antipsychotics/rasvumus

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Pharmacogenetics of leptin in antipsychotic-associated weight gain and obesity-related complications.

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Second-generation antipsychotics can greatly improve symptoms of psychosis-spectrum disorders. Unfortunately, these drugs are associated with weight gain, which increases a patient's risk for developing chronic diseases including Type 2 diabetes, cardiovascular diseases or other obesity-related

A model for antipsychotic-induced obesity in the male rat.

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BACKGROUND Weight gain is a common and severe side effect of antipsychotic drugs. A usual tool to study the side effects of psychotropic drugs is animal models. However, attempts to create an animal model of antipsychotic-induced weight gain were not successful so far. Female rodents are sensitive

Mechanism of the neuroleptic-induced obesity in female rats.

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1. Obesity is an undesirable side effect of neuroleptics which affects 50% approximately of patients under a program of chronic administration. 2. An animal model of neuroleptic-induced obesity and hyperphagia has been developed in female rats treated chronically with sulpiride (20 mg/Kg/ip. for 21

Effects of a nutritional intervention in obese postmenopausal women on atypical antipsychotics.

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OBJECTIVE To investigate the effects of a nutritional intervention on the body weight, body composition, blood glucose and lipid levels of obese postmenopausal women taking atypical antipsychotics in Greece. METHODS In a case-control design, 25 obese postmenopausal women treated with antipsychotic

Improved body weight and metabolic outcomes in overweight or obese psychiatric patients switched to amisulpride from other atypical antipsychotics.

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Switching to a different second-generation antipsychotic (SGA) with a lower risk of weight gain is recommended for overweight or obese psychiatric patients undergoing SGA treatment. However, there have been no complete reports regarding the long-term metabolic effects of switching to amisulpride. In

Dysmetabolic features of the overweight patients receiving antipsychotic drugs: a comparison with normal weight and obese subjects.

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BACKGROUND Extensive research indicates that obesity, defined by a body mass index (BMI) greater or equal to 30, is common in patients treated with antipsychotic drugs and is frequently associated with carbohydrate and lipid abnormalities leading to metabolic syndrome and diabetes. In contrast, the

Endocrine and metabolic abnormalities involved in obesity associated with typical antipsychotic drug administration.

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In this study, the authors assessed the endocrine system and glucose tolerance in obese and non-obese women chronically treated with typical antipsychotic drugs (AP). In particular, we tested the hypotheses that these subjects display hypogonadism and increased insulin resistance compared to healthy

Obesity and related metabolic abnormalities during antipsychotic drug administration: mechanisms, management and research perspectives.

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Excessive body weight gain (BWG) is a common side effect of some typical and atypical antipsychotic drugs (APs). Convergent evidence suggests a hierarchy in the magnitude of BWG that may be induced by diverse agents, being very high for clozapine and olanzapine; high for quetiapine, zotepin,

Susceptibility genes for the side effect of antipsychotics on body weight and obesity.

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Antipsychotic-induced body weight gain is becoming a major health concern since the increasing use of this medication in different mental disorders with a high prevalence in different populations. The percentage of patients gaining weight following antipsychotic medication can reach up to 80%

Amantadine in the treatment of neuroleptic-induced obesity in rats: behavioral, endocrine and neurochemical correlates.

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The efficacy of the antiviral agent Amantadine (AM, 5-100 mg/kg/sc, ip or intrahypothalamically, 12.5-100 micrograms bilaterally) in influencing body weight and food intake in drug-free rats, and in preventing neuroleptic-induced weight gain, was assessed in adult female rats. In drug-free rats,

Effect of GLP-1 receptor agonist treatment on body weight in obese antipsychotic-treated patients with schizophrenia: a randomized, placebo-controlled trial.

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Schizophrenia is associated with cardiovascular co-morbidity and a reduced life-expectancy of up to 20 years. Antipsychotics are dopamine D2 receptor antagonists and are the standard of medical care in schizophrenia, but the drugs are associated with severe metabolic side effects such as obesity and

Obesity, dyslipidaemias and smoking in an inpatient population treated with antipsychotic drugs.

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OBJECTIVE The prevalence of cardiovascular disease in people with schizophrenia is known to be above population norms. In addition, many antipsychotic drugs have been associated with weight gain and some with dyslipidaemia. Our aims were to determine the apparent and actual prevalence of the

Different Immune Signature in Youths Experiencing Antipsychotic-Induced Weight Gain Compared to Untreated Obese Patients.

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OBJECTIVE To assess cytokine and chemokine levels in youth experiencing antipsychotic-induced weight gain (AIWG) compared to obese patients, hypothesizing a different "immune signature" between the two kinds of obesity. METHODS We compared a group of youth experiencing AIWG (N 19, mean age 159

Decreased 5-HT2cR and GHSR1a interaction in antipsychotic drug-induced obesity.

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Second generation antipsychotics (SGAs), notably atypical antipsychotics including olanzapine, clozapine and risperidone, can cause weight gain and obesity side effects. Antagonism of serotonin 2c receptors (5-HT2cR) and activation of ghrelin receptor type 1a (GHSR1a) signalling have been identified

Potential mechanisms of atypical antipsychotic-induced metabolic derangement: clues for understanding obesity and novel drug design.

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Beside the therapeutic improvement over first-generation antipsychotics, the fact that prescription of atypical agents is also associated to the emergence of severe metabolic derangement in patients is not a mystery anymore. Body weight gain, dyslipidemia, adiposity, impaired glucose homeostasis,

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