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Effects of antipsychotics on fat deposition and changes in leptin and insulin levels

Magnetic resonance imaging study of previously untreated people with schizophrenia

Department of Psychiatry Nanjing Brain Hospital and Nanjing Medical University, Nanjing, China, and Department of Biomedical Science, University of Sheffield, Sheffield, UK

ZHI-JIAN YAO, MD

Department of Psychiatry Nanjing Brain Hospital and Nanjing Medical University, Nanjing, China, and Department of Biomedical Science, University of Sheffield, Sheffield, UK

WEN LIU, MD

Department of Radiological Science, Nanjing Brain Hospital and Nanjing Medical University, Nanjing

QUN FANG, MD

Clinical Science Centre, Nanjing Brain Hospital and Nanjing Medical University, Nanjing

GAVIN P. REYNOLDS, PhD

Department of Biomedical Science, University of Sheffield, Sheffield

Correspondence: Gavin P. Reynolds, Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, UK. Tel: (0) 114 222 4662; fax: (0) 114 276 5413; e-mail: g.p.reynolds{at}sheffield.ac.uk

Declaration of interest None.

Funding detailed in Acknowledgements.

Background Weight gain is a common consequence of antipsychotic drug treatment and can lead to further morbidity.

Aims To assess the effects of antipsychotic drug therapy on abdominal fat deposition, on insulin and leptin secretion, and on circulating glucose and lipids.

Method Abdominal body fat was determined by magnetic resonance imaging in a group of previously untreated patients with schizophrenia, before and after 10 weeks’ antipsychotic drug treatment. Body mass and blood concentrations of glucose, insulin, leptin and lipids were also measured.

Results Significant increases in both subcutaneous and intra-abdominal fat were identified after antipsychotic drug treatment. A three-fold increase in leptin secretion as well as significant increases in levels of circulating lipids and non-fasting glucose were also identified.

Conclusions Patients first receiving antipsychotic drugs experience substantial deposition of both subcutaneous and intra-abdominal fat, reflecting a loss of the normal inhibitory control of leptin on body mass. Along with fat deposition, the increase in levels of fasting lipids and in non-fasting glucose may provide early signs of drug-induced progression towards the metabolic syndrome.

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