Resveratrol

high-resolution terminology - matching measurements at high-resolution

Resveratrol

Description

Resveratrol is a natural bioactive phenol prouced by several plants with antioxidant and anti-inflammatory effects. Dietary intake as nutraceutical is discussed for targeting mitochondria with a wide spectrum of action in degenerative diseases.

Resveratrol and mitObesity

Work in progress by Gnaiger E 2020-01-20 linked to a preprint in preparation on BME and mitObesity.

	Year	Reference	Organism	Tissue;cell
Cassereau 2020 Exp Neurol	2020	Cassereau J, Chevrollier A, Codron P, Goizet C, Gueguen N, Verny C, Reynier P, Bonneau D, Lenaers G, Procaccio V (2020) Oxidative stress contributes differentially to the pathophysiology of Charcot-Marie-Tooth disease type 2K. Exp Neurol 323:113069.	Human	Fibroblast
Banday 2020 J Am Heart Assoc	2020	Banday AA, Lokhandwala MF (2020) Renal dopamine oxidation and inflammation in high salt fed rats. J Am Heart Assoc 9:e014977.	Rat	Kidney
Gabandé-Rodríguez 2019 Cells	2019	Gabandé-Rodríguez E, M Gómez de Las Heras M, Mittelbrunn M (2019) Control of inflammation by calorie restriction mimetics: on the crossroad of autophagy and mitochondria. Cells 2019;9:E82.
Rodriguez-Enriquez 2019 Toxicol Appl Pharmacol	2019	Rodríguez-Enríquez S, Pacheco-Velázquez SC, Marín-Hernández Á, Gallardo-Pérez JC, Robledo-Cadena DX, Hernández-Reséndiz I, García-García JD, Belmont-Díaz J, López-Marure R, Hernández-Esquivel L, Sánchez-Thomas R, Moreno-Sánchez R (2019) Resveratrol inhibits cancer cell proliferation by impairing oxidative phosphorylation and inducing oxidative stress. Toxicol Appl Pharmacol 370:65-77.	Rat	Heart Liver
Zhou 2018 Toxicology	2018	Zhou Q, Fu X, Wang X, Wu Q, Lu Y, Shi J, Klaunig JE, Zhou S (2018) Autophagy plays a protective role in Mn-induced toxicity in PC12 cells. Toxicology 394:45–53.	Rat	Other cell lines
Cardoso 2017 Biochim Biophys Acta	2017	Cardoso GMF, Pletsch JT, Parmeggiani B, Grings M, Glanzel NM, Bobermin LD, Amaral AU, Wajner M, Leipnitz G (2017) Bioenergetics dysfunction, mitochondrial permeability transition pore opening and lipid peroxidation induced by hydrogen sulfide as relevant pathomechanisms underlying the neurological dysfunction characteristic of ethylmalonic encephalopathy. Biochim Biophys Acta 1863:2192-2201.	Rat	Nervous system
Most 2017 Eur J Clin Nutr	2017	Most J, Penders J, Lucchesi M, Goossens GH, Blaak EE (2017) Gut microbiota composition in relation to the metabolic response to 12-week combined polyphenol supplementation in overweight men and women. Eur J Clin Nutr 71:1040-5.	Human	Skeletal muscle
Da Silva 2017 Neurotox Res	2017	Da Silva JC, Amaral AU, Cecatto C, Wajner A, Dos Santos Godoy K, Ribeiro RT, de Mello Gonçalves A, Zanatta Â, da Rosa MS, Loureiro SO, Vargas CR, Leipnitz G, de Souza DOG, Wajner M (2017) α-Ketoadipic acid and α-aminoadipic acid cause disturbance of glutamatergic neurotransmission and induction of oxidative stress in vitro in brain of adolescent rats. Neurotox Res 32:276-90.	Rat	Nervous system
Layne 2017 Contemp Clin Trials	2017	Layne AS, Krehbiel LM, Mankowski RT, Anton SD, Leeuwenburgh C, Pahor M, Sandesara B, Wu SS, Buford TW (2017) Resveratrol and exercise to treat functional limitations in late life: Design of a randomized controlled trial. Contemp Clin Trials 6:58–63.	Human	Skeletal muscle
De Moura 2017 Neurotox Res	2017	de Moura Alvorcem L, da Rosa MS, Glänzel NM, Parmeggiani B, Grings M, Schmitz F, Wyse ATS, Wajner M, Leipnitz G (2017) Disruption of energy transfer and redox status by sulfite in hippocampus, striatum, and cerebellum of developing rats. Neurotox Res 32:264-75.	Rat	Nervous system
Pollack 2017 J Gerontol A Biol Sci Med Sci	2017	Pollack RM, Barzilai N, Anghel V, Kulkarni AS, Golden A, O'Broin P, Sinclair DA, Bonkowski MS, Coleville AJ, Powell D, Kim S, Moaddel R, Stein D, Zhang K, Hawkins M, Crandall JP (2017) Resveratrol improves vascular function and mitochondrial number but not glucose metabolism in older adults. J Gerontol A Biol Sci Med Sci 72:1703–9.	Human	Skeletal muscle
Fisar 2016b Folia Biol (Praha)	2016	Fisar Z, Hroudova J, Singh N, Koprivova A, Maceckova D (2016) Effect of simvastatin, coenzyme Q10, resveratrol, acetylcysteine and acetylcarnitine on mitochondrial respiration. Folia Biol (Praha) 62:53-66.	Pig	Nervous system
Timmers 2016 Diabetes Care	2016	Timmers S, de Ligt M, Phielix E, van de Weijer T, Hansen J, Moonen-Kornips E, Schaart G, Kunz I, Hesselink MK, Schrauwen-Hinderling VB, Schrauwen P (2016) Resveratrol as add-on therapy in subjects with well-controlled type 2 diabetes: a randomized controlled trial. Diabetes Care 39:2211-17.	Human	Skeletal muscle
Most 2016 Am J Clin Nutr	2016	Most J, Timmers S, Warnke I, Jocken JW, van Boekschoten M, de Groot P, Bendik I, Schrauwen P, Goossens GH, Blaak EE (2016) Combined epigallocatechin-3-gallate and resveratrol supplementation for 12 wk increases mitochondrial capacity and fat oxidation, but not insulin sensitivity, in obese humans: a randomized controlled trial. Am J Clin Nutr 104:215-27.	Human	Skeletal muscle
Morato 2015 Cell Death Differ	2015	Morató L, Ruiz M, Boada J, Calingasan NY, Galino J, Guilera C, Jové M, Naudí A, Ferrer I, Pamplona R, Serrano M, Portero-Otín M, Beal MF, Fourcade S, Pujol A (2015) Activation of sirtuin 1 as therapy for the peroxisomal disease adrenoleukodystrophy. Cell Death Differ 22:1742-53.	Mouse	Nervous system
Williams 2014 PLoS One	2014	Williams CB, Hughes MC, Edgett BA, Scribbans TD, Simpson CA, Perry CG, Gurd BJ (2014) An examination of resveratrol's mechanisms of action in human tissue: impact of a single dose in vivo and dose responses in skeletal muscle ex vivo. PLoS One 9:e102406.	Human	Skeletal muscle
Beaudoin 2014 J Physiol	2014	Beaudoin MS, Perry CC, Arkell A, Chabowski A, Simpson JA, Wright DC, Holloway GP (2014) In the ZDF rat, impairments in mitochondrial palmitoyl-CoA respiratory kinetics that precede the development of diabetic cardiomyopathy are prevented by resveratrol supplementation. J Physiol 592:2519-33.	Rat	Heart
Hirzel 2013 J Recept Signal Transduct Res	2013	Hirzel E, Lindinger PW, Maseneni S, Giese M, Rhein VV, Eckert A, Hoch M, Krähenbühl S, Eberle AN (2013) Differential modulation of ROS signals and other mitochondrial parameters by the antioxidants MitoQ, resveratrol and curcumin in human adipocytes. J Recept Signal Transduct Res 33:304-12.	Human	Fat Other cell lines
Beaudoin 2013 Am J Physiol Regul Integr Comp Physiol	2013	Beaudoin MS, Snook LA, Arkell AM, Simpson JA, Holloway GP, Wright DC (2013) Resveratrol supplementation improves white adipose tissue function in a depot-specific manner in Zucker diabetic fatty rats. Am J Physiol Regul Integr Comp Physiol 305:542-51.	Rat	Fat
Smith 2013 J Physiol	2013	Smith BK, Perry CG, Herbst EA, Ritchie IR, Beaudoin MS, Smith JC, Neufer PD, Wright DC, Holloway GP (2013) Submaximal ADP-stimulated respiration is impaired in ZDF rats and recovered by resveratrol. J Physiol 591:6089-101.	Rat	Skeletal muscle
Chowdhury 2012 Brain	2012	Chowdhury SK, Smith DR, Saleh A, Schapansky J, Marquez A, Gomes S, Akude E, Morrow D, Calcutt NA, Fernyhough P (2012) Impaired adenosine monophosphate-activated protein kinase signalling in dorsal root ganglia neurons is linked to mitochondrial dysfunction and peripheral neuropathy in diabetes. Brain 135:1751-66.	Mouse Rat	Nervous system
Cumero 2012 Br J Pharmacol	2012	Cumero S, Fogolari F, Domenis R, Zucchi R, Mavelli I, Contessi S (2012) F0F1-ATPsynthase as a molecular target of 3-Iodothyronamine. Br J Pharmacol 166:2331-47		Heart
Jung 2012 J Med Food	2012	Jung HY, Lee AN, Song TJ, An HS, Kim YH, Kim KD, Kim IB, Kim KS, Han BS, Kim CH, Kim KS, Kim JB (2012) Korean mistletoe (Viscum album coloratum) extract improves endurance capacity in mice by stimulating mitochondrial activity. J Med Food 15:621-8.	Mouse	Liver Kidney
Timmers 2011 Cell Metab	2011	Timmers S, Konings E, Bilet L, Houtkooper RH, van de Weijer T, Goossens GH, Hoeks J, van der Krieken S, Ryu D, Kersten S, Moonen-Kornips E, Hesselink MK, Kunz I, Schrauwen-Hinderling VB, Blaak EE, Auwerx J, Schrauwen P (2011) Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab 14:612-22.	Human	Skeletal muscle
Morselli 2011 J Cell Biol	2011	Morselli E, Mariño G, Bennetzen MV, Eisenberg T, Megalou E, Schroeder S, Cabrera S, Bénit P, Rustin P, Criollo A, Kepp O, Galluzzi L, Shen S, Malik SA, Maiuri MC, Horio Y, López-Otín C, Andersen JS, Tavernarakis N, Madeo F, Kroemer G (2011) Spermidine and resveratrol induce autophagy by distinct pathways converging on the acetylproteome. J Cell Biol 192:615–29.	Human Caenorhabditis elegans Saccharomyces cerevisiae
Bellance 2009 Int J Biochem Cell Biol	2009	Bellance N, Benard G, Furt F, Begueret H, Smolková K, Passerieux E, Delage JP, Baste JM, Moreau P, Rossignol R (2009) Bioenergetics of lung tumors: Alteration of mitochondrial biogenesis and respiratory capacity. Int J Biochem Cell Biol 41:2566-77.	Human	Fibroblast
Jarolim 2004 FEMS Yeast Res	2004	Jarolim S, Millen J, Heeren G, Laun P, Goldfarb DS, Breitenbach M (2004) A novel assay for replicative lifespan in Saccharomyces cerevisiae. FEMS Yeast Res 5:169-77.	Saccharomyces cerevisiae Fungi

1. Zhao Y, Chen B, Shen J, Wan L, Zhu Y, Yi T, Xiao Z (2017) The beneficial effects of Quercetin, Curcumin, and Resveratrol in obesity. Oxid Med Cell Longev 2017:1459497. - https://www.ncbi.nlm.nih.gov/pubmed/29138673
2. Li B, Xiao X, Miao Y, Guo L, Zhen J, Li X, Jiang B, Hu Z (2020) Resveratrol alleviates obesity-associated podocyte injury in ovariectomized obese rats. Exp Ther Med 19:123-30. - https://www.ncbi.nlm.nih.gov/pubmed/31853281
3. Yang YSH, Li ZL, Shih YJ, Bennett JA, Whang-Peng J, Lin HY, Davis PJ, Wang K (2019) Herbal medicines attenuate PD-L1 expression to induce anti-proliferation in obesity-related cancers. Nutrients 11 pii: E2979. - https://www.ncbi.nlm.nih.gov/pubmed/31817534
4. Yang AJT, Frendo-Cumbo S, MacPherson REK (2019) Resveratrol and metformin recover prefrontal cortex AMPK activation in diet-induced obese mice but reduce BDNF and synaptophysin protein content. J Alzheimers Dis 71:945-56. - https://www.ncbi.nlm.nih.gov/pubmed/31450493

MitoPedia: BME and mitObesity

» Body mass excess and mitObesity | BME and mitObesity news | Summary |

Term	Abbreviation	Description
BME cutoff points	BME cutoff	Obesity is defined as a disease associated with an excess of body fat with respect to a healthy reference condition. Cutoff points for body mass excess, BME cutoff points, define the critical values for underweight (-0.1 and -0.2), overweight (0.2), and various degrees of obesity (0.4, 0.6, 0.8, and above). BME cutoffs are calibrated by crossover-points of BME with established BMI cutoffs.
Body fat excess	BFE	In the healthy reference population (HRP), there is zero body fat excess, BFE, and the fraction of excess body fat in the HRP is expressed - by definition - relative to the reference body mass, M°, at any given height. Importantly, body fat excess, BFE, and body mass excess, BME, are linearly related, which is not the case for the body mass index, BMI.
Body mass	m [kg]; M [kg·x-1]	The body mass M is the mass (kilogram [kg]) of an individual (object) [x] and is expressed in units [kg/x]. Whereas the body weight changes as a function of gravitational force (you are weightless at zero gravity; your floating weight in water is different from your weight in air), your mass is independent of gravitational force, and it is the same in air and water.
Body mass excess	BME	The body mass excess, BME, is an index of obesity and as such BME is a lifestyle metric. The BME is a measure of the extent to which your actual body mass, M [kg/x], deviates from M° [kg/x], which is the reference body mass [kg] per individual [x] without excess body fat in the healthy reference population, HRP. A balanced BME is BME° = 0.0 with a band width of -0.1 towards underweight and +0.2 towards overweight. The BME is linearly related to the body fat excess.
Body mass index	BMI	The body mass index, BMI, is the ratio of body mass to height squared (BMI=M·H-2), recommended by the WHO as a general indicator of underweight (BMI<18.5 kg·m-2), overweight (BMI>25 kg·m-2) and obesity (BMI>30 kg·m-2). Keys et al (1972; see 2014) emphasized that 'the prime criterion must be the relative independence of the index from height'. It is exactly the dependence of the BMI on height - from children to adults, women to men, Caucasians to Asians -, which requires adjustments of BMI-cutoff points. This deficiency is resolved by the body mass excess relative to the healthy reference population.
Comorbidity		Comorbidities are common in obesogenic lifestyle-induced early aging. These are preventable, non-communicable diseases with strong associations to obesity. In many studies, cause and effect in the sequence of onset of comorbidities remain elusive. Chronic degenerative diseases are commonly obesity-induced. The search for the link between obesity and the etiology of diverse preventable diseases lead to the hypothesis, that mitochondrial dysfunction is the common mechanism, summarized in the term 'mitObesity'.
Healthy reference population	HRP	A healthy reference population, HRP, establishes the baseline for the relation between body mass and height in healthy people of zero underweight or overweight, providing a reference for evaluation of deviations towards underweight or overweight and obesity. The WHO Child Growth Standards (WHO-CGS) on height and body mass refer to healthy girls and boys from Brazil, Ghana, India, Norway, Oman and the USA. The Committee on Biological Handbooks compiled data on height and body mass of healthy males from infancy to old age (USA), published before emergence of the fast-food and soft-drink epidemic. Four allometric phases are distinguished with distinct allometric exponents. At heights above 1.26 m/x the allometric exponent is 2.9, equal in women and men, and significantly different from the exponent of 2.0 implicated in the body mass index, BMI [kg/m2].
Height of humans	h [m]; H [m·x-1]	The height of humans, h, is given in SI units in meters [m]. Humans are countable objects, and the symbol and unit of the number of objects is N [x]. The average height of N objects is, H = h/N [m/x], where h is the heights of all N objects measured on top of each other. Therefore, the height per human has the unit [m·x-1] (compare body mass [kg·x-1]). Without further identifyer, H is considered as the standing height of a human, measured without shoes, hair ornaments and heavy outer garments.
Length	l [m]	Length l is an SI base quantity with SI base unit meter m. Quantities derived from length are area A [m2] and volume V [m3]. Length is an extensive quantity, increasing additively with the number of objects. The term 'height' h is used for length in cases of vertical position (see height of humans). Length of height per object, LUX [m·x-1] is length per unit-entity UX, in contrast to lentgth of a system, which may contain one or many entities, such as the length of a pipeline assembled from a number NX of individual pipes. Length is a quantity linked to direct sensory, practical experience, as reflected in terms related to length: long/short (height: tall/small). Terms such as 'long/short distance' are then used by analogy in the context of the more abstract quantity time (long/short duration).
MitObesity drugs		Bioactive mitObesity compounds are drugs and nutraceuticals with more or less reproducible beneficial effects in the treatment of diverse preventable degenerative diseases implicated in comorbidities linked to obesity, characterized by common mechanisms of action targeting mitochondria.
Obesity		Obesity is a disease resulting from excessive accumulation of body fat. In common obesity (non-syndromic obesity) excessive body fat is due to an obesogenic lifestyle with lack of physical exercise ('couch') and caloric surplus of food consumption ('potato'), causing several comorbidities which are characterized as preventable non-communicable diseases. Persistent body fat excess associated with deficits of physical activity induces a weight-lifting effect on increasing muscle mass with decreasing mitochondrial capacity. Body fat excess, therefore, correlates with body mass excess up to a critical stage of obesogenic lifestyle-induced sarcopenia, when loss of muscle mass results in further deterioration of physical performance particularly at older age.
VO2max	VO2max; VO2max/M	Maximum oxygen consumption, VO2max, is and index of cardiorespiratory fitness, measured by spiroergometry on human and animal organisms capable of controlled physical exercise performance on a treadmill or cycle ergometer. VO2max is the maximum respiration of an organism, expressed as the volume of O2 at STPD consumed per unit of time per individual object [mL.min-1.x-1]. If normalized per body mass of the individual object, M [kg.x-1], mass specific maximum oxygen consumption, VO2max/M, is expressed in units [mL.min-1.kg-1].