11 research outputs found
Restoration of cardiac metabolic flexibility by acetate in high fat diet-induced obesity is independent of ANP/BNP modulation
No full textThe present study hypothesized that cardiac metabolic inflexibility is dependent on cardiac ANP/BNP alteration and HDAC activity. We further sought to investigate the therapeutic potential of SCFA, acetate in high fat diet (HFD)-induced obese rat model. Adult male Wistar rats were assigned into groups (n = 6/group): Control, Obese, Sodium acetate (NaAc)-treated and Obese+ NaAc-treated groups received distilled water once daily (oral gavage), 40% HFD ad libitum, 200 mg/kg NaAc once daily (oral gavage) and 40% HFD+NaAc respectively. The treatments lasted for 12 weeks. HFD resulted in increased food intake, body weight and cardiac mass. It also caused insulin resistance and enhanced β-cell function, increased fasting insulin, lactate, plasma and cardiac triglyceride, total cholesterol, lipid peroxidation, TNF-α, IL-6, HDAC and cardiac troponin T and γ-Glutamyl transferase and decreased plasma and cardiac GSH with unaltered cardiac ANP and BNP. However, these alterations were averted when treated with acetate. Taken together, these results indicate that obesity induces defective cardiac metabolic flexibility, which is accompanied by elevated level of HDAC and not ANP/BNP alteration. The results also suggest that acetate ameliorates obesity-induced cardiac metabolic inflexibility by suppression of HDAC and independent of ANP/BNP modulation.The presentation of the authors' names and (or) special characters in the title of the pdf file of the accepted manuscript may differ slightly from what is displayed on the item page. The information in the pdf file of the accepted manuscript reflects the original submission by the author
Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model.
No full textBackgroundAdipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats.Materials and methodsTwenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks.ResultsHFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin.ConclusionTaken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin
Effects of melatonin on circulating obestatin concentration in HFD-induced obese rats.
No full textData are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*p#p<0.05 VS. OBS). Control (CTL), Melatonin (MLT), Obesity (OBS).</p
Fig 3 -
No full textEffect of melatonin on plasma, adipose and liver malondialdehyde (A-C) in HFD-induced obese rats. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*pp<0.05 vs. OBS). Control (CTL); Melatonin (MLT); Obesity (OBS).</p
Melatonin attenuates excess body weight but not food intake in HFD-induced obese animals.
No full textMelatonin attenuates excess body weight but not food intake in HFD-induced obese animals.</p
Fig 6 -
No full textEffects of melatonin on plasma, adipose and liver nitric oxide concentration (A-C) in HFD-induced obese rats. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*p#p<0.05 VS. OBS). Control (CTL); Melatonin (MLT); Obesity (OBS).</p
Fig 4 -
No full textEffects of melatonin on plasma, adipose and liver Glucose-6-phosphate dehydrogenase (A-C) and glutathione (D-F) in HFD-induced obese rats. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*p#p<0.05 VS. OBS). Control (CTL); Melatonin (MLT); Obesity (OBS); Glucose 6 phosphate dehydrogenase (G6PD); Glutathione (GSH).</p
Fig 2 -
No full textEffects of melatonin on plasma, adipose and liver triglyceride (A-C) and total cholesterol (D-F) in HFD-induced obese rats. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*pp<0.05 vs. OBS). Control (CTL); Melatonin (MEL); Obesity (OBS); Total cholesterol (TC).</p
Fig 1 -
No full textEffects of melatonin on blood glucose (A), insulin (B) and insulin resistance (C) HFD-induced obese animals. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*pp<0.05 vs. OBS). Control (CTL); Melatonin (MLT); Obesity (OBS).</p
Fig 5 -
No full textEffects of melatonin on plasma, adipose and liver interleukin-6 (A-C) and uric acid concentration (D-F) HFD-induced obese rats. Data are expressed as mean ± SD. n = 6 and analyzed by one-way ANOVA followed by Bonferroni post hoc test. (*p#p<0.05 VS. OBS). Control (CTL), Melatonin (MLT), Obesity (OBS).</p
