Biomedical subjects

Palmiero Monteleone

Publications and source records attributed to Palmiero Monteleone.

27 records · Page 2Linked to original sources

PubMed2003

Circulating levels of neuroactive steroids in patients with binge eating disorder: a comparison with nonobese healthy controls and non-binge eating obese subjects.

OBJECTIVES: Increased plasma levels of allopregnenolone (3alpha,5alpha-tetrahydroprogesterone [3alpha,5alpha-THP]), dehydroepiandrosterone (DHEA), and DHEA sulphate (DHEA-S) have been reported in patients with anorexia nervosa or bulimia nervosa. To assess whether those changes are related to malnutrition, we investigated plasma levels of neuroactive steroids in women with binge eating disorder (BED) who compulsively binge as bulimic patients, but do not incur malnutrition. METHODS: Sixty-eight women participated in the study (31 nonobese healthy controls, 9 nonobese patients with BED, 16 obese patients with BED, and 12 obese non-binge eating women). Blood samples were collected in the morning for determination of plasma levels of 3alpha,5alpha-THP, DHEA, DHEA-S, and cortisol. RESULTS: Nonobese BED women had significantly higher plasma levels of DHEA, DHEA-S, and 3alpha,5alpha-THP than nonobese healthy women. Similarly, obese individuals with BED exhibited significantly higher neurosteroid plasma levels than non-binge eating obese subjects. No significant differences in plasma cortisol levels were observed among the groups. DISCUSSION: This study shows increased plasma levels of neuroactive steroids in BED patients. These findings could have been influenced by methodologic limitations (e.g., the absence of diurnal sampling). However, they suggest that if malnutrition is involved in the determination of increased plasma levels of neuroactive steroids in people with anorexia or bulimia nervosa, then different factors may induce similar effects in people with BED. Alternatively, common unknown factors could be responsible for neurosteroid changes in anorexia nervosa, bulimia nervosa, and BED.

Adult↗

PubMed2003

Differential responses of circulating ghrelin to high-fat or high-carbohydrate meal in healthy women.

The effects of specific nutritional factors on ghrelin secretion have not been investigated in humans. Therefore, we assessed ghrelin responses to a high-carbohydrate meal (1217 kcal with 77% carbohydrates, 10% protein, and 13% lipids) and to an isocaloric high-fat meal (15% carbohydrates, 10% proteins, and 75% lipids) in 14 nonobese healthy women. Eleven subjects also rated their hunger feelings on visual analog scales. Circulating ghrelin abruptly fell after both meals, but, after the carbohydrate meal, its maximum percent decrease was significantly greater than after the fat meal (P = 0.02). Plasma insulin and glucose levels rose after the meals, but their increases were significantly higher after the carbohydrate meal than after the fat meal. No significant change was observed in circulating leptin after both meals. Moreover, compared with the fat meal, the carbohydrate meal had a significantly greater suppressant effect on hunger feelings. Plasma ghrelin changes were significantly associated with hunger changes (P < 0.007). These findings show that circulating ghrelin is differently suppressed by diet manipulations. The mechanisms responsible for such a phenomenon and its possible implication in the physiology of human satiety remain to be elucidated.

Adult↗

PubMed2003

Opposite changes in circulating adiponectin in women with bulimia nervosa or binge eating disorder.

Adiponectin is a recently discovered peripheral peptide that is secreted exclusively by differentiated adipocytes. It has been shown to enhance insulin sensitivity, control body weight, regulate lipid homeostasis, and prevent atherosclerosis. Dysregulation of both lipid and glucose metabolism and changes in body weight and body fat mass have been reported in bulimia nervosa (BN) and/or binge eating disorder (BED); hence, investigation of adiponectin secretion is of obvious interest in these eating disorders. To this purpose, we measured plasma levels of adiponectin, glucose, cholesterol, triglycerides, and thyroid hormones in 60 drug-free women, including 20 patients with BN, 20 patients with BED, and 20 healthy controls. Compared with healthy women, BN women exhibited significantly increased circulating adiponectin levels (P < 0.002) and cholesterol concentrations (P < 0.005), whereas BED women had significantly reduced plasma levels of adiponectin (P < 0.005) and increased concentrations of glucose (P < 0.01), cholesterol (P < 0.05), and triglycerides (P < 0.02). Moreover, plasma levels of adiponectin were significantly correlated to the frequency of binge/vomiting episodes (r = 0.65, P = 0.002) in bulimics but not to the frequency of bingeing in BED patients. Because we did not include a group of obese patients who did not binge eat, the specificity of our findings in the BED should be considered cautiously. However, on the basis of present results, it is tempting to speculate that the increased production of adiponectin in BN may represent a compensatory mechanism to counteract the possible development of insulin resistance, whereas the decreased secretion of adiponectin in individuals with BED may be a risk factor for the development of glucose intolerance.

Adiponectin↗

PubMed2002

Correlations between negative symptoms and peripheral G protein levels in mononuclear leukocytes of deficit and nondeficit schizophrenics. Preliminary results.

Receptor-coupled G proteins were measured in mononuclear leukocytes (MNL) of 17 drug-treated patients with deficit schizophrenia (DS) and 16 drug-treated patients with nondeficit schizophrenia (NDS). No significant difference was found in MNL levels of G(alphas), G(alphai), G(alphaq) and G(beta) proteins between the two groups; however, MNL levels of G(alphas) were inversely correlated to the severity of negative symptoms in DS patients, while MNL levels of G(alphaq) were positively correlated to negative symptoms in NDS patients. Since G(alphas) and G(alphaq) are coupled to D-1 and 5-HT(2) receptors, respectively, these findings may support the hypothesis that a prevalent dysfunction of D-1 receptors is involved in the pathophysiology of negative symptoms in DS, whereas a prevalent dysfunction of 5-HT(2) receptors underlies negative symptoms in NDS. These results must be regarded as preliminary because of the possible interference of antipsychotic drugs on the explored parameters.

Adult↗

PubMed2002

Is the time course of clozapine response correlated to the time course of clozapine plasma levels? A one-year prospective study in drug-resistant patients with schizophrenia.

The relationship between the time course of clinical response to clozapine and the time course of clozapine plasma levels has never been investigated. In the present study, we assessed prospectively the clinical response to clozapine and the plasma levels of the drug and its major metabolites in 32 drug-resistant patients with schizophrenia kept on a fixed dose of 600 mg/day for 1 year Four of the patients met response criteria at week 4 of treatment. At weeks 8, 12, and 24, new responders were 7, 6, and 6, respectively. Nine patients never achieved clinical response. In responders at week 4, clozapine and clozapine-N-oxide plasma levels were significantly higher than in both new responders at weeks 8, 12, and 24 and nonresponders. In new responders at weeks 8, 12, and 24, in spite of a fixed clozapine daily dose, mean drug plasma levels progressively rose up to when clinical response occurred; then, the levels remained stable over time. Nonresponders exhibited mean clozapine plasma levels constantly below the value of 260 ng/ml, with N-demethylation as the preferred metabolic route. The present findings show, for the first time, that the time course of the clinical response to clozapine may be linked to the time course of plasma levels of clozapine and its major metabolites.

Adult↗

PubMed2002

Pronounced early increase in circulating leptin predicts a lower weight gain during clozapine treatment.

Weight gain is a widely reported side effect of clozapine, but no predictive factor has been identified so far. We investigated whether pretreatment values of circulating leptin or its early changes during clozapine administration could predict the long-term weight gain induced by the drug. Body weight and plasma levels of leptin were prospectively measured in 22 patients (13 men and 9 women) with drug-resistant schizophrenia undergoing a long-term treatment with clozapine. At the end of the second week of clozapine administration, circulating leptin increased much more than weight gain, and this increase was inversely correlated to body weight increase observed after 6 and 8 months of treatment. These findings suggest that early changes in leptin secretion may predict long-term weight gain in the course of clozapine administration.

Adult↗

PubMedDate not supplied

Leptin secretion is related to chronicity and severity of the illness in bulimia nervosa.

OBJECTIVE: A reduction in circulating leptin has been reported in some patients with BN, but not in others. The reasons for such diversity have not been explained. Therefore, we measured plasma levels of leptin and other hormones in a large sample of patients with eating disorders and in healthy controls and explored differences between bulimics with low plasma leptin levels and those with normal concentrations of the hormone. METHOD: One hundred and twenty-seven women participated in the study. They were 33 patients with AN, 56 women with BN, and 38 healthy volunteers. All were drug free for at least 6 weeks. Blood samples were collected in the morning for determination of hormone levels. Eating-related psychopathology and depressive symptoms were rated by using specific psychopathological scales. RESULTS: As compared with healthy women, both underweight AN and normal-weight BN patients exhibited decreased plasma levels of leptin, prolactin, and 17beta-estradiol. Plasma levels of cortisol were increased in AN but not in BN women. In bulimics, circulating leptin was inversely correlated with the duration of the illness and the frequency of bingeing/vomiting. Moreover, 29 bulimics had anorexic-like plasma leptin concentrations; the remaining 27 had circulating leptin similar to normal controls. The former had a significantly longer duration of the illness and a higher frequency of bingeing/vomiting compared with the latter. Moreover, a higher number of patients with concomitant borderline personality disorder were found in bulimics with low leptin concentrations. No significant differences between the two groups emerged in BW, BMI, mean plasma levels of cortisol, PRL, 17beta-estradiol and other clinical parameters. CONCLUSIONS: Present data show that leptin production is decreased in the subgroup of bulimic patients with a more chronic disease and with a greater severity of the bingeing/vomiting behavior. These findings support the idea that factors other than body weight changes (especially chronic malnutrition and bingeing behavior) may impair profoundly and persistently leptin secretion in patients with BN.

Adult↗

PubMedDate not supplied

Opposite changes in the serum brain-derived neurotrophic factor in anorexia nervosa and obesity.

OBJECTIVE: A role for the brain-derived neurotrophic factor (BDNF) in the regulation of eating behavior has been recently demonstrated. Therefore, the possibility exists that alterations in BDNF production and/or activity are involved in the pathophysiology of anorexia nervosa (AN) and obesity. METHODS: We measured morning serum levels of BDNF in 22 women with AN, 24 women with obesity (body mass index [BMI] > 30 kg/m2), and 27 nonobese healthy women. All the subjects were drug-free and underwent a clinical assessment by means of rating scales measuring both eating-related psychopathology and depressive symptoms. RESULTS: As compared with the nonobese healthy controls, circulating BDNF was significantly reduced in AN patients and significantly increased in obese subjects. No significant difference was observed in serum BDNF concentrations between AN women with or without a comorbid depressive disorder. Moreover, serum BDNF levels were significantly and positively correlated with the subjects' body weight and BMI. CONCLUSION: The BDNF changes observed in AN and obesity are likely secondary adaptive mechanisms aimed at counteracting the change in energy balance that occurs in these syndromes.

Adult↗

PubMedDate not supplied

Investigation of the serotonin transporter regulatory region polymorphism in bulimia nervosa: relationships to harm avoidance, nutritional parameters, and psychiatric comorbidity.

OBJECTIVE: Genes involved in 5HT transmission have been supposed to contribute to the biologic vulnerability for bulimia nervosa (BN). Because a long (L) and a short (S) variant of the promoter region of the 5HT transporter gene have been identified, we tested whether the 5HTT gene-linked polymorphic region (5HTTLPR) could represent a susceptibility factor for BN and/or could be related to nutritional parameters, harm avoidance personality dimension, and psychiatric comorbidity. METHODS: A total of 219 white women (125 bulimics and 94 healthy control subjects) underwent a blood sample collection for 5HTTLPR genotyping and a clinical evaluation assessing comorbidity for axis I and II psychiatric disorders, harm avoidance personality dimension, and body composition (only patients). RESULTS: The distribution of the 5HTTLPR genotypes did not significantly differ between patients and control subjects, although the L allele was significantly more frequent in the former. Bulimic individuals carrying at least one copy of the S allele had significantly lower mean body mass index and body fat mass values and significantly higher mean harm avoidance score than patients with the LL genotype. No significant association was found between the 5HTTLPR genotype and comorbid axis I and II psychiatric disorders. CONCLUSIONS: These findings support the view that polymorphic variants of the 5HTT promoter region do not play a part in predisposing to BN, whereas they seem to predispose bulimic individuals to nutritional impairment and increased harm avoidance.

Adolescent↗