Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

Cioffi, Federica; Senese, Rosalba; Lasala, Pasquale; Ziello, Angela; Mazzoli, Arianna; Crescenzo, Raffaella; Liverini, Giovanna; Lanni, Antonia; Goglia, Fernando; Iossa, Susanna

doi:10.3390/nu9040323

Cited by 69 publications

(54 citation statements)

References 51 publications

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“…As before mentioned, oxidative stress is critically involved in NAFLD pathogenesis, because caused lipid peroxidation increasing ROS production. In particular, high fructose micro-environmental stimulates ROS formation [4,6,7,35] and this study confirmed the exacerbated ROS production not only in mitochondria, but also in other cytoplasm compartments (Fig. 4c).…”

Section: Representative Immunoblots Are Shownsupporting

confidence: 82%

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l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Montesano

Senesi

Vacante

et al. 2019

J Endocrinol Invest

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Purpose Nonalcoholic fatty liver disease (NAFLD) is defined by excessive lipid accumulation in the liver and involves an ample spectrum of liver diseases, ranging from simple uncomplicated steatosis to cirrhosis and hepatocellular carcinoma. Accumulating evidence demonstrates that high fructose intake enhances NAFLD development and progression promoting inhibition of mitochondrial β-oxidation of long-chain fatty acids and oxidative damages. l-Carnitine (LC), involved in β-oxidation, has been used to reduce obesity caused by high-fat diet, which is beneficial to ameliorating fatty liver diseases. Moreover, in the recent years, various studies have established LC anti-oxidative proprieties. The objective of this study was to elucidate primarily the underlying anti-oxidative mechanisms of LC in an in vitro model of fructose-induced liver steatosis. Methods Human hepatoma HepG2 cells were maintained in medium supplemented with LC (5 mM LC) with or without 5 mM fructose (F) for 48 h and 72 h. In control cells, LC or F was not added to medium. Fat deposition, anti-oxidative, and mitochondrial homeostasis were investigated. Results LC supplementation decreased the intracellular lipid deposition enhancing AMPK activation. However, compound C (AMPK inhibitor-10 μM), significantly abolished LC benefits in F condition. Moreover, LC, increasing PGC1 α expression, ameliorates mitochondrial damage-F induced. Above all, LC reduced ROS production and simultaneously increased protein content of antioxidant factors, SOD2 and Nrf2. Conclusion Our data seemed to show that LC attenuate fructose-mediated lipid accumulation through AMPK activation. Moreover, LC counteracts mitochondrial damages and reactive oxygen species production restoring antioxidant cellular machine. These findings provide new insights into LC role as an AMPK activator and anti-oxidative molecule in NAFLD.

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Section: Representative Immunoblots Are Shownsupporting

confidence: 82%

“…Numerous data suggest that chronic exposure to a highfructose microenvironment could lead to a decrease in the mitochondrial biogenesis and a concomitant increase in mitochondrial oxidative stress production [35] in hepatocytes.…”

Section: Representative Immunoblots Are Shownmentioning

confidence: 99%

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Montesano

Senesi

Vacante

et al. 2019

J Endocrinol Invest

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“…Since there was no increased 4‐HNE and HEX formation in the stomach of sucrose‐fed compared to starch‐fed rats, the observed oxidative stress in sucrose‐fed rats is likely not a consequence of enhanced lipid oxidation during digestion. An alternative explanation may be the metabolic conversion of fructose to uric acid in the liver, which is accompanied by mitochondrial oxidative stress and dysfunction, and hepatic steatosis in rats . Indeed, in the present study, hepatic oxidative stress was observed in rats on the sucrose diets, indicated by the increased hepatic TBARS concentrations, along with increased liver weight and fat accumulation in the mesenterium and retroperitoneum.…”

Section: Discussionmentioning

confidence: 45%

Combined Consumption of Beef‐Based Cooked Mince and Sucrose Stimulates Oxidative Stress, Cardiac Hypertrophy, and Colonic Outgrowth of Desulfovibrionaceae in Rats

Hecke

Vrieze

Boon

et al. 2018

Molecular Nutrition Food Res

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Scope High red meat and sucrose consumption increases the epidemiological risk for chronic diseases. Mechanistic hypotheses include alterations in oxidative status, gut microbiome, fat deposition, and low‐grade inflammation. Methods and results For 2 weeks, 40 rats consumed a diet high in white or red meat (chicken‐based or beef‐based cooked mince, respectively), and containing corn starch or sucrose in a 2 × 2 factorial design. Lard was mixed with lean chicken or beef to obtain comparable dietary fatty acid profiles. Beef (vs chicken)‐fed rats had higher lipid oxidation products (malondialdehyde, 4‐hydroxy‐2‐nonenal, and hexanal) in stomach content and blood, and lower blood glutathione. Sucrose (vs corn starch)‐fed rats showed increased blood lipid oxidation products and glutathione peroxidase activity, higher liver weight and malondialdehyde concentrations, and mesenterial and retroperitoneal fat accumulation. Beef–sucrose‐fed rats had increased cardiac weight, suggesting pathophysiological effects on the cardiovascular system. The colonic microbiome of beef–sucrose‐fed rats showed an outgrowth of the sulfate‐reducing family of the Desulfovibrionaceae, and lower abundance of the Lactobacillus genus, indicating intestinal dysbiosis. Blood C‐reactive protein, a marker for inflammation, was not different among groups. Conclusions Consumption of a cooked beef‐based meat product with sucrose increased oxidative stress parameters and promoted cardiac hypertrophy and intestinal dysbiosis.

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“…Previously, it has been demonstrated that probiotic therapy with L. plantarum strains improves urinary oxalate, calcium, uric acid, creatinine and serum uric acid levels in rats with increased renal calcium oxalate deposition [35]. A diet rich in fructose can lead to the induction of marked oxidative stress and mitochondrial dysfunction [36]. Oxidative stress arising from a high-fructose diet has been shown to suppress antioxidant enzymes in different tissues [37][38][39][40][41].…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus helveticus and Lactobacillus plantarum modulate renal antioxidant status in a rat model of fructose-induced metabolic syndrome

Korkmaz

Sadı

Kocabaş

et al. 2019

Arch biol sci (Beogr)

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High dietary fructose intake causes a metabolic disorder and augments the risk of chronic kidney disease most likely due to oxidative stress. Probiotics could have antioxidant, antiinflammatory and immunoregulatory properties. The present study examined the influence of Lactobacillus helveticus and Lactobacillus plantarum supplementation on dietary fructose-induced metabolic changes and renal antioxidant/oxidant status of rats. Male Wistar rats were divided into four groups as follows: control; fructose; fructose plus L. helveticus; fructose plus L. plantarum. Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. The probiotic supplementation was applied by gastric gavage once a day for six weeks. Several metabolic parameters in the plasma, gene and protein expressions of the main antioxidant enzymes in renal tissues of rats were measured. Dietary fructose-induced elevations in plasma insulin, triglyceride, VLDL, creatinine as well as renal urea levels were alleviated after treatment with L. helveticus and L. plantarum. Moreover, L. helveticus and L. plantarum supplementation recovered the changes in renal protein expression level of SOD1, SOD2 and CAT. In conclusion, supplementation with L. helveticus and L. plantarum has an improving effect on specific metabolic parameters and renal antioxidative enzymes in a fructose-induced metabolic disorder.

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Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

Cited by 69 publications

References 51 publications

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

l-Carnitine counteracts in vitro fructose-induced hepatic steatosis through targeting oxidative stress markers

Combined Consumption of Beef‐Based Cooked Mince and Sucrose Stimulates Oxidative Stress, Cardiac Hypertrophy, and Colonic Outgrowth of Desulfovibrionaceae in Rats

Lactobacillus helveticus and Lactobacillus plantarum modulate renal antioxidant status in a rat model of fructose-induced metabolic syndrome

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