당뇨 유발 동물 모델에서 Leptin, Adiponectin, Adiponectin 수용체 mRNA 발현에 대한 항우울제의 영향The Effects of Antidepressants on the Leptin, Adiponectin, and Adiponectin Receptor mRNA Expression in Model Diabetogenic Rats
- Authors
- 조근호; 이희진; 김대진; 이영식; 기백석
- Issue Date
- 2010
- Publisher
- 대한신경정신의학회
- Keywords
- 항우울제; 아디포넥틴; 대사증후군; 체중 증가; Antidepressant; Adiponectin; Metabolic syndrome; Weight gain
- Citation
- 신경정신의학, v.49, no.2, pp 217 - 225
- Pages
- 9
- Journal Title
- 신경정신의학
- Volume
- 49
- Number
- 2
- Start Page
- 217
- End Page
- 225
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/33854
- ISSN
- 1015-4817
- 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 4subgroups 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.
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