scholarly journals Oxidative stress and mitochondrial uncoupling protein 2 expression in hepatic steatosis induced by exposure to xenobiotic DDE and high fat diet in male Wistar rats

PLoS ONE ◽  
2019 ◽  
Vol 14 (4) ◽  
pp. e0215955 ◽  
Author(s):  
Vincenzo Migliaccio ◽  
Rosaria Scudiero ◽  
Raffaella Sica ◽  
Lillà Lionetti ◽  
Rosalba Putti
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
High Fat ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Male Wistar Rats

Thyroxine 5'-deiodinase in brown adipose tissue of myopathic hamsters

1986 ◽  
Vol 251 (1) ◽  
pp. E8-E13 ◽  
Author(s):  
J. Kopecky ◽  
L. Sigurdson ◽  
I. R. Park ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
High Fat ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Endogenous Production ◽  
Deiodinase Activity ◽  
Brown Adipose

Myopathic Syrian hamsters (BIO 14.6) have less brown adipose tissue (BAT) than normal. The trophic response of this tissue to cold is smaller than normal and trophic responses to diet and to photoperiod are absent. The objective was to find out whether activity of thyroxine 5'-deiodinase in their BAT was increased normally in response to cold and thus whether a defect in endogenous production of 3,5,3'-triiodothyronine might underlie the attenuated trophic response. The effect of feeding a high-fat diet on activity of 5'-deiodinase was also studied. Cold acclimation increased thyroxine 5'-deiodinase activity in BAT of the myopathic hamster, but the total remained smaller than normal because of the smaller size. The cold-induced increase in concentration of mitochondrial uncoupling protein was also smaller than normal. The level of serum 3,5,3'-triiodothyronine was low in myopathic hamsters and remained lower than normal when they were cold-exposed or cold acclimated. Feeding the high-fat diet to myopathic hamsters resulted in a greater than normal suppression of thyroxine 5'-deiodinase activity than in normal hamsters; the normal increases in protein content and in concentration of mitochondrial uncoupling protein were absent. We conclude that the defective trophic response of BAT of the myopathic hamster is not secondary to defective regulation of its thyroxine 5'-deiodinase activity because this activity does not appear to be obligatorily linked to hypertrophy of BAT. The low level of serum 3,5,3'-triiodothyronine in the myopathic hamster may be secondary to reduced capacity for peripheral thyroxine deiodination in its BAT.

scholarly journals Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Liver Lipid ◽  
Control Group ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Male Wistar Rats

Background Adipose 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 methods Twenty-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. Results HFD 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. Conclusion Taken 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.

Attenuation of arsenic induced high fat diet exacerbated oxidative stress mediated hepatic and cardiac injuries in male Wistar rats by piperine involved antioxidative mechanisms

2020 ◽  
Vol 142 ◽  
pp. 111477 ◽  
Author(s):  
Tiyasa Dey ◽  
Auroma Ghosh ◽  
Sanatan Mishra ◽  
Palash Kumar Pal ◽  
Aindrila Chattopadhyay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Wistar Rats ◽  
High Fat ◽  
Male Wistar Rats

scholarly journals Response of Cardiac Tissue Oxidative Stress After Aerobic Exercise and Capsaicin Administrations in Rats Fed High-Fat Diet

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Maryam Davaran ◽  
Ahmad Abdi ◽  
Javad Mehrabani ◽  
Asieh Abbassi Daloii
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Cardiac Tissue ◽  
Aerobic Training ◽  
Normal Diet ◽  
High Fat ◽  
Male Wistar Rats ◽  
Oxidative Effects ◽  
Antioxidant Effects

Background: Oxidative stress harms cells and impairs the balance between oxidative and antioxidative factors. Exercise and capsaicin have anti-inflammatory and antioxidant effects, as well as some benefits on the cardiovascular system. Objectives: The aim of the present study was to examine the effect of aerobic training with capsaicin on heart changes oxidative stress in rats fed a high-fat diet (HFD). Methods: In this experimental study, 40 male Wistar rats were fed a normal diet (ND, n = 8) or HFD (n = 32) for 8 weeks. After eight weeks, all rats were divided into five groups: ND, HFD, high-fat diet-training (HFDT), high-fat diet-capsaicin (HFDCap), high-fat diet-training-capsaicin (HFDTCap). Training groups performed a progressive aerobic running program (at 15 - 25 m/min, 30 - 60 min/day, and 5 days/week) on a motor-driven treadmill for eight weeks. Capsaicin (4 mg/kg/day) was administered orally, by gavage, once a day. Results: The results showed significant increase in cardiac SOD, GPx and CAT levels in HFDT (P < 0.001), HFDCap (P < 0.001) and HFDTCap (P < 0.001) groups. Also, a significant increase in the amount of this index was observed in the HFDTCap compared to the HFDT and HFDCap groups (P < 0.05). The level of malondialdehyde (MDA) in all experimental groups was significantly lower than the HFD group (P < 0.001). Conclusions: Exercise and capsaicin improve HFD-induced oxidative stress. Therefore, exercise and capsaicin can be used as an appropriate alternative treatment for obesity and its associated inflammatory and oxidative effects.

scholarly journals Cell Autonomous Neuroprotection by the Mitochondrial Uncoupling Protein 2 in a Mouse Model of Glaucoma

2019 ◽  
Author(s):  
Daniel T. Hass ◽  
Colin J. Barnstable
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Ganglion Cell ◽  
Cell Survival ◽  
Retinal Ganglion Cell ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Retinal Ganglion ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein

AbstractGlaucoma is a group of disorders associated with retinal ganglion cell (RGC) degeneration and death. There is a clear contribution of mitochondrial dysfunction and oxidative stress toward glaucomatous RGC death. Mitochondrial uncoupling protein 2 (Ucp2) is a well-known regulator of oxidative stress that increases cell survival in acute models of oxidative damage. The impact of Ucp2 on cell survival during sub-acute and chronic neurodegenerative conditions however is not yet clear. Herein, we test the hypothesis that increased Ucp2 expression will improve retinal ganglion cell survival in a mouse model of glaucoma. We show that increasing retinal ganglion cell but not glial Ucp2 expression in transgenic animals decreases glaucomatous RGC death, but also that the PPAR-γ agonist rosiglitazone, an endogenous transcriptional activator of Ucp2, does not significantly alter RGC loss during glaucoma. Together, these data support a model whereby increased Ucp2 expression mediates neuroprotection during a long-term oxidative stressor, but that transcriptional activation alone is insufficient to elicit a neuroprotective effect, motivating further research in to the post-transcriptional regulation of Ucp2.

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