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C Burlet

Publications and source records attributed to C Burlet.

At least 19 recordsLinked to original sources
PubMed1995

Neurotensin decreases with fasting in the ventromedian nucleus of obese Zucker rats.

Neurotensin (NT) inhibits food intake when injected either in brain ventricles or in hypothalamic nuclei such as the ventromedian nucleus (VMN). NT concentrations are lower in obese than in lean Zucker rats in several hypothalamic nuclei, including the VMN. In this experiment, we studied the influence of the feeding state on NT concentrations in different brain areas of 10-week-old lean (n = 27) and obese (n = 27) Zucker rats that were fasted for 48 hours and then refed for 6 hours. NT level was measured in the microdissected areas by radioimmunoassay. Obese rats ingested approximately 50% more food than lean rats in the ad libitum (ad lib) condition (P < .001) and 12% more during the refeeding time (NS). NT concentrations in the median eminence (ME) were 50% lower in obese than in lean rats (P < .001). This decrease could be related to a 20% decrease in the arcuate nucleus (ARC) of the obese rats (P < .04). NT concentrations in the ME and ARC, which are important for the control of pituitary hormone secretion by NT, were not changed by the feeding state in both genotypes. NT varied with the feeding state in the VMN only (P < .04). Concentrations were 45% lower in fasted (FD) obese rats than in ad lib or refed (RF) obese rats (1.09 +/- 0.25 ng/mg protein v 1.98 +/- 0.36 ad lib and 1.62 +/- 0.11 RF, P < .05). They remained unchanged in lean rats. NT variations in the VMN of obese rats could contribute synergistically with other neuropeptides to the abnormal feeding behavior of these rats.

3-Hydroxybutyric Acid↗
PubMed1995

The immunological impairment of arcuate neuropeptide Y neurons by ricin A chain produces persistent decrease of food intake and body weight.

Neuropeptide Y is demonstrated as a potent orexigenic peptide when injected into the rat hypothalamic paraventricular nuclei. The neuropeptide Y innervation of paraventricular nuclei originates from both hypothalamic arcuate nuclei and brainstem neurons, whose specific role in the control of food intake is still under discussion. To assess the role of the arcuate neuropeptide Y in the regulation of food intake, we propose a new method for immunologically impairing the neuronal secretion of neuropeptide Y from a unique brain site. The monoclonal antibody to the neuropeptide Y precursor epitope, the C-flanking peptide, was microinjected with two cellular toxins (the ricin A chain and the monensin) into the hypothalamic arcuate nuclei or paraventricular nuclei. One microinjection into the arcuate nuclei reduced the food intake and body weight gain for 10 days. It prevented the food intake stimulation usually induced by a 12 h food deprivation. This decrease of food intake was not due to the aversive properties of monoclonal antibody or cellular toxins, or the immunoneutralization of the biologically active neuropeptide Y, because (i) the acute effect of the microinjection into the arcuate nuclei promoted a transient increase of the food intake likely induced by a strong release of neuropeptide Y from the arcuate neurons which were immunologically damaged, and (ii) the C-flanking peptide monoclonal antibody binds neither neuropeptide Y nor its receptors. The microinjection was inefficient when C-flanking peptide monoclonal antibody was replaced by non-specific rat immunoglobulins or when the C-flanking peptide monoclonal antibody/toxins mixture was injected into the paraventricular nuclei. The data bring further arguments in two domains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Putative neuropeptide Y antagonist failed to decrease overeating in obese Zucker rats.

A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which stimulates food intake and increases early in life in obese rats, plays a major role in the development of this hyperphagia. The aim of our experiment was to test a proposed NPY antagonist namely PYX-2 in obese hyperphagic Zucker rats in order to know if it could be an interesting drug for limiting their food intakes. Four doses of PYX-2 (50-1000 pmol) were injected in a counterbalanced order in the lateral brain ventricles of 10 adult male Zucker rats. Food intake was recorded 0.5, 1, 2, 3, 6, and 23 h after PYX-2 injection and compared either to the rat's spontaneous food intake or to the food intake following injection of artificial CSF (vehicle) only. It was not modified by any dose of PYX-2 whatever the time considered (1 h after injection: 4.3 +/- 0.5 (1000 pmol) vs 4.6 +/- 0.8 (CSF) g; 23 h period: 27.0 +/- 1.9 (1000 pmol) vs 26.6 +/- 2.9 (CSF) g; N.S.). Thus, PYX-2, the putative NPY antagonist, totally failed to inhibit food intake in the obese rats. The absence of effect of PYX-2 on food intake can be explained by the structure of PYX-2, a modified 27-36 amino acid sequence that may not be recognized by the Y1-type NPY receptors which are involved in the regulation of feeding behavior.

Amino Acid Sequence↗
PubMed1994

Increased threshold concentrations of neuropeptide Y for a stimulatory effect on food intake in obese Zucker rats--changes in the microstructure of the feeding behavior.

A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which strongly stimulates food intake and increases early in life in obese rats, plays a major role in the development of this hyperphagia. The aim of our experiment was to measure the feeding responses of lean (n = 8) and obese (n = 17) male Zucker rats to several doses of exogenous NPY injected in the lateral brain ventricle. We analyzed the microstructure of the rats' feeding behavior with an automatic device for 8 h post-injection. NPY stimulated food intake both in the lean and obese rats in a dose-dependent manner (P < 0.001). However, the minimal effective dose was always 3-4 times greater in the obese rats than in the lean ones (range: 0.43-0.53 vs. 0.12-0.18 microgram/brain; P < 0.001). Meal size, meal duration and time spent eating significantly increased in the lean rats (P < 0.05 or less). The last two parameters also increased in the obese rats but with the highest dose (5 micrograms) only. The obese Zucker rats were therefore less sensitive to NPY than the lean ones, probably because of their already high endogenous NPY levels. The modifications in the eating behavior indicate that NPY could overcome the satiety signals.

Animals↗
PubMed1994

Hypothalamic neuropeptides could mediate the anorectic effects of fenfluramine.

Oxytocin, vasopressin and corticotrophin releasing factor have anorectic properties when injected centrally. We studied the kinetics of these neuropeptides by injecting fenfluramine, a drug which reduces food intake, in Long Evans rats. The drug was injected daily through a double chronic cannula implanted above the paraventricular nucleus of the hypothalamus; the rats had free access to pure macronutrients. The rats lost weight during the treatment. Their total caloric intake decreased mostly because the carbohydrate intake decreased, while the protein intake increased slightly. The synthesis and release of brain oxytocin and vasopressin were increased and the release of corticotrophin releasing factor was stimulated. The neuropeptides could be involved in fenfluramine-triggered mechanisms.

Animals↗
PubMed1994

Changes in hemodynamic and metabolic parameters following induced brain death in the pig.

Changes in hemodynamic and metabolic parameters (systemic oxygen delivery, [DO2], oxygen consumption [VO2], arterial lactate content) in brain-dead and control pigs in the absence of any inotropic or fluid support were studied. Brain death was induced by the inflation of a Foley catheter balloon placed into the subdural space of the animals. Serial atrial natriuretic peptide (ANP) determinations were performed to evaluate concomitant changes occurring in the endocrine function of the heart. Experiments were completed by a volume expansion protocol to provide a dynamic evaluation of these parameters. A significant increase in heart rate (from 113 +/- 5 to 176 +/- 11 beats/min), pulmonary capillary wedge pressure (from 7 +/- 1 to 12 +/- 3 mmHg), dP/dt (from 2040 +/- 340 to 4200 +/- 660 mmHg/sec-1), cardiac output (from 2.4 +/- 0.2 to 3.3 +/- 0.4 L/min), mean arterial pressure (from 66 +/- 8 to 93 +/- 14 mmHg), and systemic oxygen delivery (from 360 +/- 30 to 530 +/- 90 ml/min-1), was observed following brain death induction. These parameters returned below basal values within 60 min. On the contrary, serum lactate and VO2 remained unchanged. Following volume expansion, brain-dead pigs exhibited impaired hemodynamic response, with a significant decrease in dP/dt, MAP, and DO2. These changes were accompanied by a significant decrease in VO2 and a significant increase in lactate plasma levels. At the same time, a similar increase in ANP release was observed in both groups in response to volume expansion, suggesting that despite impaired myocardial contractility, endocrine function of the heart was preserved following brain death. We conclude that brain death leads to early impaired left ventricular contractility, which could be responsible for the changes observed in aerobic to anaerobic metabolism in response to rapid volume infusion. These results suggest that the use of fluid infusion to reduce the need in inotropic support in conventional therapeutic modalities should be used with care in the management of a brain-dead potential organ donor.

Animals↗
PubMed1994

Macronutrient type independently of energy intake modulates hypothalamic neuropeptide Y in Long-Evans rats.

Neuropeptide Y (NPY) induces a robust feeding response when it is injected in the hypothalamus. It stimulates both carbohydrate and fat intakes. Diets rich in either macronutrient are known to induce obesity and to modify feeding behavior. The aim of the present study was to determine the effects of long-term ingestion of these diets on hypothalamic NPY in relation with food intake and body weight gain and composition. For this purpose, three groups of weanling Long-Evans rats were fed either a well-balanced diet, a high-carbohydrate (HC) diet (high starch plus 25% sucrose solution), or a high-fat (HF) diet during 14 weeks. Body weight and food intake were recorded during this period. At the end of the experiment, NPY was measured in several microdissected brain areas, and some adipose tissues (AT) depots were sampled. HF rats weighed significantly more than the two other groups (p < 0.02). They were also fattier (+ 30-50% in AT weights; p < 0.01). Energy intake (EI) of the HC rats was significantly greater than that of the control (+ 15%; p < 0.02) and HF rats (+ 34%; p < 0.01) during the week preceding killing. EI of HF rats over the whole experiment was lower than that of the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Estimation of myocardial interstitial norepinephrine release after brain death using cardiac microdialysis.

Brain death is a pathophysiological condition associated with major hemodynamic changes, temporary myocardial ischemia, and histological damage of the heart. These modifications could be related to a major local release of norepinephrine from myocardial sympathetic nerve endings leading to norepinephrine cardiotoxicity. This study was designed to evaluate the utility of cardiac microdialysis to measure interstitial myocardial norepinephrine release resulting from brain death. The dialysis probe consisted in a 10 x 0.20-mm dialysis fiber with a 18,000 mol wt cutoff. Dialysis probes were implanted into the right and left ventricular walls of the beating heart in anesthetized pigs and perfused with Ringer solution at 2 microliters/min. Dialysate norepinephrine concentration was measured using HPLC with electrochemical detection. The relative recovery rate of norepinephrine in vivo was 34 +/- 4%. Interstitial fluid concentrations were obtained using the following formula: [C]interstitium = [C]dialysate/Recovery in vivo. After brain death, a transient increase in interstitial norepinephrine concentration was observed (from 0.74 +/- 0.20 to 4.50 +/- 0.60 ng/ml and 0.76 +/- 0.20 to 6.2 +/- 0.9 ng/ml in left and right ventricle, respectively, P < 0.01) which far exceeded plasma level increase (from 0.50 +/- 0.10 ng/ml to 0.91 +/- 0.20 ng/ml, P < 0.05). This increase in myocardial norepinephrine was, moreover, biphasic, with a second peak occurring 40 min after brain death. The present study confirms the onset of a dramatic increase in cardiac norepinephrine release from myocardial nerve endings following brain death, and demonstrate the utility of the new cardiac microdialysis technique to assess changes in interstitial fluid content.

Animals↗
PubMed1994

Muscle bioenergetics in obese Zucker rats.

The purpose of this study was to investigate the energetic metabolism in obese Zucker rats, using phosphorus nuclear magnetic resonance spectroscopy at rest and during a 2-Hz muscle stimulation and subsequent recovery. Animals were anesthetized with ketamine (150 mg/kg ip). Fed obese rats and 2-day-fasted obese rats were compared with their normally fed and 2-day-fasted lean litter mates. No differences were found between the two groups for ATP, total creatine, phosphocreatine (PCr), and intracellular pH. Starvation in lean rats resulted in a significant fall in inorganic phosphate (Pi), increased resting ADP level, and decreased PCr and ADP recovery after stimulation. The obese rats exhibited a decreased PCr/Pi and increased ADP at rest and a decreased PCr resynthesis and ADP metabolization rate after stimulation. Muscle stimulation in fasted obese rats induced higher PCr depletion and more pronounced acidosis. These results suggest an in vivo mitochondrial metabolism dysfunction in fasted lean as well as in fed and fasted obese rats.

Adenosine Diphosphate↗
PubMed1994

[Corticotropin-releasing factor and anorexia nervosa: reactions of the hypothalamus-pituitary-adrenal axis to neurotropic stress].

The aim of this study is to obtain CRF (Corticotropin Releasing Factor) stimulation at a suprahypothalamic level with a psychological stressor and to evaluate its response in anorexia nervosa. CRF plays a major role in the mechanisms underlying the hypothalamo-pituitary-adrenal (HPA) system's response to stress. Animal studies clearly showed that CRF is involved both in the adaptation to a novel environment and the regulation of eating behaviour. CRF's staietogenic effect is mediated via the paraventricular nucleus. Three groups of age matched young women were studied: 8 patients meeting the DSM III-R criteria for anorexia nervosa, 8 underweight healthy volunteers and 10 normal weight volunteers. All subjects were submitted to an auditory stimulation test ("psychosocial stress test") consisting of an intellectual task in which maximal performance is impossible to achieve, the subjects being permanently disturbed by various meaningful noises. Subjects were asked to answer self-rating scales for anxiety and tension prior to and after the test. CRF reactivity was measured by salivary cortisol (RIA). After the test, anorexia nervosa patients exhibit a significantly higher salivary cortisol response compared to the normal weight volunteers. In most of cases, salivary cortisol response was not correlated with the psychological variables. The range of the response is very explosive in two anorectic patients. Our data are consistent with the hyperactivity of the corticotropic axis stress response in anorexia nervosa, but request further investigations to prove that.

Acoustic Stimulation↗
PubMed1993

Neuropeptide Y projection from arcuate nucleus to parvocellular division of paraventricular nucleus: specific relation to the ingestion of carbohydrate.

Neuropeptide Y (NPY) injection into the hypothalamic paraventricular nucleus (PVN) stimulates feeding behavior and specifically carbohydrate intake in rats. The present study investigated the relation between endogenous levels of NPY and natural ingestion for carbohydrate. It also examined the possible importance of a specific NPY projection in this relationship, which traverses from cell bodies in the arcuate nucleus (ARC) to terminals in the parvocellular division of the PVN (pPVN). Sprague-Dawley rats were given pure macronutrient diets (carbohydrate, protein and fat), and their daily nutrient intake was recorded for 3 weeks. The rats were sacrificed, and 8 hypothalamic nuclei were micropunched and examined via RIA for endogenous NPY levels. The results demonstrate a strong, positive correlation between daily carbohydrate intake and hypothalamic NPY levels. The relationship was specific to the pPVN (r = +0.71; P < 0.001), ARC (r = +0.57; P < 0.001) and dorsomedial nucleus (DMN, r = +0.52; P < 0.01), and was not observed in any other hypothalamic area, including the magnocellular division of the PVN. In the pPVN, the NPY levels of animals that consumed > 50 kcal of carbohydrate (49 pg/microgram protein) were almost twice that of animals that consumed < 20 kcal of carbohydrate (28 pg/microgram protein: P < 0.01). Furthermore, NPY levels in the ARC were positively correlated with NPY in the pPVN and DMN but not any other nuclei. No relation between hypothalamic NPY and measures of protein or fat ingestion was detected. Levels of NPY were also unrelated to total caloric intake, to body weight at sacrifice, and to body weight gain during the 3-week measurement period. These results, together with other findings, provide support for a role of endogenous NPY and its projection from the ARC to the pPVN, perhaps via the DMN, in controlling natural appetite for carbohydrate.

Animals↗
PubMed1993

Microdialysis in the estimation of interstitial myocardial neuropeptide Y release.

The purpose of this study was to investigate the feasibility of cardiac microdialysis for the in vivo estimation of cardiac interstitial peptide concentrations, and, to determine the changes in neuropeptide Y release in myocardial tissue during experimental brain death in pigs. Using a specifically designed concentric flexible probe, perfused with Ringer solution containing 0.5% of bovine serum albumin at a flow rate of 2 microliters/min, allowed us to obtain a 23 +/- 2% relative recovery rate in vitro. Based on these in vitro recovery data, a regional study of the kinetics of interstitial NPY levels following brain death was obtained by monitoring the changes in NPY dialysate levels recorded from dialysis probes implanted into the right and left ventricular walls of the beating heart in vivo. Basal dialysate NPY levels determined by radioimmunoassay were of 95.2 +/- 7.0 and 93.2 +/- 9.1 pmol/l in left and right ventricle, respectively. Brain death was followed by a sustained 2 h increase in NPY dialysate levels in both ventricles (peak levels: 173.2 +/- 30.9 pmol/l in left ventricle, and 149.7 +/- 23.9 pmol/l in right ventricle), which then returned to control levels. We conclude that cardiac microdialysis is a simple and promising new tool for evaluating the role of peptides in cardiovascular regulation.

Animals↗
PubMed1993

Galanin in the hypothalamus of fed and fasted lean and obese Zucker rats.

Galanin (GAL), a 29 aminoacid peptide, is widely distributed in the central nervous system and especially in the hypothalamus. It strongly stimulates food intake when it is injected in the paraventricular nucleus (PVN) of normal rats. The obese Zucker rat with a well-established hyperphagia is characterized by a general dysregulation of some important neuropeptides involved in the regulation of feeding behavior e.g. neurotensin, NPY or CCK and the aim of this study was to measure GAL in different microdissected brain areas in lean (Fa/Fa) and obese (fa/fa) male Zucker rats. As feeding status may modulate the central peptide concentrations, it was measured in ad libitum fed rats and in 48-h fasted rats of both genotypes. GAL was measured by a specific radioimmunoassay in the arcuate nuclei (ARC) and parvocellular (PVNp) and magnocellular (PVNm) parts of the PVN as well as in the median eminence (ME), median preoptic area (MPOA), supraoptic (SON) and dorsomedian (DMN) nuclei. Two-way analysis of variance revealed a very significant effect of genotype in the PVNp (P < 0.001), SON (P < 0.001) and in the ME (P < 0.02). No significant variations at all were noted in the ARC, PVNm, MPOA and DMN. GAL concentrations were more than doubled in the PVNp and SON of ad lib obese rats when compared to the ad lib lean rats (P < 0.005). On the other hand, in the ME where GAL concentration was about 4-fold greater than in the other areas, there was a 20 to 30% decrease in GAL concentrations in the obese rat (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

K(+)-stimulated neuropeptide Y release into the paraventricular nucleus and relation to feeding behavior in free-moving rats.

Neuropeptide Y (NPY) strongly stimulates food intake when it is injected in the central nervous system and especially in the hypothalamus. The major site of NPY synthesis in the hypothalamus is the arcuate nucleus which projects to the paraventricular nucleus. These two nuclei form the arcuate-paraventricular axis, a local circuit in the control of food intake. It was demonstrated that neuropeptide Y concentration in the paraventricular nucleus can be modified by ingestive or metabolic factors. Actually, these modifications cannot be associated with the existence of a release of neuropeptide Y in this nucleus. That is why we used push-pull perfusion during the light phase in freely-behaving rats with food and water available. Perfusates were collected with standard artificial cerebrospinal fluid (CSF) as medium and hyperosmotic CSF obtained by addition of potassium chloride (55 mM). Hyperosmotic perfusion was repeated a second time for some animals. Results clearly demonstrated that neuropeptide Y is released into the paraventricular nucleus during normal perfusion with a mean value of 35.5 +/- 1.5 pg/tube. The potassium perfusion produced an increase in the release of neuropeptide Y (peak at 71.4 +/- 7.1 pg/tube; p < 0.01), and this phenomenon was reproduced with the second potassium stimulation (peak at 47.7 +/- 2.3 vs pg/tube; p < 0.05). Neuropeptide Y release returned to normal values after or between stimulations. Behavioral analysis showed that these stimulations were associated with an increase in food intake. Neuropeptide Y is therefore physiologically released into the paraventricular nucleus of the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Elevated neuropeptide Y in the arcuate nucleus of young obese Zucker rats may contribute to the development of their overeating.

Neuropeptide Y (NPY) mediates feeding behavior through a local hypothalamic network formed by the arcuate and paraventricular nuclei (the AP axis). In the hypothalamus, NPY is mainly synthesized in neurons of the arcuate nucleus. These neurons project to the paraventricular nucleus, the site where NPY has the strongest stimulatory effects on food intake of Sprague-Dawley rats. In the adult Zucker fatty rat (a genetic model of obesity with a well-established hyperphagia), NPY concentrations in these nuclei are higher than in its lean counterpart. We measured hypothalamic NPY before the appearance of altered eating behavior, e.g., in very young (16-d-old) lean and obese Zucker pups, and in pups at an age when overeating had begun, e.g., a few days after weaning at 30 d. At 30 d, NPY concentrations were significantly higher in obese than in lean rats in the arcuate nucleus (14.2 +/- 0.7 vs. 11.6 +/- 0.5 pmol/mg protein, P < 0.01). This difference was not observed at 16 d. A 160% increase was noted in the paraventricular nuclei of obese rats between 16 and 30 d of life compared with a 100% increase in the lean rats (P < 0.001). Neuropeptide Y concentration was greater in 30-d-old rats than in 16-d-old rats in other areas involved in the regulation of feeding behavior, such as the dorsomedian nuclei and lateral hypothalamus, but the values did not differ between genotypes. Higher NPY concentration was therefore detected early in young obese rats in the main hypothalamic site of NPY synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗