentials↗

PubMed1988

Integrated metabolic control of food intake after 2-deoxy-D-glucose and nicotinic acid injection.

We measured the minute-to-minute respiratory quotient (RQ), total metabolic rate, and the intensity and energy cost of locomotor activity in unrestrained rats with a recently developed open-circuit metabolic device. These measures permitted calculation of the resting metabolic rate (designated métabolisme de fond or MF). Simultaneous monitoring of the meal patterns of the animals allowed correlations between MF and feeding behavior. The major hypotheses proposed to account for the onset of feeding were challenged by pharmacological inhibition of the utilization of glucose and/or lipids. When injected together, 2-deoxy-D-glucose, which blocks glucose utilization, and nicotinic acid, which blocks lipid utilization, had a synergistic effect on MF and on the feeding response. The RQ, which reflects the relative rate of glucose-to-lipid utilization, showed that neither the inhibition of utilization of glucose nor the inhibition of utilization of lipids could account for the magnitude of the feeding response. The signal that best accounted for these examples of experimentally induced feeding is ischymetric (power or rate of energy) in nature rather than solely glucostatic or solely lipostatic.

Animals↗

PubMed1988

[Physiology of food intake and regulation of body weight].

Feeding is often influenced by competitive needs or by environmental factors. Nevertheless, in physiological conditions hunger is elicited by depletion of macronutrients. The first question is what specific signals cause food intake? Recent data suggest that the signal comes not from exclusive depletion of carbohydrates or of anyone type of the major macronutrients but from overall decreased cellular power production (hypoischymetric signal). Locomotion free metabolic rate has been shown to decrease preceding hunger and to increase in order to determine satiety. Satiation, which occurs largely before ingested nutrients can cross the intestinal barrier and replete the inner milieu, obeys a specific mechanism. Following the stimulation by ingestion of the oro-gastro-intestinal receptors metabolic hormones such as glucagon and insulin are released and enhance metabolism of endogenous reserves. The so-induced endogenous "meal" brings about an anticipatory hypermetabolism which inhibits further ingestion. Post-absorptive satiety subsequently will replace the pre-absorptive state of satiation. The long term regulation of body weight is more subtle. When the actual body weight exceeds its defended value, responsiveness towards signals of hunger diminishes. This hyporesponsiveness seems to be a consequent of an enlargement of the microscopic fat depot at the level of hypothalamic receptive structures which parallels the peripheral increase of the macroscopic fat depot. Thus, hunger promoting signals become less effective and feeding decreases. A symmetrical process takes place in case of body weight loss which results in central hyperresponsiveness to hunger related stimuli and thus facilitates feeding and body weight recovery.

Body Weight↗

PubMed1988

Correlation between metabolic and behavioral effects of dexfenfluramine treatment.

The consequences of dexfenfluramine (dFF) treatments on food intake (FI), locomotor activity (LA), respiratory quotient (RQ), and on changes in metabolic rate (MR) and in RQ that are induced by LA and FI, were investigated in 12 female Wistar rats fed ad libitum. Reduction of FI induced by dFF was correlated with an overall decrease in RQ that expresses increased lipogenesis. For a given amount of activity, MR and RQ changes were enhanced by dFF. On the other hand, dFF appeared to increase energy expenditure in relation to FI only to the extent that the energetic cost of LA itself was not taken into account. It is concluded that the anorexia induced by dFF may be due to the peripheral consequences of dFF treatments on the peripheral metabolism of glucides and lipids according to a lipostatic, glucostatic, or an ischymetric mechanism, and that the increase in energy expenditure previously reported after feeding, may reflect an increase in the energy produced in relation to LA rather than an increase in the thermic effect of feeding per se.

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

Dextrofenfluramine increases energy cost of muscular effort.

A peripheral action of dextrofenfluramine (d.FF) was investigated. The effects of d.FF on total energy expenditure (TEE), locomotor activity (LA), and respiratory quotient (RQ) were quantitatively monitored for 22 hours by a computerized metabolic device. The precise temporal evolution of RQ allowed calculation of glucidic versus lipidic substrates used in all instances. It appeared that in d.FF-treated rats, TEE and resting energy expenditure (REE) were not significantly changed, RQ and LA were significantly decreased. Moreover, in d.FF-treated rats. LA induced a two to five fold increase energy expenditure over vehicle-treated control subjects and it was observed that there was an LA related increase in RQ which was not observed in control subjects. Therefore, d.FF causes LA to be a highly inefficient process by inducing what seems to be an exaggerated catabolism of glucides. These may be only partially used for muscular contraction because it was calculated from relative changes in RQ and TEE during LA that 70% of the catabolized glucides seems to be diverted toward lipogenesis. This process probably represents the way futile cycles are triggered by d.FF in order to exacerbate LA associated energy cost.

Animals↗

PubMed1986

Short-term control of feeding: limitation of the glucostatic theory.

In the rat, the short-term effect on spontaneous feeding of intravenous administration of either glucose or glucose plus insulin was investigated. The infusions lasted 4 hours and covered 170% of rats's previously measured spontaneous caloric intake, while control infusions of saline and saline plus insulin were also made. Feeding patterns in subjects' home cages were recorded. Glycaemia and glycosuria were measured in order to asses glucose utilization. When it was infused alone, glucose was utilized at 95% and so covered 160% of oral caloric requirements, while the reduction of oral intake was only 40%. When insulin was co-infused with glucose, utilization reached 100% and oral feeding was reduced by 70%. Saline infusions did not affect oral feeding, and insulin brought about the expected increase in feeding. It is proposed that the mechanism which sustains feeding should depend on multiple macronutrients utilization rather than on one specific chemical family. Furthermore, the fact that insulin has a clear-cut effect, despite its lipogenetic, i.e., metabolite-sequestering properties, favors the ischymetric hypothesis (based on cellular power-production), rather than the energostatic one (based on yields of nutrients).

Animals↗

PubMed1985

Spontaneous and 2DG induced metabolic changes and feeding: the ischymetric hypothesis.

A computer-controlled calorimeter which simultaneously measured respiratory exchanges, locomotor activity, and meal patterns, was used to study Total Metabolic Rate (TM), Locomotor Free Metabolic Rate (LFM), and Respiratory Quotient (RQ) in relation to spontaneous and 2DG induced Food Intake in freely-feeding rats. It appeared that spontaneous and 2DG induced feeding was preceded by a consistant drop of LFM starting about five minutes before a meal and reaching its nadir at the onset of a meal. The simultaneous determination of the RQ did not show any systematic change that would have reflected either a lipo- or a gluco-privic origin of the LFM drop and meal onset. Therefore, the results are in agreement with the ischymetric hypothesis of the control of food intake which proposes that the final signal triggering hunger and satiety is the intensity of cell power production (measured in this experiment through the LFM parameter) which is independent of the glucidic lipidic or protidic origin of the substrate(s) supplying power production.

Animals↗

PubMed1985

Iontophoretic application of angiotensin II, vasopressin and oxytocin in the region of the anterior hypothalamus in the rat.

The anterior hypothalamus has been implicated in the regulation of hydromineral balance, drinking, vasopressin release, sodium excretion and blood pressure control. Using anaesthetized rats, we have looked at the activity of cells in this region through using a recording electrode cemented to a 7 barrelled iontophoretic electrode inserted ventrally. Cells were tested for their responsiveness to iontophoretic application (Io) of angiotensin II (AII), vasopressin (AVP) and oxytocin (Ox). Of the 47 cells found to responsive to Io glutamate, 23 increased firing to AII, 18 to AVP and 6 to Ox. Nine cells responsive to AVP also responded to AII. Two cells responded to both Ox and AII. It appears that this rostral diencephalic area has neurons sensitive to more than one of the hormones implicated in the various responses involved in hydromineral regulation.

Angiotensin II↗

PubMed1985

Neuronal responses in subfornical organ and other regions to angiotensin II applied by various routes.

Effects of Angiotensin II (AII) and of signals of hydromineral deficiencies on neuronal firing in the subfornical organ (SFO) and the surrounding regions of the rat were examined. AII was applied in three ways: electrophoresis, intracarotid injection, or intracerebroventricular injection. Seventeen SFO neurons (52%) were facilitated by electrophoretic AII and one (3%) was inhibited (AII-responding neurons). Neurons in other regions (cerebral cortex, nucleus triangularis septi, hippocampus, nucleus periventricularis) were also facilitated (23%) or inhibited (14%). Prostaglandin (PG)F2, a universal vasoconstrictor, produced an effect similar to that by AII on neuronal activity of the SFO and surrounding regions, and this effect was antagonized by (NO2-), a vasoplegic agent. Intracarotid injection of AII caused biphasic facilitation of SFO activity. The second increase correlates with changes in blood pressure. Intraventricular injection of AII caused drastic and long lasting excitation of SFO activity. Simultaneous intraventricular application of NO2- blocked the AII effect on SFO neurons but not on blood pressure. Hypovolemia or cerebrospinal fluid withdrawal that might cause mechanical stimulation of circumventricular organs increased SFO neuronal activity. These results are compatible with the vasoconstriction hypothesis of an indirect effect of AII through change in diameter of the vasa that surround neurons.

Action Potentials↗