1,720,983 research outputs found
UCP2 and SOD2: adaptive and protective role during mitochondrial ROS production in rat liver.
No full textThe endocrine pancreas of diet-induced obese rat. Different effect on insulin secretion and blood glucose regulation according to the different types of dietary fatty acids.
No full textHigh fat diet and DDE combined effects on metallothionein expression and synthesis in rat tissues.
No full textDiet impact on mitochondrial bioenergetics and dynamics in Hormonal and neuroendocrine regulation of energy balance
No full textOxidative stress and mitochondrial uncoupling protein 2 expression in hepatic steatosis induced by exposure to xenobiotic DDE and high fat diet in male Wistar rats.
Full text linkOxidative stress plays a key role in steatohepatitis induced by both xenobiotic agents and high fat diet (HFD). The present study aimed to evaluate hepatic oxidative stress and anti- oxidant systems response in rats exposed to HFD and/or non-toxic dose of dichlorodiphe- nyldichloroethylene (DDE), the first metabolite of dichlorodiphenyltrichloroethane. Groups of 8 rats were so treated for 4 weeks: 1- standard diet (N group); 2- standard diet plus DDE (10 mg/kg b.w.) (N+DDE group); 3- HFD (D group); 4- HFD plus DDE (D+DDE group). Oxi- dative stress was analyzed by determining malondialdehyde as lipid peroxidation product, while the anti-oxidant systems were evaluating by measuring the levels of the principal cyto- solic and mitochondrial antioxidant proteins and enzymes, namely superoxide dismutase 1 and 2 (SOD1, SOD2), glutathione peroxidase 1 (GPx1) and uncoupling protein 2 (UCP2) involved in the control of hepatic reactive oxygens species (ROS) accumulation. The results showed malondialdehyde accumulation in livers of all groups, confirming the pro-oxidant effects of both HFD and DDE, but with a greater effect of DDE in absence of HFD. In addi- tion, we found different levels of the analyzed anti-oxidant systems in the different groups. DDE mainly induced UCP2 and SOD2, while HFD mainly induced GPx1. Noteworthy, in the condition of simultaneous exposure to DDE and HFD, the anti-oxidant response was more similar to the one induced by HFD than to the response induced by DDE. Present findings confirmed that both HFD and xenobiotic exposure induced hepatic oxidative stress and showed that the anti-oxidant defense response was not the same in the diverse groups, sug- gesting that UCP2 induction could be an adaptive response to limit excessive ROS damage, mainly in condition of xenobiotic exposure
Physiological impact associated with chronic simultaneous exposure to high-fat diet and persistent organic pollutant p,p ́-diphenyldichloroethene (DDE): effects on hepatic mitochondrial functions.
No full textChronic exposure to high fat feeding and environmental pollutants: effect on mitochondrial function in different tissues in rats
No full textHigh-Lard and High-Fish Oil Diets Differ in Their Effects on Insulin Resistance Development, Mitochondrial Morphology and Dynamic Behaviour in Rat Skeletal Muscle
No full textFish oil (mainly omega 3 polyunsaturated fatty acids), differently from lard (mainly saturated fatty acids) has been sug- gested to have anti-inflammatory effects associated with amelioration of insulin sensibility. An important role in skele- tal muscle insulin resistance development has been recently attributed to mitochondrial dynamic behavior. Mitochon- dria are dynamic organelles that frequently undergo fission/fusion processes and a shift toward fission process has been associated with skeletal muscle mitochondrial dysfunction and insulin resistance development. The present work aimed to evaluate if the replacement of lard with fish oil in high-fat diet positively affect skeletal muscle mitochondrial dy- namic behavior in association with the improvement of insulin-resistance. Body weight gain, systemic insulin-resistance (glucose/insulin ratio), serum TNFα levels and skeletal muscle lipid content were assessed in rats fed a high-lard or high-fish-oil diet for 6 weeks. In skeletal muscle sections, immunohistochemical analysis were performed to detect the presence of insulin receptor substrate 1 (IRS1) and tyrosine phosphorylated IRS1 (key factor in insulin signalling path- way) as well as to detect the main proteins involved in mitochondrial fusion (MFN2 and OPA1) and fission (DRP1 and Fis1) processes. Skeletal muscle mitochondrial ultrastructural features were assessed by electron microscopy. High-fish oil feeding induced lower body weight gain, systemic inflammation and insulin-resistance development as well as skeletal muscle lipid accumulation compared to high-lard feeding. Skeletal muscle sections from high-fish oil fed rats exhibited a greater number of immunoreactive fibers for MFN2 and OPA1 proteins as well as weaker immunostaining for DRP1 and Fis1 compared to sections from high-lard fed rats. Electron microscopy observations suggested a promi- nent presence of fission events in L rats and fusion events in F rats. The positive effect of the replacement of lard with fish oil in high-fat diet on systemic and skeletal muscle insulin sensibility was associated to changes in mitochondrial dynamic behavior
Time-dependent effects on body weight gain and hepatic oxidative stress in rats exposed to both high fat feeding and low doses of persistent organic pollutant
No full textBackground: Oxidative stress plays an important role into obesity associated metabolic comorbidities. Moreover, exposure to persistent organic pollutants (POPs) is associated with hepatic cellular stress due to detoxification processes. Little is known on the impact associated with chronic simultaneous exposure to both high-fat diet and low doses of persistent organic pollutants, such as p,p ́-diphenyldichloroethene (DDE), (DDT’s major metabolite with the highest persistence).
Aim: The present work aimed to investigate the effect of different periods of simultaneous exposure to low dose of POP and high-fat feeding on body weight gain and hepatic injury. Given that liver is the main organ involved in response to both high fat diet and toxic injury, we evaluated the development of oxidative stress at the hepatic level.
Methods: Three groups of 8 rats were so treated for 4 or 16 weeks: 1) standard diet (10% fat J/J) (N rats); 2) high-fat diet (45% fat J/J) (D rats); 3) high-fat diet plus DDE (10 mg/kg b.w. by gavage) (D+DDE rats). DDE dose used in this work was comparable to the admissible daily intake. Body weight gain and hepatic lipid content were determined. Hepatic oxidative stress was assessed by determining H2O2 production and TBARs content.
Results: D rats showed higher body weight gain, hepatic lipid content, H2O2 production and TBARs content compared to control rats after both 4 and 16 weeks. Similar variations were found in D+DDE rats after 4 weeks of treatment. On the other hand, after 16 weeks of treatment D+DDE rats showed lower body weight gain and hepatic lipid content compared to D rats. Moreover, they showed higher H2O2 production and TBARs content compared to D rats.
Conclusion: Short period exposure to DDE associated with high fat feeding elicited the same alterations in body weight gain and hepatic oxidative stress found in response to the only exposure to high fat diet. A prolonged period of exposure revealed DDE treatment toxicity as showed by decreased body weight gain and hepatic lipid content and increased oxidative stress
Effect of chronic exposure to high fat feeding and environmental pollutants on mitochondria in brown adipose tissue in rat.
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