scholarly journals Understanding the Effects of Antipsychotics on Appetite Control

2022 ◽  
Vol 8 ◽  
Author(s):  
Sayani Mukherjee ◽  
Silje Skrede ◽  
Edward Milbank ◽  
Ramaroson Andriantsitohaina ◽  
Miguel López ◽  
...  
Keyword(s):  
Side Effects ◽  
Receptor Binding ◽  
First Generation ◽  
Antipsychotic Drugs ◽  
Molecular Mechanisms ◽  
Extrapyramidal Side Effects ◽  
Appetite Control ◽  
Drug Induced ◽  
Increased Risk

Antipsychotic drugs (APDs) represent a cornerstone in the treatment of schizophrenia and other psychoses. The effectiveness of the first generation (typical) APDs are hampered by so-called extrapyramidal side effects, and they have gradually been replaced by second (atypical) and third-generation APDs, with less extrapyramidal side effects and, in some cases, improved efficacy. However, the use of many of the current APDs has been limited due to their propensity to stimulate appetite, weight gain, and increased risk for developing type 2 diabetes and cardiovascular disease in this patient group. The mechanisms behind the appetite-stimulating effects of the various APDs are not fully elucidated, partly because their diverse receptor binding profiles may affect different downstream pathways. It is critical to identify the molecular mechanisms underlying drug-induced hyperphagia, both because this may lead to the development of new APDs, with lower appetite-stimulating effects but also because such insight may provide new knowledge about appetite regulation in general. Hence, in this review, we discuss the receptor binding profile of various APDs in relation to the potential mechanisms by which they affect appetite.

Tardive Dyskinesia: A Concern for the Pediatrician

PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 553-556
Author(s):  
HARVEY S. SINGER
Keyword(s):  
Side Effects ◽  
Tardive Dyskinesia ◽  
Children And Adolescents ◽  
Behavior Disorders ◽  
Antipsychotic Drugs ◽  
Extrapyramidal Side Effects ◽  
Body Movements ◽  
Neuroleptic Therapy

Antipsychotic drugs, such as the phenothiazines (chlorpromazine, fluphenazine, thioridazine), butyrophenones (haloperiodol), and diphenylbutylpiperidines (pimozide) are used in children and adolescents to treat a variety of clinical entities including psychoses, tics, behavior disorders, and movement problems. Because virtually all of these drugs have a potential to affect body movements and posture, they have also been termed neuroleptics.1 Most physicians are aware of the more common acute extrapyramidal side effects of these drugs, such as oculogyria, pseudoparkinsonism, dystonia, and restlessness (akathisia). Despite the widespread use of neuroleptics, however, little is known about the long-term neurologic consequences of such treatment. Of particular concern, based originally on data in adults, is the risk of severe and persistent tardive dyskinesia developing in persons receiving neuroleptic therapy.

scholarly journals Antipsychotics and glucose metabolism: how brain and body collide

2019 ◽  
Vol 316 (1) ◽  
pp. E1-E15 ◽  
Author(s):  
Chantel Kowalchuk ◽  
Laura N. Castellani ◽  
Araba Chintoh ◽  
Gary Remington ◽  
Adria Giacca ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Gain ◽  
Glucose Metabolism ◽  
First Generation ◽  
Clinical Evidence ◽  
Mental Illnesses ◽  
Therapeutic Effects ◽  
Direct Effects ◽  
Increased Risk

Since the serendipitous discovery of the first antipsychotic (AP) drug in the 1950s, APs remain the cornerstone of treatment for schizophrenia. A shift over the past two decades away from first-generation, conventional APs to so-called “atypical” (or 2nd/3rd generation) APs parallels acknowledgment of serious metabolic side-effects associated in particular with these newer agents. As will be reviewed, AP drugs and type 2 diabetes are now inextricably linked, contributing to the three- to fivefold increased risk of type 2 diabetes observed in schizophrenia. However, this association is not straightforward. Biological and lifestyle-related illness factors contribute to the association between type 2 diabetes and metabolic disease independently of AP treatment. In addition, APs have a well-established weight gain propensity which could also account for elevated risk of insulin resistance and type 2 diabetes. However, compelling preclinical and clinical evidence now suggests that these drugs can rapidly and directly influence pathways of glucose metabolism independently of weight gain and even in absence of psychiatric illness. Mechanisms of these direct effects remain poorly elucidated but may involve central and peripheral antagonism of neurotransmitters implicated not only in the therapeutic effects of APs but also in glucose homeostasis, possibly via effects on the autonomic nervous system. The clinical relevance of studying “direct” effects of these drugs on glucose metabolism is underscored by the widespread use of these medications, both on and off label, for a growing number of mental illnesses, extending safety concerns well beyond schizophrenia.

Delayed and Often Persistent

2016 ◽  
Author(s):  
Susan H. Fox
Keyword(s):  
Side Effects ◽  
Tardive Dyskinesia ◽  
Movement Disorder ◽  
Movement Disorders ◽  
Antipsychotic Drugs ◽  
Dopamine D2 Receptor ◽  
Treatment Options ◽  
D2 Receptor ◽  
Drug Induced ◽  
Tardive Dystonia

Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.

scholarly journals The Pathophysiology of Gestational Diabetes Mellitus

2018 ◽  
Vol 19 (11) ◽  
pp. 3342 ◽  
Author(s):  
Jasmine Plows ◽  
Joanna Stanley ◽  
Philip Baker ◽  
Clare Reynolds ◽  
Mark Vickers
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Molecular Mechanisms ◽  
Overweight And Obesity ◽  
Chronic Hyperglycemia ◽  
Increased Risk

Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist—including insulin and lifestyle interventions—there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.

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