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Olanzapine-induced metabolic syndrome is partially mediated by oxytocinergic system dysfunction in female
Elsie D Oduor1, Peter W Mwangi1, Boniface M Chege1,2
1Department of Human Anatomy and Medical Physiology, University of Nairobi, Nairobi, Kenya.
Introduction:
Olanzapine (OLZ), a second-generation antipsychotic, is associated with the development of metabolic syndrome with unclear underlying pathophysiologic mechanisms. Oxytocin (OT) influences feeding, lipid, and glucose metabolism. This study investigates whether dysfunction in the oxytocinergic system contributes to the development of olanzapine-induced metabolic syndrome.
Methods:
Twenty five (25) female Sprague-Dawley rats were housed under standard conditions and studied over 12 weeks. During the first 6-week induction phase, rats were randomized into 3 groups: normal control (vehicle treatment; normal saline; n = 5), low dose (4 mg/kg olanzapine [OLZ]; n = 5), and high dose (8 mg/kg OLZ; n = 15). In the last 6-week treatment phase, the high dose group was re-randomized into 3 groups: negative control (8 mg/kg OLZ; n = 5), positive control (8 mg/kg OLZ + 500 mg/kg metformin; n = 5), and test group (8 mg/kg OLZ + 1 mg/kg oxytocin [OT]; n = 5). The normal control and low dose groups continued unchanged. Body weight, food intake, glucose levels, OGTT, lipid profile, visceral fat, hepatic index, hepatic triglycerides, and steatosis were assessed.
Results:
At induction end, high-dose OLZ increased food intake (179 ± 5 g), body weight (239 ± 3 g), blood glucose (7.8 ± 0.3 mmol/L), and impaired glucose tolerance (846 ± 25 mmol/L·min) compared to controls (p < 0.0001). Post-treatment, the test group displayed reduced food intake (163 ± 2 g vs. 197 ± 6 g), body weight (297 ± 2 g vs. 376 ± 6 g), blood glucose (5.8 ± 0.3 mmol/L vs. 9.8 ± 0.2 mmol/L), and improved glucose tolerance (711 ± 14 vs. 853 ± 9 mmol/L·min) compared to negative controls (p < 0.0001). LDL-C, total cholesterol, serum and hepatic triglycerides, visceral adipose, and hepatic mass and steatosis were also significantly decreased in the test group compared to negative control group (p < 0.01).
Conclusion:
OLZ-induced metabolic abnormalities were mitigated by oxytocin, indicating that the oxytocinergic system hypofunction may be implicated in its pathophysiology. These results highlight OT's therapeutic potential and call for further clinical research to explore its role in the management of antipsychotic-induced metabolic syndrome.
Insights
Oxytocin (OT) treatment mitigated metabolic abnormalities caused by olanzapine (OLZ) in rats. This suggests oxytocinergic system dysfunction contributes to OLZ-induced metabolic syndrome, highlighting OT
Area of Science:
- Metabolic Syndrome Research
- Neuroendocrinology
- Pharmacology
Background:
- Second-generation antipsychotics like olanzapine (OLZ) are linked to metabolic syndrome.
- The exact mechanisms behind OLZ-induced metabolic syndrome are not fully understood.
- Oxytocin (OT) plays a role in regulating metabolism, including feeding, lipid, and glucose homeostasis.
Purpose of the Study:
- To investigate the potential contribution of oxytocinergic system dysfunction to olanzapine-induced metabolic syndrome.
- To evaluate the therapeutic effect of oxytocin on metabolic abnormalities associated with olanzapine treatment.
Main Methods:
- Female Sprague-Dawley rats were administered varying doses of olanzapine over 12 weeks.
- Groups included normal controls, low-dose OLZ, and high-dose OLZ.
- The high-dose OLZ group was further divided into negative control, metformin (positive control), and oxytocin (test) groups for the final 6 weeks.
- Key metabolic parameters such as body weight, food intake, glucose tolerance, and lipid profiles were assessed.
Main Results:
- High-dose olanzapine significantly increased body weight, food intake, blood glucose, and impaired glucose tolerance.
- Oxytocin treatment in the high-dose OLZ group led to significant reductions in food intake, body weight, and blood glucose levels.
- Oxytocin also improved glucose tolerance and reduced LDL-C, total cholesterol, triglycerides, visceral fat, and hepatic steatosis compared to the negative control group.
Conclusions:
- Olanzapine-induced metabolic abnormalities were significantly mitigated by oxytocin administration.
- These findings suggest that hypofunction of the oxytocinergic system may play a role in the pathophysiology of olanzapine-induced metabolic syndrome.
- Oxytocin demonstrates therapeutic potential for managing antipsychotic-induced metabolic syndrome, warranting further clinical investigation.
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