513 Melatonin Administration Prevents Inflammation Processes and Reduces Liver Injury in Zucker Rats After Ischemia/Reperfusion

Kireev, Roman; Samuel, Betty Annie; Sara, Christine; Elena, Valera-Nuñez; Conde-Moreno, Elisa; Tresguerres, Jesús A.F.

doi:10.1016/s0168-8278(11)60515-1

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“…We previously have shown that oral melatonin reduced plasma levels of IL‐6, TNF‐ α , and C‐reactive protein in ZDF rats, thus improving the pro‐inflammatory state . Similarly, oral administration of melatonin to ZDF rats after ischemia/reperfusion resulted in both reduced gene expressions and levels of pro‐inflammatory cytokines, including TNF‐ α and IL‐1 β , while enhancing the levels of anti‐inflammatory cytokines, such as IL‐10, leading to lower liver injury .…”

Section: Discussionmentioning

confidence: 88%

“…Additionally, melatonin enhanced respiration rate and the increased acceptor control ratio value (ACR) in liver isolated mitochondria from streptozotocin‐induced type 1 diabetic rats and partially reduced liver damage . Furthermore, melatonin treatment was found to limit liver injury induced by ischemia/reperfusion in Zucker fatty rats (ZF), a model of obesity, and to prevent associated low‐grade inflammation . It is also noteworthy that some liver conditions and treatments modify melatonin secretion and, consequently, alter its biological and antioxidant capabilities .…”

Section: Introductionmentioning

confidence: 99%

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Melatonin reduces hepatic mitochondrial dysfunction in diabetic obese rats

Agil

El-Hammadi

Jiménez-Aranda

et al. 2015

Journal of Pineal Research

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Hepatic mitochondrial dysfunction is thought to play a role in the development of liver steatosis and insulin resistance, which are both common characteristics of obesity and type 2 diabetes mellitus (T2DM). It was hypothesized that the antioxidant properties of melatonin could potentially improve the impaired functions of hepatic mitochondria in diabetic obese animals. Male Zucker diabetic fatty (ZDF) rats and lean littermates (ZL) were given either melatonin (10 mg/kg BW/day) orally for 6 wk (M‐ZDF and M‐ZL) or vehicle as control groups (C‐ZDF and C‐ZL). Hepatic function was evaluated by measurement of serum alanine transaminase and aspartate transaminase levels, liver histopathology and electron microscopy, and hepatic mitochondrial functions. Several impaired functions of hepatic mitochondria were observed in C‐ZDF in comparison with C‐ZL rats. Melatonin treatment to ZDF rats decreases serum levels of ALT (P < 0.001), alleviates liver steatosis and vacuolation, and also mitigates diabetic‐induced mitochondrial abnormalities, glycogen, and lipid accumulation. Melatonin improves mitochondrial dysfunction in M‐ZDF rats by increasing activities of mitochondrial citrate synthase (P < 0.001) and complex IV of electron transfer chain (P < 0.05) and enhances state 3 respiration (P < 0.001), respiratory control index (RCR) (P < 0.01), and phosphorylation coefficient (ADP/O ratio) (P < 0.05). Also melatonin augments ATP production (P < 0.05) and diminishes uncoupling protein 2 levels (P < 0.001). These results demonstrate that chronic oral melatonin reduces liver steatosis and mitochondria dysfunction in ZDF rats. Therefore, it may be beneficial in the treatment of diabesity.

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Section: Discussionmentioning

confidence: 88%