J Korean Neuropsychiatr Assoc.
2010 Mar;49(2):217-225.
The Effects of Antidepressants on the Leptin, Adiponectin, and Adiponectin Receptor mRNA Expression in Model Diabetogenic Rats
- Affiliations
-
- 1Department of Psychiatry, Eulji Hospital, Seoul, Korea.
- 2Department of Addiction Rehabilitation with Social Welfare, Seongnam, Korea.
- 3Department of Psychiatry, Seoul St. Mary's Hospital, The Catholic University College of Medicine, Seoul, Korea.
- 4Department of Psychiatry, Chung-Ang University College of Medicine, Seoul, Korea. knozodr@hanmail.net
Abstract
OBJECTIVES
Weight gain and glucose intolerance are the most common symptoms of metabolic syndrome. Certain patients complain of weight-change and hyperglycemia after receiving antidepressants. Our study evaluated the effects of antidepressants on serum glucose and energy metabolism.
METHODS
Subjects were 32 Otsuka Long-Evans Tokushima Fatty (OLETF) and 35 wild-type Long-Evans Tokushima Otsuka (LETO) rats. From age 11 weeks, the rats were divided into 4 subgroups within each strain. We administered the designated antidepressant-amitriptyline, fluoxetine, or mirtazapine-to these subgroups, allocating the fourth as the control. After exactly 4 weeks' medication, we sacrificed the animals and checked their weight, glucose, insulin, leptin, adiponectin, and expression of adiponectin receptor mRNA.
RESULTS
Fluoxetine subgroups in both strains gained the least weight. The glucose, triglyceride, and cholesterol levels of all OLETF antidepressant subgroups did not differ from the controls. Adiponectins in amitriptyline- and mirtazapine-subgroups were higher than control. All antidepressant subgroups showed elevated expressions of adiponectin receptor mRNA in fat, muscle, and the pancreas.
CONCLUSION
Amitriptyline and mirtazapine seem to regulate adiponectin and expression of adiponectin receptor mRNA. Even though the underlying mechanisms were different, we conclude none of the antidepressants would have negative influences on energy metabolism in diabetogenic animals.