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Melatonin Reduces Aggravation of Renal Ischemia-Reperfusion Injury in Obese Rats by Maintaining Mitochondrial
Anongporn Kobroob1, Aphisek Kongkaew2, Orawan Wongmekiat3
1Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand.
Abstract:
This study examined the potential benefits of melatonin against renal ischemia and reperfusion (IR) injury in obesity and explored the underlying mechanisms. Obesity was induced in Wistar rats by feeding a high-fat diet for 16 weeks. Three obese groups that underwent renal IR induction (30-min renal ischemia followed by 24-h reperfusion) were randomly assigned to receive melatonin at ischemic onset, reperfusion onset, or pretreatment for 4 weeks before IR induction. Groups of vehicle-treated obese and normal-diet-fed rats that underwent sham or IR induction were also included in the study. The results showed that renal functional and structural impairments after IR incidence were aggravated in obese rats compared to normal-diet-fed rats. The obese-IR rats also exhibited oxidative stress, mitochondrial dysfunction, apoptosis, and mitochondrial dynamics and mitophagy imbalances, which were all considerably improved upon melatonin treatment, irrespective of the treatment time. This study suggests the prophylactic and therapeutic efficacy of melatonin in IR-induced acute kidney injury (AKI) in obese individuals, which may improve the prognosis of AKI in these populations. The benefits of melatonin are likely mediated by the modification of various signaling molecules within the mitochondria that maintain mitochondrial redox balance and lead to the protection of mitochondrial homeostasis and integrity.
Insights
Melatonin effectively treats kidney damage from ischemia-reperfusion injury in obese rats by improving mitochondrial function and reducing oxidative stress. This suggests melatonin offers both preventive and therapeutic benefits for acute kidney injury in obesity.
Area of Science:
- Nephrology
- Endocrinology
- Mitochondrial Biology
Background:
- Obesity exacerbates renal ischemia-reperfusion (IR) injury, leading to significant kidney damage.
- Obese individuals face heightened risks of acute kidney injury (AKI) due to comorbidities.
- Understanding protective mechanisms against AKI in obesity is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the protective effects of melatonin against renal IR injury in an obese rat model.
- To elucidate the underlying mechanisms by which melatonin mitigates kidney damage in obesity.
- To assess the prophylactic and therapeutic potential of melatonin for AKI in obese populations.
Main Methods:
- Obesity was induced in Wistar rats using a high-fat diet for 16 weeks.
- Renal IR injury was induced (30 min ischemia, 24 h reperfusion).
- Melatonin was administered at different time points: ischemic onset, reperfusion onset, or 4 weeks pretreatment.
Main Results:
- Obese rats showed aggravated renal functional and structural impairments post-IR compared to normal-diet rats.
- Melatonin treatment significantly improved renal function, reduced oxidative stress, and enhanced mitochondrial function in obese-IR rats.
- Melatonin effectively corrected imbalances in mitochondrial dynamics and mitophagy, irrespective of administration timing.
Conclusions:
- Melatonin demonstrates both prophylactic and therapeutic efficacy in mitigating IR-induced AKI in obese rats.
- Melatonin's benefits are linked to improved mitochondrial redox balance and homeostasis.
- Melatonin treatment holds promise for improving AKI prognosis in obese individuals.
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