Volume 10, Issue 4 (2024)
Pharm Biomed Res 2024, 10(4): 345-354 |
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Khadiza Begum1 
, Md Abdur Rahman Ripon1 , Tabassum Akter1 , Md Monirul Islam1 , Rahima Begum1 , Mohammad Salim Hossain *1
, Md Abdur Rahman Ripon1 , Tabassum Akter1 , Md Monirul Islam1 , Rahima Begum1 , Mohammad Salim Hossain *1
1- Department of Pharmacy, Noakhali Science and Technology University, Noakhali, Bangladesh.
Abstract: (708 Views)
Background: Nowadays, metabolic syndromes represent one of the major public health challenges worldwide and are twice as prevalent in patients with neuropsychiatric disorders. This could be due to antipsychotic consumption, especially atypical ones, such as olanzapine (OLA), a second-generation antipsychotic used in the management of schizophrenia.
Objectives: This study explores the potential of chronic OLA exposure to modulate inflammatory pathways in a context of metabolic dysfunction using high-fat diet (HFD) induced obese mice (female).
Methods: A total of 1 mg/kg of OLA and HFD were given for 6 weeks to an obese mice group as treatment. Then, body weight, abdominal fat weight, lipid profiles (serum triglycerides (TG), total cholesterol (TC), and high-density lipoprotein cholesterol [HDL-C]), and liver functions (serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase, and alkaline phosphatase [ALP]) were assessed against the HFD control group. The relative gene expression of PPAR-ɣ, MCP-1, and GLUT4 were also compared.
Results: This treatment of OLA (1 mg/kg) induced a significant decrease in TG, SGOT, and serum glutamic-pyruvic transaminase levels, and a non-significant decrease in body weight, abdominal fat mass, TC, HDL-C, ALP level and the expression of MCP-1 and PPAR-γ; however, GLUT4 was significantly increased.
Conclusion: After chronic OLA exposure, the results indicate that the declination of body and organ weight, lipid levels, liver function markers, and MCP-1 and PPAR-ɣ expression except for GLUT4 shows its effects in changing the metabolic disturbances in obese mice.
Objectives: This study explores the potential of chronic OLA exposure to modulate inflammatory pathways in a context of metabolic dysfunction using high-fat diet (HFD) induced obese mice (female).
Methods: A total of 1 mg/kg of OLA and HFD were given for 6 weeks to an obese mice group as treatment. Then, body weight, abdominal fat weight, lipid profiles (serum triglycerides (TG), total cholesterol (TC), and high-density lipoprotein cholesterol [HDL-C]), and liver functions (serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase, and alkaline phosphatase [ALP]) were assessed against the HFD control group. The relative gene expression of PPAR-ɣ, MCP-1, and GLUT4 were also compared.
Results: This treatment of OLA (1 mg/kg) induced a significant decrease in TG, SGOT, and serum glutamic-pyruvic transaminase levels, and a non-significant decrease in body weight, abdominal fat mass, TC, HDL-C, ALP level and the expression of MCP-1 and PPAR-γ; however, GLUT4 was significantly increased.
Conclusion: After chronic OLA exposure, the results indicate that the declination of body and organ weight, lipid levels, liver function markers, and MCP-1 and PPAR-ɣ expression except for GLUT4 shows its effects in changing the metabolic disturbances in obese mice.
Type of Study: Original Research |
Subject:
Clinical Pharmacy
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