Distribution of Resveratrol Metabolites in Liver, Adipose Tissue, and Skeletal Muscle in Rats Fed Different Doses of This Polyphenol

Andrés‐Lacueva, Cristina; Macarulla, M. T.; Rotches-Ribalta, María; Boto‐Ordóñez, María; Urpí-Sardà, Mireia; Rodríguez, Víctor M.; Portillo, Marı́a P.

doi:10.1021/jf3001108

Cited by 88 publications

(51 citation statements)

References 47 publications

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“…Its metabolites remain in the plasma significantly longer (Pervaiz and Holme, 2009). It is distributed to the liver, kidney, heart, and brain, among others (Andres-Lacueva et al , 2012; Clark et al , 2012; Walle, 2011). Greater than 50% of resveratrol and its metabolites are protein bound in plasma (Burkon and Somoza, 2008; Jannin et al , 2004).…”

Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

282

205

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Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

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Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

282

205

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“…In this regard, Lasa et al [115] have recently taken a further step suggesting the anti-obesity effect of some RES metabolites after their in vitro exposure at 25 µM to mouse pre-adipocytes for 24 hours. Unfortunately, the disposition of RES in human adipose tissue is not known, and these rather high metabolite concentrations have not been detected yet in animal adipose tissues after high RES supplementation [247,315]. Azorín-Ortuño et al [251] described that 100 nM RES or DH-RES, but not their corresponding glucuronide metabolites, decreased fatty acid binding protein type-4 (FABP4) levels in macrophages exposed to oxidized LDL particles.…”

Section: Potential Clinical Effects Vs Human Evidencementioning

confidence: 99%

Resveratrol and Clinical Trials: The Crossroad from In Vitro Studies to Human Evidence

Tomé‐Carneiro

Larrosa²,

González‐Sarrías

et al. 2013

CPD

399

294

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Resveratrol (3,5,4’-trihydroxy-trans-stilbene) is a non-flavonoid polyphenol that may be present in a limited number of food-stuffs such as grapes and red wine. Resveratrol has been reported to exert a plethora of health benefits through many different mechanisms of action. This versatility and presence in the human diet have drawn the worldwide attention of many research groups over the past twenty years, which has resulted in a huge output of in vitro and animal (preclinical) studies. In line with this expectation, many resveratrol-based nutraceuticals are consumed all over the world with questionable clinical/scientific support. In fact, the confirmation of these benefits in humans through randomized clinical trials is still very limited. The vast majority of preclinical studies have been performed using assay conditions with a questionable extrapolation to humans, i.e. too high concentrations with potential safety concerns (adverse effects and drug interactions), short-term exposures, in vitro tests carried out with non-physiological metabolites and/or concentrations, etc. Unfortunately, all these hypothesis-generating studies have contributed to increased the number of ‘potential’ benefits and mechanisms of resveratrol but confirmation in humans is very limited. Therefore, there are many issues that should be addressed to avoid an apparent endless loop in resveratrol research. The so-called ‘Resveratrol Paradox’, i.e., low bioavailability but high bioactivity, is a conundrum not yet solved in which the final responsible actor (if any) for the exerted effects has not yet been unequivocally identified. It is becoming evident that resveratrol exerts cardioprotective benefits through the improvement of inflammatory markers, atherogenic profile, glucose metabolism and endothelial function. However, safety concerns remain unsolved regarding chronic consumption of high RES doses, specially in medicated people. This review will focus on the currently available evidence regarding resveratrol’s effects on humans obtained from randomized clinical trials. In addition, we will provide a critical outlook for further research on this molecule that is evolving from a minor dietary compound to a possible multi-target therapeutic drug.

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“…It has been described that only a small proportion of this molecule reaches plasma and tissues after its oral intake [30], [31]. The concentrations of glucuronide and sulfate metabolites are relatively higher [32]–[34].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Metabolites Modify Adipokine Expression and Secretion in 3T3-L1 Pre-Adipocytes and Mature Adipocytes

et al. 2013

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ObjectiveDue to the low bioavailability of resveratrol, determining whether its metabolites exert any beneficial effect is an interesting issue.Methods3T3-L1 maturing pre-adipocytes were treated during differentiation with 25 µM of resveratrol or with its metabolites and 3T3-L1 mature adipocytes were treated for 24 hours with 10 µM resveratrol or its metabolites. The gene expression of adiponectin, leptin, visfatin and apelin was assessed by Real Time RT-PCR and their concentration in the incubation medium was quantified by ELISA.ResultsResveratrol reduced mRNA levels of leptin and increased those of adiponectin. It induced the same changes in leptin secretion. Trans-resveratrol-3-O-glucuronide and trans-resveratrol-4′-O-glucuronide increased apelin and visfatin mRNA levels. Trans-resveratrol-3-O-sulfate reduced leptin mRNA levels and increased those of apelin and visfatin.ConclusionsThe present study shows for the first time that resveratrol metabolites have a regulatory effect on adipokine expression and secretion. Since resveratrol has been reported to reduce body-fat accumulation and to improve insulin sensitivity, and considering that these effects are mediated in part by changes in the analyzed adipokines, it may be proposed that resveratrol metabolites play a part in these beneficial effects of resveratrol.

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Distribution of Resveratrol Metabolites in Liver, Adipose Tissue, and Skeletal Muscle in Rats Fed Different Doses of This Polyphenol

Cited by 88 publications

References 47 publications

Mitochondrial function in hypoxic ischemic injury and influence of aging

Mitochondrial function in hypoxic ischemic injury and influence of aging

Resveratrol and Clinical Trials: The Crossroad from In Vitro Studies to Human Evidence

Resveratrol Metabolites Modify Adipokine Expression and Secretion in 3T3-L1 Pre-Adipocytes and Mature Adipocytes

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