M J Meile

French National Centre for Scientific Research, Lutetia Parisorum, Île-de-France, France

Are you M J Meile?

Claim your profile

Publications (9)28.63 Total impact

  • Annales D Endocrinologie - ANN ENDOCRINOL. 01/2004; 65(4):246-247.
  • C Rouch, M J Meile, M Orosco
    [Show abstract] [Hide abstract]
    ABSTRACT: In previous studies, we showed that carbohydrate and protein ingestion, respectively, increased and decreased hypothalamic extracellular serotonin and the plasma ratio tryptophan over its competitor amino acids (Trp/LNAAs), reflecting serotonin synthesis. Serotonin levels returned towards baseline 2 h after either meal while the ratio remained altered. The question addressed is the ability of serotonin to respond expectedly to a second meal of the alternate nutrient. Rats were fed with sequential meals of either carbohydrates first and then casein 2 h later or in reverse order. Hypothalamic serotonin was measured using microdialysis. Permanent blood sampling allowed to track in parallel plasma amino acids. A carbohydrate meal increased hypothalamic serotonin, so did a subsequent casein meal. Conversely, following a casein meal that reduced serotonin, a carbohydrate meal also decreased it. The plasma ratio Trp/LNAAs was enhanced by a carbohydrate meal and remained high for 2h. A subsequent casein meal reversed this change but the ratio remained higher than basal values. A first casein meal reduced the ratio that was not increased again by a subsequent carbohydrate meal. It is obvious that ingestion of specific nutrients induce long-lasting metabolic and neurochemical variations that prevent subsequent changes to occur. The lack of expected changes to a second meal addresses again the hypothesis of alternate appetites for carbohydrates and proteins driven by serotonin changes.
    Nutritional Neuroscience 05/2003; 6(2):117-24. · 1.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In neonatal Wistar rats injected with streptozotocin (STZ) at birth (n0-STZ model), a recognized model of beta-cell regeneration, we investigated the capacity of early treatment with glucagon-like peptide 1 (GLP-1) or exendin-4 to promote beta-cell regeneration and thereby improve islet function in the long term, when animals become adults. To this end, n0-STZ rats were submitted to GLP-1 or exendin-4 from postnatal day 2 to day 6 only, and their beta-cell mass and pancreatic functions were tested on day 7 and at 2 months. On day 7, both treatments increased body weight, decreased basal plasma glucose, decreased insulinemia, and increased pancreatic insulin content in n0-STZ rats. At the same age, the beta-cell mass, measured by immunocytochemistry and morphometry methods, was strongly increased in n0-STZ/GLP-1 and n0-STZ/Ex rats compared with n0-STZ rats, representing 51 and 71%, respectively, of the beta-cell mass in Wistar rats, whereas n0-STZ beta-cell mass represented only 21% of the Wistar control value. Despite such early improved beta-cell mass, which is maintained at adult age, the basal and glucose-stimulated insulin secretion (in vivo after intravenous glucose load or in vitro using perfused pancreas) were not improved in the 2-month-old n0-STZ rats previously treated with GLP-1 or exendin-4 compared with untreated n0-STZ rats. However, both treated groups significantly exhibited a decreased basal plasma glucose level and an increased plasma glucose clearance rate compared with the 2-month-old untreated n0-STZ group at adult age. These findings in the n0-STZ model indicate for the first time that GLP-1 or exendin-4 applied during the neonatal diabetic period exert both short- and long-term beneficial effects on beta-cell mass recovery and glucose homeostasis. However, the increase in beta-cell mass, which is still present in the adult n0-STZ rats previously treated, contrasts with the poor beta-cell responsiveness to glucose. Further studies are needed to understand the dissociation between beta-cell regeneration and the lack of improvement in beta-cell function.
    Diabetes 08/2001; 50(7):1562-70. · 7.90 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sodium (Na+) depletion induces sodium appetite to replenish Na+ loss. It appears to be a consequence of enhanced levels of aldosterone (Aldo) and angiotensin II (AII) in the plasma as well as in the brain. Mineralocorticoid pretreatment modifies the sensitivity of septo-preoptic neurons to locally applied AII and Aldo. Therefore, we investigated septo-preoptic neuronal sensitivities to AII and Aldo, as well as to the specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (Los) and to the specific AII type-2 receptor (AT-2) non-peptide antagonist PD123319 after one Na+ depletion without repletion. We found that one Na+ depletion induced increases in the proportion of neurons inhibited by iontophoretic application of AII (20.5% vs. 7.8%, p=0.004) whereas, the proportion of neurons excited by Aldo was increased, (23.7% vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensitivity to AII after one application of Aldo was increased in the furosemide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhibited by application of losartan was enhanced, (26.4% vs. 9.3%, p=0.03). No significant changes were found in response to PD123319 by itself. Moreover, there were more neurons which co-localized responses to both Los and PD123319 in the furosemide group than in the control group (29.7% vs. 8.6%, p=0.027). It is known that multidepletions induce an increased need-free sodium appetite and our present findings could well form part of the neuronal basis of this behavior.
    Brain Research 04/1998; 787(1):171-4. · 2.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A previous study has shown that DOCA pretreatment altered the responsiveness of neurons to microiontophoretic administration of angiotensin II (AII) and aldosterone (Aldo). This result coincided with an increase in activity in the septo-preoptic region and a decrease in activity of the central nucleus of the amygdala. The latter region is anatomically linked to the bed nucleus of the stria terminalis (BNST). Single unit activity was recorded in the BNST in response to iontophoretic application of AII, non-peptide AII-receptor antagonists or Aldo in DOCA-pretreated and in non-pretreated rats. DOCA-pretreatment significantly decreased the responsiveness to AII (28 cells (18.5%) vs. 8 cells (14.0%) u = 0.018 for excitation and 3 cells (8.6%) vs. 0 cells 0%, u = 0.011 for inhibition, P < 0.05) and to Aldo (24 cells (21.4%) vs. 4 cells (10.2%), u = 0.026 for excitation, and 3 cells (2.6%) vs. 0 cells, u = 0.009 for inhibition, P < 0.05) of the neurons localised in the BNST. A significant decrease was found in the inhibitory responses to iontophoretic application of losartan, an AII type-1 receptor (AT-1) antagonist (u = 0.042, P < 0.05). No significant differences were recorded with iontophoretic application of PD 123319, a specific AII-type-2 (AT-2) receptor antagonist. Therefore AT-1 receptors are likely responsible for the decreased responsiveness of the BNST correlated with the decrease in the activity within the amygdala.
    Regulatory Peptides 10/1996; 66(1-2):59-63. · 2.06 Impact Factor
  • R Caulliez, M J Meile, S Nicolaidis
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to elucidate the role of the neuropil located in the LHA in the acquisition of the association between a taste (conditioned stimulus = saccharin) and a visceral distress (unconditioned stimulus = lithium chloride) leading to long delayed learning of a conditioned taste aversion (CTA). In 82 male rats guide-cannulae were directed bilaterally into the basolateral LHA where bilateral microinjections were made after the conditioned stimulus and before the unconditioned stimulus. We found that: (1) tetrodotoxin, a non-specific blocker of neuronal activity disrupted the acquisition of the CTA; (2) SCH 23390, a specific D1 receptor blocker also disrupted learning of the CTA, while sulpiride, a D2 receptor blocker, did not; (3) neither the specific blockade of D1 nor of D2 receptors could prevent the visceral distress-induced decrease in water intake, showing that the visceral distress was actually experienced; and (4) the sham taste aversion learning (i.e. without visceral distress) revealed that neither the D1 nor the D2 receptors blockade induced by themselves either a taste preference or a taste aversion towards saccharin, indicating that the impaired acquisition of the CTA was not due to a superimposed taste preference that could have been induced by the intra-LHA D1 receptors blockade. It is concluded that the neuropil in the LHA is necessary in the process of the acquisition of long delayed learning and that it uses a D1 receptor specific mechanism.
    Brain Research 09/1996; 729(2):234-45. · 2.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dynamic changes in VMH and PVN monoamines and immunoreactive insulin (IRI) were investigated by microdialysis in freely-moving genetically obese Zucker rats in order to relate possible disturbances to the impaired regulation of food intake of this model. Serotonin (5-HT), 5-HIAA and dopamine (DA) increased at the beginning of spontaneous meals while DOPAC decreased. Although similar in normal and obese rats, these changes were much more dramatic in the latter, as if more "signal" for satiety were necessary at the VMH-PVN level. Glucoprivic feeding or satiety are induced in normal rats by intravenous infusions of insulin or insulin+glucose respectively. The Zucker rat is resistant to these treatments. The monoaminergic changes brought about by these infusions were similar in obese and normal rats (decreases in 5-HT and DA and increases in 5-HIAA and DOPAC), but the occurrence of meals, in the obese, showed a superim-position of monoaminergic changes resembling those related to spontaneous feeding. The monoaminergic effects of insulin must therefore be dissociated from its effects on feeding. Hypothalamic insulin itself might be the brain signal. At the beginning of meals presented for the first time, VMH-PVN IRI increased earlier and with a smaller magnitude in the obese. When the rats were accustomed to scheduled meals, a similar anticipatory increase in IRI was found in both obese and lean rats. This suggests that brain insulin is more than a satiety signal. In addition, in response to an i.v. insulin infusion, IRI increased twice as much in obese rats despite lower basal levels. Whatever the origin of hypothalamic insulin, the larger response of the obese Zucker rat, known to be insulin resistant, may reflect the inefficiency of the peptide in reducing feeding and body weight in this pathological model.
    Obesity research 01/1996; 3 Suppl 5:655S-665S. · 4.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Using microdialysis in freely moving rats, we have been able to observe changes in monoamines from the ventromedial and paraventricular hypothalamic nuclei before, during, and after spontaneous feeding. Because the genetically obese Zucker rat shows abnormalities related both to feeding and monoamines, it was of interest to investigate possible particularities in the monoaminergic variations around spontaneous feeding. The profile of changes in Zucker rats was grossly similar to that of Wistar rats: increases in 5-hydroxy-tryptamine (5-HT), 5-hydroxyindolacetic acid (5-HIAA), and dopamine (DA), and decrease in dihydroxyphenylacetic acid (DOPAC). However, the release in monoamines (5-HT and DA) was more dramatic and longer-lasting than in Wistar rats, while the changes in the metabolites were proportionnally less pronounced. This suggests that high concentrations of these feeding-related amines are released and remain in the synaptic cleft of the obese rat, possibly because they are required in larger amounts to bring about satiety. The hyperphagia of the obese Zucker rat may therefore be the result of a resistance to these prandially released satiety-promoting neurosubstances.
    Physiology & Behavior 07/1995; 57(6):1103-6. · 3.16 Impact Factor
  • A Mokhtarian, M J Meile, P C Even
    [Show abstract] [Hide abstract]
    ABSTRACT: A method is described for stress-free periodic sampling of blood and/or intravenous infusions in the normal awake and behaving mouse. The surgical procedure consists of the permanent implantation of a Silastic-rubber catheter in the right external jugular vein. The free end of the catheter is then pulled subcutaneously up to the skull and fixed on the skull with a form of dental acrylic that sticks firmly on the bone and thus does not require anchor screws in the skull. This technique allowed us to perform glucose tolerance tests in the mouse, and to follow the time course of blood glucose levels in individuals.
    Physiology & Behavior 12/1993; 54(5):895-8. · 3.16 Impact Factor

Publication Stats

277 Citations
28.63 Total Impact Points

Institutions

  • 1998
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 1996
    • Collège de France
      Lutetia Parisorum, Île-de-France, France