Melatonin reduces obesity and restores adipokine patterns and metabolism in obese ( ob/ob ) mice

Favero, Gaia; Stacchiotti, Alessandra; Castrezzati, Stefania; Bonomini, Francesca; Aglietta, Massimo; Rodella, Luigi Fabrizio

doi:10.1016/j.nutres.2015.07.001

Cited by 76 publications

(67 citation statements)

References 64 publications

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“…Previous studies have shown lower adiponectin mRNA expression in leptin-deficient ob/ob and leptin receptor-deficient db/db mice 29–31 , as well as in obese Zucker fa/fa rats lacking functional leptin receptors 32 , and that leptin significantly increases Adipoq expression in WAT 18, 23, 33, 34 and in the heart 35 . Interestingly, we found lower amounts of adiponectin protein in WAT of ob/ob mice consistent with other studies 30, 36, 37 , but leptin replacement failed to normalize its levels. This in vivo observation prompted us to hypothesize that the restored circulating levels of adiponectin with an increase in Adipoq mRNA expression but without changes in the protein levels in WAT is due to an increased expression and secretion in WAT.…”

Section: Discussionsupporting

confidence: 92%

“…The stimulatory effect of leptin on circulating adiponectin levels in ob/ob mice could be involved in the amelioration in oxidative stress and inflammation observed in these animals, since a negative correlation between adiponectin and 8-isoprostane and SAA after leptin replacement was found. An increase in the expression of adiponectin receptors Adipor1 and Adipor2 , which were reduced in ob/ob in agreement with a previous work 37 , is unlikely to mediate these improvements, since their expression was unaffected after leptin administration.…”

Section: Discussionsupporting

confidence: 91%

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Normalization of adiponectin concentrations by leptin replacement in ob/ob mice is accompanied by reductions in systemic oxidative stress and inflammation

Frühbeck

Catalán

Rodríguez

et al. 2017

Sci Rep

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The circulating concentrations of adiponectin, an antidiabetic adipokine, have been shown to be reduced in obesity, in relation to an increase in inflammation. The aim of the present work was to assess the effect of leptin replacement on adiponectin levels and expression as well as on markers of oxidative stress and inflammation in leptin-deficient ob/ob mice. Twelve-week-old male mice (n = 7–10 per group) were treated with either saline (wild type and ob/ob mice) or leptin (ob/ob mice) for 18 days. A third group of ob/ob mice was treated with saline and pair-fed to the amount of food consumed by the leptin-treated group. Leptin replacement restored values of adiponectin (P < 0.001), reduced circulating 8-isoprostane and serum amyloid A (SAA) levels (P < 0.05 for both), and significantly downregulated the increased gene expression of osteopontin (Spp1, P < 0.05), Saa3 (P < 0.05), Cd68 (P < 0.01), Il6 (P < 0.01) and NADPH oxidase (Nox1 and Nox2, P < 0.01) in the perirenal WAT and Spp1 (P < 0.05) in the liver of ob/ob mice. In cultured adipocytes from ob/ob mice, leptin increased (P < 0.05) the mRNA expression and secretion of adiponectin. We concluded that circulating concentrations of adiponectin are positively regulated by leptin and ameliorate obesity-associated oxidative stress and inflammation in mice.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Normalization of adiponectin concentrations by leptin replacement in ob/ob mice is accompanied by reductions in systemic oxidative stress and inflammation

Frühbeck

Catalán

Rodríguez

et al. 2017

Sci Rep

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“…A recent study demonstrated that melatonin has effects on inflammation, fat deposition, and energy metabolism in ob/ob mice [30]. In this study, we found that melatonin treatment for 12 weeks significantly decreased body weight and liver weight in HFD mice.…”

Section: Discussionsupporting

confidence: 64%

Melatonin improves non-alcoholic fatty liver disease via MAPK-JNK/P38 signaling in high-fat-diet-induced obese mice

et al. 2016

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BackgroundMelatonin can regulate lipid metabolism, increase insulin sensitivity, regulate glucose metabolism and reduce body weight. This study is aimed to determine the effects and mechanism of action of melatonin on non-alcoholic fatty liver disease (NAFLD) in high-fat-diet (HFD) induced obese mice.MethodsNAFLD was induced by HFD in C57BL/6 mice. A total of 24 mice were randomly assigned to 4 groups. Groups A and B were fed with HFD for 36 weeks while groups C and D were fed with a regular diet (RD). During the last 12 weeks, Groups A and C were treated with 10 mg/kg melatonin while Groups B and D were treated with water in the same volume by intragastric administration. Body and liver weight, blood glucose, serum transaminases and lipid levels, and markers of hepatic inflammation were measured. Histological analyses were also performed on liver tissue.ResultsAfter 12 weeks of treatment with melatonin, body weights (Group A: before 53.11 ± 0.72 vs after 12w treatment 39.48 ± 0.74) and liver weights (A 1.93 ± 0.09 g vs B 2.92 ± 0.19 g vs C 1.48 ± 0.09 g vs D 1.49 ± 0.10 g), fasting plasma glucose, alanine transaminase (A 24.33 ± 11.90 IU/L vs B 60.80 ± 10.18 IU/L vs C 13.01 ± 3.49 IU/L vs D 16.62 ± 2.00 IU/L), and low-density cholesterol (A 0.24 ± 0.06 mmol/L vs B 1.57 ± 0.10 mmol/L vs C 0.28 ± 0.06 mmol/L vs D 0.29 ± 0.03 mmol/L) were significantly decreased in HFD mice. HFD fed mice treated with melatonin showed significantly less liver steatosis. Treatment of HFD fed mice with melatonin led to a significant decrease in the expression of TNF-α, IL-1β, and IL-6 measured using quantitative real-time polymerase chain reaction (qRT-PCR). HFD fed mice demonstrated increased phosphorylation of P38 and JNK1/2, which was reduced by melatonin treatment.ConclusionsThe study concluded that melatonin could improve NAFLD by decreasing body weight and reduce inflammation in HFD induced obese mice by modulating the MAPK-JNK/P38 signaling pathway.

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“…Similar to the results of the present study, Gonciarz et al [83] found no change of circulating resistin after melatonin supplementation. However, in the Favero et al study [103], melatonin supplementation reduced resistin levels in obese ( ob/ob ) mice. The links between resistin and obesity need further investigations.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie‐Restricted Diet

Szewczyk-Golec

Rajewski²,

Gackowski

et al. 2017

Oxidative Medicine and Cellular Longevity

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Obesity is one of the major global health problems. Melatonin deficiency has been demonstrated to correlate with obesity. The aim of the study was to estimate the effect of melatonin on oxidative stress and adipokine levels in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin (n = 15) or placebo (n = 15) for 30 days with a calorie-restricted diet. Serum levels of melatonin, 4-hydroxynonenal (HNE), adiponectin, omentin-1, leptin, and resistin, as well as erythrocytic malondialdehyde (MDA) concentration and Zn/Cu-superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities, were measured at baseline and after supplementation. Significant body weight reduction was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and GPx activities statistically increased, whereas the MDA concentrations were reduced. In the placebo group, a significant rise in the HNE and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. Melatonin supplementation facilitated body weight reduction, improved the antioxidant defense, and regulated adipokine secretion. The findings strongly suggest that melatonin should be considered in obesity management. This trial is registered with CTRI/2017/07/009093.

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Melatonin reduces obesity and restores adipokine patterns and metabolism in obese ( ob/ob ) mice

Cited by 76 publications

References 64 publications

Normalization of adiponectin concentrations by leptin replacement in ob/ob mice is accompanied by reductions in systemic oxidative stress and inflammation

Normalization of adiponectin concentrations by leptin replacement in ob/ob mice is accompanied by reductions in systemic oxidative stress and inflammation

Melatonin improves non-alcoholic fatty liver disease via MAPK-JNK/P38 signaling in high-fat-diet-induced obese mice

Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie‐Restricted Diet

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