Acido Ursolico

[LiborioAsahi]

fregatene dei dati quantitativi sui topi. Non sono attendibili. è il principio che conta, per le quantità meglio basarsi su studi con cavie umane!

[Trokji]

va bene!!

[orange]

Facciamo bim bum bam per vedere a chi tocca sta volta fare da cavia?

[LiborioAsahi]

purtroppo ho perso io. Procuratemi la sbobba da assumere. E in fretta.

[D. Ace]

inizia a sbucciare mele XD

[Bomb Jack]

Originariamente inviato da LiborioAsahi

purtroppo ho perso io. Procuratemi la sbobba da assumere. E in fretta.

[Bomb Jack]

...intanto avevo trovato questi, ma sono solo sul dimagrimento e solo sui topi:

Mol Nutr Food Res. 2010 Nov;54(11):1609-17.
Ursolic acid stimulates lipolysis in primary-cultured rat adipocytes.

Li Y, Kang Z, Li S, Kong T, Liu X, Sun C.
Source

Department of Nutrition and Food Hygiene, Public Health College, Harbin Medical University, Harbin, PR China.

Abstract

Ursolic acid (UA) is a pentacyclic triterpenic acid with many biological functions naturally existing in many kinds of food. To investigate whether UA can accelerate lipolysis, primary-cultured rat adipocytes were treated with UA, and glycerol release in the culture medium was measured. UA stimulated lipolysis significantly. Furthermore, the lipolytic effect of UA was inhibited by the protein kinase A (PKA) specific inhibitor H89, suggesting that UA exerted its lipolytic function through the cAMP-dependent PKA pathway. Downstream targets of the PKA pathway, hormone-sensitive lipase (HSL) and perilipin A were checked, UA enhanced lipolysis by promoting the translocation of HSL from the cytosol to the lipid droplets and inhibiting the expression of perilipin A. Additionally, adipose triglyceride lipase (ATGL), a novel rate-limiting lipase in the lipolytic catabolism, was upregulated by UA. UA-induced expression of ATGL could not be blocked by H89, suggesting that ATGL upregulation is not regulated by the PKA pathway. These findings suggest that UA significantly stimulates lipolysis by translocating HSL, decreasing perilipin A expression by the PKA pathway, and up-regulating ATGL in primary cultured adipocytes. Thus, UA is a promising candidate for the treatment of obesity.

PMID:20521271 [PubMed - indexed for MEDLINE]

Arch Pharm Res. 2009 Jul;32(7):983-7. Epub 2009 Jul 31.
Anti-lipase and lipolytic activities of ursolic acid isolated from the roots of Actinidia arguta.

Kim J, Jang DS, Kim H, Kim JS.
Source

Diabetic Complications Research Center, Division of Traditional Korean Medicine (TKM) Integrated Research, Korea Institute of Oriental Medicine (KIOM), Daejeon, 305-811, Korea.

Abstract

The aim of this study was to investigate the anti-obestic effects of ursolic acid isolated from the roots of Actinidia arguta, as well as the mechanism of action of this compound. This was conducted by testing whether ursolic acid inhibited the elevation of the rat plasma triacylglycerol levels after oral administration of a lipid emulsion containing corn oil in rats. Ursolic acid prevented the elevation of plasma triacylglycerol levels 2 h after oral administration of the lipid emulsion at a dose of 100 mg/kg. Furthermore, ursolic acid inhibited phosphodiesterase activity in vitro with an IC(50) of 51.21 muM and enhanced lipolysis in rat fat cells. We suggest that the inhibitory effects of ursolic acid, isolated from the roots of A. arguta, on obesity, might be attributable to the inhibition of lipid absorption through the inhibition of pancreatic lipase and by enhancing lipolysis in fat cells.

PMID:19641878 [PubMed - indexed for MEDLINE]

Phytother Res. 2010 Jan;24(1):49-53.
Stimulation of glucose uptake by triterpenoids from Weigela subsessilis.

Lee MS, Thuong PT.
Source

Department of Food and Nutrition, Chungnam National University, 220 Gung-dong, Yuseong-gu, Daejeon 305-764, Republic of Korea. myunglee@cnu.ac.kr

Abstract

Four ursane-type triterpenoids, corosolic acid (1), ilekudinol B (2), ursolic acid (3) and pomolic acid (4), were isolated from an EtOAc-soluble extract of the leaves of Weigela subsessilis. These bioactive compounds were evaluated for their glucose uptake activity and produced moderate to strong enhancement both in basal- and insulin-stimulated L6 muscle cells. In particular, corosolic acid exhibited the most potent activity, increasing uptake by basal- and insulin-stimulated myotubes by 2.63- and 3.33-fold, respectively; ilekudinol B produced 1.6- and 2.9-fold, ursolic acid produced 1.84- and 2.64-fold, and pomolic acid produced 1.6- and 2.8-fold increases. No cytotoxicities were observed for corosolic acid, ursolic acid and ilekudinol B in myoblasts, while pomolic acid at doses of 25 and 50 microm reduced cell viability by 19% and 21.8% upon 24 h treatment and by 48.6% and 54.1% upon 48 h treatment, respectively. These results suggest that ursane-type triterpenoids from W. subsessilis might enhance glucose uptake by acting as insulin mimics and as insulin sensitizers and that they could be useful as nontoxic diabetes treatment agents.
(c) 2009 John Wiley & Sons, Ltd.

PMID:19548274 [PubMed - indexed for MEDLINE]

[rockclimber]

Originariamente inviato da Guru

mRNA Expression Signatures of Human Skeletal Muscle Atrophy Identify a Natural Compound that Increases Muscle Mass.
Kunkel SD, Suneja M, Ebert SM, Bongers KS, Fox DK, Malmberg SE, Alipour F, Shields RK, Adams CM.
Source
Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USA; Department of Veterans Affairs Medical Center, Iowa City, IA 52246, USA.
Abstract
Skeletal muscle atrophy is a common and debilitating condition that lacks a pharmacologic therapy. To develop a potential therapy, we identified 63 mRNAs that were regulated by fasting in both human and mouse muscle, and 29 mRNAs that were regulated by both fasting and spinal cord injury in human muscle. We used these two unbiased mRNA expression signatures of muscle atrophy to query the Connectivity Map, which singled out ursolic acid as a compound whose signature was opposite to those of atrophy-inducing stresses. A natural compound enriched in apples, ursolic acid reduced muscle atrophy and stimulated muscle hypertrophy in mice. It did so by enhancing skeletal muscle insulin/IGF-I signaling and inhibiting atrophy-associated skeletal muscle mRNA expression. Importantly, ursolic acid's effects on muscle were accompanied by reductions in adiposity, fasting blood glucose, and plasma cholesterol and triglycerides. These findings identify a potential therapy for muscle atrophy and perhaps other metabolic diseases.

Sembra molto promettente.

Stando a quanto scrivono, non solo aumenta la muscolatura attraverso l'aumentata risposta di questa ad IGF-1 ed insulina (il che, aggiungo io, potrebbe fargli avere anche un ruolo nel trattamento del diabete o almeno della sindrome x), ma riduce anche il grasso corporeo.

Di integratori ce ne sono ma non ne ho visti in Italia.
Diciamo anche che, fin'ora, era proposto come antiossidante/antitumorale, visto che ci sono studi a riguardo.

giusto per completezza l'articoloc compare cu cell metabolism..impact factor 17.95...sti cazzi.

[mistersalvo]

io ho trovato una crema titolata la 90%

Acido Ursolico estratto dal Rosmarinus officinalis con
eccellenti proprietà nel ripristino della funzionalità
della pelle sottoposta a stress da raggi UV-A e UVB, grazie all’effetto Antiinfiammatorio, per inibizione
di elastasi e ciclossigenasi. Per azione rigenerante
sulle fibre di collagene è indicato per la riduzione
delle rughe. Indicato quindi come Rigenerante e
Anti Age. Favorisce inoltre la crescita di capelli
sani e forti.
Tit. 90% Acido Ursolico

[LoStefo]

Originariamente inviato da mistersalvo

io ho trovato una crema titolata la 90%

Acido Ursolico estratto dal Rosmarinus officinalis con
eccellenti proprietà nel ripristino della funzionalità
della pelle sottoposta a stress da raggi UV-A e UVB, grazie all’effetto Antiinfiammatorio, per inibizione
di elastasi e ciclossigenasi. Per azione rigenerante
sulle fibre di collagene è indicato per la riduzione
delle rughe. Indicato quindi come Rigenerante e
Anti Age. Favorisce inoltre la crescita di capelli
sani e forti.
Tit. 90% Acido Ursolico

Ne prendo una fornitura vitalizia! Come si chiama la crema mister?

[mistersalvo]

è della sochim

[LoStefo]

Grazie!

[Bomb Jack]

La discussione dello studio (dove si spiega tutto):

Landmark studies using rodent models showed that diverse atrophy-inducing stresses (including fasting, systemic illness, and muscle disuse) generate similar patterns of changes in skeletal mRNA expression (Sacheck et al., 2007). We translated those findings to humans by determining the effect of fasting on global skeletal muscle mRNA expression in human skeletal muscle. Our fasting protocol was well tolerated by subjects, relatively simple to execute, and required only a few subjects to discern important changes in skeletal muscle mRNA expression. For example, it allowed us to demonstrate, for the first time, fasting-mediated induction of atrogin-1 and MuRF1mRNAs in human skeletal muscle.
In human skeletal muscle, fasting altered levels of >500 skeletal muscle mRNAs (approximately 3% of the total mRNAs examined). However, only a few of these mRNAs are known to play central roles in muscle atrophy in mice (includingatrogin-1, MuRF1, ZFAND5, and PGC-1α). Likewise, most mRNAs that were altered by fasting in both human and mouse muscle (which formed the basis for our first Connectivity Map query), and most mRNAs that were altered by both fasting and SCI in human muscle (which formed the basis for our second Connectivity Map query), have undefined roles in muscle atrophy. Although we do not yet know the functional roles of most mRNAs whose levels are altered by fasting or SCI, or the precise mechanisms that regulate them in the setting of an atrophy-inducing stress, we used these data to query the Connectivity Map. This unbiased approach singled out one compound as a predicted inhibitor of atrophy-inducing stress: ursolic acid.
A water-insoluble pentacyclic triterpenoid, ursolic acid is the major waxy component in apple peels (Frighetto et al., 2008). It is also found in many other edible plants. Interestingly, because it exerts beneficial effects in animal models of diabetes and hyperlipidemia (Liu, 1995,Wang et al., 2009), ursolic acid is thought to be the active component in a variety of folkloric antidiabetic herbal medicines (Liu, 1995,Liu, 2005). As predicted by the Connectivity Map, we found thatursolic acid reduced skeletal muscle atrophy in the setting of two distinct atrophy-inducing stresses (fasting and muscle denervation). A major strength of the Connectivity Map is that it takes into account positive and negative changes in mRNA expression that together constitute an authentic mRNA expression signature. Thus, by querying the Connectivity Map with signatures of muscle atrophy, we were, in effect, querying with the reciprocal signature of muscle hypertrophy. Indeed, ursolic acid not only reduced muscle atrophy but also induced muscle hypertrophy.
The strategy that led us to ursolic acid implied that ursolic acid might increase muscle mass by inhibiting atrophy-associated skeletal muscle gene expression. Indeed, we found that acute ursolic acid treatment of fasted mice reducedatrogin-1 and MuRF1 mRNAs in association with reduced muscle atrophy. Similarly, chronic ursolic acid treatment of unstressed mice reduced atrogin-1 and MuRF1 mRNAs and induced muscle hypertrophy. Interestingly, ursolic acid-induced muscle hypertrophy was also associated with induction or repression of >60 other skeletal muscle mRNAs, including IGF1 mRNA (which was induced). Although previous studies showed that increased skeletal muscle IGF1expression is sufficient to inhibit atrophy and promote hypertrophy, we noted that, following a hypertrophic stimulus such as mechanical loading, increased IGF1 gene expression is a late event (Adams et al., 1999). We therefore asked whether ursolic acid might stimulate earlier events in insulin/IGF-I signaling by examining skeletal muscle Akt activation, a critical node in the insulin and IGF-I signaling cascades. Indeed, in muscles that had hypertrophied secondary to chronic ursolic acid treatment, Akt phosphorylation was increased. Interestingly, this increase in skeletal muscle Aktactivity can potentially account for many of ursolic acid's effects, including reduced atrophy-associated gene expression, reduced muscle atrophy, increased muscle hypertrophy, and reduced adiposity (Izumiya et al., 2008,Lai et al., 2004). However, additional studies will be needed to determine whether Akt is required for the effects of ursolic acid, and whether other pathways (such as the calcineurin/NFAT and MAP kinase pathways) might also be involved.
Although ursolic acid increased skeletal muscle Akt phosphorylation in vivo, those experiments could not determine ifursolic acid acted directly on skeletal muscle, how quickly ursolic acid acted, and if the effect of ursolic acid requiredIGF-I or insulin, which are always present in healthy animals, even during fasting. To address these questions, we studied serum-starved skeletal myotubes and found that ursolic acid rapidly stimulated IGF-I receptor and insulin receptoractivity, but only if IGF-I or insulin was also present. Taken together, our data suggest that ursolic acid first enhances the capacity of pre-existing IGF-I and insulin to activate skeletal muscle IGF-I receptors and insulin receptors, respectively. This activates Akt, S6K, and ERK and alters skeletal muscle gene expression in a manner that reduces atrophy and promotes hypertrophy. Specific changes in downstream gene expression include induction of IGF1 (a feed-forward mechanism that likely contributes to ursolic acid-mediated hypertrophy), repression of atrogin-1 and MuRF1, and induction or repression of many other genes whose contributions to muscle atrophy or hypertrophy remain to be determined. Some of these changes in skeletal muscle gene expression (such as repression of atrogin-1 and MuRF1) can be explained by our finding that ursolic acid enhances IGF-I-mediated inhibition of FoxO transcription factors. However, ursolic acid might also inhibit other transcription factors that promote atrophy, such as NF-kB, and this is an important area for future investigation.
Importantly, ursolic acid alone was not sufficient to increase phosphorylation of the IGF-I receptor or the insulin receptor. Rather, its effects also required IGF-I or insulin, respectively. This suggests that ursolic acid either facilitates hormone-mediated receptor autophosphorylation or it inhibits receptor dephosphorylation. The latter possibility is supported by previous in vitro data showing that ursolic acid directly inhibits PTP1B (Zhang et al., 2006), a tyrosine phosphatase that dephosphorylates (inactivates) the IGF-I and insulin receptors (Kenner et al., 1996). However, neither global nor muscle-specific PTP1B knockout mice were found to possess increased muscle mass (Delibegovic et al., 2007,Klaman et al., 2000). This may suggest the existence of another receptor for ursolic acid, which might be closely related to PTP1B. Identifying the receptor(s) for ursolic acid is an important area for future investigation that may elucidate important mechanisms of metabolic control. Pharmacokinetic studies of ursolic acid will also be critical for fully understanding its in vivo effects.
Given the current lack of therapies for skeletal muscle atrophy, we speculate that ursolic acid might be investigated as a potential therapy for illness- and age-related muscle atrophy. It may be useful as a monotherapy or in combination with other strategies that have been considered, such as myostatin inhibition (Zhou et al., 2010). Given its capacity to reduce adiposity, fasting blood glucose, and plasma lipid levels, ursolic acid might also be investigated as a potential therapy for obesity, metabolic syndrome, and type 2 diabetes. A systematic search for ursolic acid derivatives that are more potent and/or efficacious could also be undertaken. Further work in this area may lead to new medical therapies for increasingly common metabolic diseases that reduce the absolute or relative amount of skeletal muscle.

Molto, molto interessante...
I risultati sembrano solidi anche se vanno ancora svelati alcuni meccanismi in maniera più precisa.

Ho fatto una ricerca su pubmed: sembra l'unica sostanza di origine naturale in grado di contrastare i fattori di atrofia muscolare (che, e si è scoperto anche grazie a questo studio, se vengono inibiti causano ipertrofia a prescindere).

[LiborioAsahi]

[novellino]

Originariamente inviato da LiborioAsahi

Rigorosamente a "metà" , postare anche l'etichetta costava troppa fatica