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Biomedical subjects

C Burlet

Publications and source records attributed to C Burlet.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1992

Early modification of neuropeptide Y but not of neurotensin in the suprachiasmatic nucleus of the obese Zucker rat.

Hyperphagia in the obese Zucker rat is characterized by the early modification of the dark/light (D/L) rhythm of food intake. This rhythm is mainly driven by the suprachiasmatic nucleus (SCN) and, more controversially, by the ventromedian nucleus (VMN). In the SCN of adult obese Zucker rat, the concentrations of neuropeptide Y (NPY), a potent stimulator of food intake, are increased whereas those of neurotensin (NT), an anorexigenic peptide, are decreased. However, nothing is actually known about the synchronicity of the dysregulation of the D/L rhythm and variations of these peptides. That is why we measured NPY and NT in the microdissected SCN and VMN of lean (n = 16) and obese (n = 15) Zucker rats before the occurrence of hyperphagia (day 16 of age) and a few days after weaning (day 30 of age) when the modifications are apparent. For NPY, there was a very significant effect of age (P less than 0.001) for both nuclei and a significant effect of genotype (P less than 0.02) for the SCN only. NPY concentrations increased between 16 and 30 days in both nuclei (+74% (SCN) and +70% (VMN) in the obese rat; +57% (SCN) and +67% (VMN) in the lean rat; P less than 0.001). NPY in the SCN was not different at 16 days of age between lean and obese rats but significantly increased at 30 days in the obese rat (22.6 +/- 1.2 vs. 18.6 +/- 1.5 ng/mg protein; P less than 0.05). NT was not detected in the SCN of either group at 16 days or at 30 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Alteration of pituitary-adrenal responses to adrenalectomy by the immunological targeting of CRF neurons.

We previously demonstrated that cellular toxins added to a cytotoxic IgG2a monoclonal antibody to corticotropin releasing factor (CRF-MAb) may specifically penetrate some hypothalamic CRF neurons, after central injection near the paraventricular nuclei. We attempt here to evaluate the consequential effects on the CRF neurons functioning. Such a toxic mix, 4 weeks after its central injection, caused a marked reduction (66%) of the chronic adrenocorticotropic hormone (ACTH) release in response to a bilateral adrenalectomy (7th day). This change was accompanied by a reduction in the CRF concentration (43%) measured in the median eminence. We concluded that specific internalization of toxins, by the way of CRF-MAb, leads to a long-term dysregulation of the CRF synthesis and/or neuronal transport.

Adrenalectomy↗
PubMed1992

Unexpected regulation of hypothalamic neuropeptide Y by food deprivation and refeeding in the Zucker rat.

Neuropeptide Y strongly stimulates food intake when it is injected in the hypothalamic paraventricular (PVN) and ventromedian (VMN) nuclei. In Sprague-Dawley (SD) rats, NPY synthesis in the arcuate nucleus (ARC) is increased by food deprivation and is normalized by refeeding. We have previously shown that the obese hyperphagic Zucker rat is characterized by higher NPY concentrations in this nucleus. NPY might therefore play an important role in the development of hyperphagia. The aim of the present study was to determine if the regulation by the feeding state works in the obese Zucker rat. For this purpose, 10 weeks-old male lean (n = 30) and obese (n = 30) Zucker rats were either fed ad libitum, either food-deprived (FD) for 48 hours or food-deprived for 48 h and refed (RF) for 6 hours. NPY was measured in several microdissected brain areas involved in the regulation of feeding behavior. NPY concentrations in the ARC was about 50% greater in obese rats than in lean rats (p less than 0.02) whatever the feeding state. In the VMN, NPY concentrations were higher in the lean FD rats than in the obese FD rat (p less than 0.001). Food deprivation or refeeding did not modify NPY in the ARC, in the VMN or in the dorsomedian nucleus whatever the genotype considered. On the other hand, food deprivation induced a significant decrease in NPY concentrations in the PVN of lean rats. This decrease was localized in the parvocellular part of this nucleus (43.0 +/- 1.9 (FD) vs 54.2 +/- 2.1 (Ad lib) ng/mg protein; p less than 0.005). Ad lib levels were restored by 6 hours of refeeding. These variations were not observed in the obese rat. The regulation of NPY by the feeding state in the Zucker rat was therefore very different from that described in the SD rats. Strain or age of the animals used might explain these differences. High NPY levels and absence of regulation in obese Zucker rats could contribute to the abnormal feeding behavior of these rats.

Animals↗
PubMed1992

Central effects of monosodium glutamate on feeding behavior in adult Long-Evans rats.

Monosodium glutamate (MSG) is known as a neurotoxic molecule when injected neonatally in rats, where it produces a marked decrease in food intake and an increase in adipose tissue mass. But, in adult rats subcutaneous injections of MSG produce a small, dose-dependent increase in food intake. It is not known if this action is centrally or systemically mediated. Therefore, the feeding pattern of adult rats injected intracerebroventricularly with MSG was measured. Seven days after installation of a cannula in the right lateral ventricle, rats were injected either with artificial cerebrospinal fluid or twice with 3 mg/brain MSG within a 3-day interval. The feeding pattern was recorded via a complete computerized system during 24 h. Feeding behavior was significantly modified by MSG treatments. These effects were observed immediately after drug injections, that is, upon the first meal, as well as during the 24 h that followed. For the first meal, modifications in meal size (+285%; p = 0.0001), meal duration (x10; p = 0.0005), postmeal interval (x4; p = 0.0005), and the satiety ratio (-50%; p = 0.01) were observed. During the 24-h postinjection period, modifications in meal number (-3; p = 0.0007), total amount of food eaten (+21%,; p = 0.007), time spent eating (+40%; p = 0.007), meal duration (+53%; p = 0.005), and meal size (+44%; p = 0.01) were noted. When the two MSG injections were compared, differences were also noted. For the first meal, postmeal interval (-50%; p < 0.005) and satiety ratio (-50%; p < 0.005) were decreased after the second injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1992

Long-term reduction of vasopressin excretion induced by the central injection of an immunoconjugate (antibody to vasopressin linked to ricin A chain).

We have previously demonstrated that vasopressin-producing neurons are the target of monoclonal antibodies to vasopressin microinjected into the brain tissue. At the same time, this central microinjection of vasopressin-monoclonal antibody into the supraoptic nuclei produced hydro-osmotic disorders mimicking the effects of a central diabetes insipidus. In order to investigate the increase in both duration and amplitude of the biological effects seen after the injection of vasopressin-monoclonal antibody, an immunoconjugate was constructed with the vasopressin-monoclonal antibody IgG1k isotype and the cytotoxic part of the ricin molecule, the ricin A chain. The biological parameters, such as diuresis and urine osmolality which are directly regulated by vasopressin, and vasopressin excretion, were measured after the central injection of this immunotoxin/immunoconjugate. The consequences of immunotoxin injection were also studied when immunotoxin was co-injected with monensin (50 nM) which has been shown to decrease the intracellular degradation of immunotoxin, and plasma complement, which has been shown to increase the neuronal uptake of immunotoxin. Single injection of immunotoxin near the hypothalamic supraoptic nuclei significantly increased diuresis and decreased vasopressin excretion. However, these effects were only transient and disappeared 24 h later. Four successive injections of immunotoxin (one per day) with monensin induced a decrease of vasopressin excretion which was still observed after a resting period of four days after the fourth injection. The long-term reduction of vasopressin excretion was induced in rats receiving four successive injections of a mixture consisting of immunotoxin with monensin and plasma complement. In such experiments, the vasopressin content of urine remained low (55% under the baseline value), two weeks after the fourth injection of immunotoxin. At the same time, the diuresis was increased (80% above the baseline value) and urine osmolality lowered (45% under the baseline value). When non-specific IgG replaced specific antibody, vasopressin excretion, diuresis as well as urine osmolality were unchanged. The results of this study demonstrated that the use of a specific immunotoxin results in a local interference with the vasopressinergic neurons and induces a long-term reduction of vasopressin secretion.

Animals↗
PubMed1992

Specific hypothalamic neuropeptide Y variation with diet parameters in rats with food choice.

Neuropeptide Y (NPY) preferentially stimulates carbohydrate intake rather than fat intake but there is no information on the effects of food choice on the concentration of NPY in the brain. We measured brain NPY concentrations in male adult rats that had to choose between a high fat and a high carbohydrate diet or were fed a control diet for 2 weeks. In rats with food choice, energy intake increased (+17%). NPY levels increased in the parvocellular part (PVNp) of the PVN and decreased in the lateral hypothalamus and were significantly correlated with the carbohydrate-to-fat energy ratio but not with total energy intake. This suggests that hypothalamic NPY might be involved in food choice and that PVNp is important in the regulation of feeding behaviour by NPY.

Animals↗
PubMed1992

Changes in endocrine control of electrolyte homeostasis and blood pressure following heart and heart-lung transplantation. A comparative study.

The purpose of this study was to compare the early postoperative effects of heart and heart-lung transplantation on the secretion of atrial natriuretic peptide (alpha-ANP), renin, aldosterone, and vasopressin. This was carried out from the first to the eighth postoperative day in ten heart and five heart-lung recipients. The changes in the release of these hormones were similar in both groups. Vasopressin release remained stable while that of the renin-angiotensin-aldosterone system progressively returned to more normal levels. Grafted heart tissue was capable of high alpha-ANP release early on in both heart and in heart-lung recipients. This sustained alpha-ANP release was not a function of the resulting overall atrial tissue mass. Our findings suggest that it might be the consequence of an intrinsic hypersecretion of alpha-ANP resulting from the loss of normal heart innervation occurring in both heart and heart-lung transplantation.

Adult↗
PubMed1992

Chronic and continuous intracerebroventricular infusion of neuropeptide Y in Long-Evans rats mimics the feeding behaviour of obese Zucker rats.

Neuropeptide Y (NPY), a member of the pancreatic polypeptide family, strongly stimulates food intake when injected centrally in animals. It is found in abundance in the brain and particularly in areas involved in the regulation of feeding behaviour. Moreover, in these areas, NPY concentrations are higher in the obese hyperphagic Zucker rat. The aim of the present experiment was to reproduce in normal Long-Evans rats the high central levels of NPY measured in Zucker rats. We therefore continuously infused NPY in the brain lateral ventricle through osmotic mini-pumps and studied the effects of this infusion on different parameters of the feeding behaviour. Male adult Long-Evans rats were fed ad libitum on a high carbohydrate (HC) diet and on a high fat (HF) diet given simultaneously in two separate cups. NPY was infused at a rate of 0.44 micrograms/h (n = 11) and rats infused with artificial cerebrospinal fluid (n = 11) served as controls. The infusions lasted 14 days. Total food intake markedly increased in NPY infused rats starting on the first day after pump installation (33.7 +/- 1.7 vs. 14.8 +/- 0.6 g/day; P less than 0.0001). This effect lasted for nine days. In these rats, the average food intake during the infusion period (21.0 +/- 1.6 g/day) was also significantly greater than during the pre-infusion period (13.1 +/- 0.5 g/day; P less than 0.0001) and the post-infusion period (10.6 +/- 0.4 g/day; P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗