beta 3 e dimagrimento localizzato (solo x esperti)

[x]

ecco il sito anche se avevo un altro che non trovo...questo link dovresti conoscerlo cmq http://www.ricercaitaliana.it/prin/u...067481_002.htm

sto recuperando materiale amico...chiaramente in inglese

Ancora grazie, mister! Posta tutto quello che puoi.

Ascolta, di quella famosa ricerca di Cinti di cui hai messo il link (ricercaitaliana) hai per caso la bibliografia: il testo riporta i riferimenti, ma non la bibliografia...

[x]

i soggetto sono sempre animali...e ripetiamo, gli animali hanno una maggior % di tessuto adiposo bruno...l'uomo ne ha troppo poca per poter trarre giovamento da beta3 agonisti selettivi...vai acercare alcuni studi sulla sinefrina (synephrine in inglese)la cui fonte principale è il citrus aurantium (aracio amaro), ma le qualità lipolitiche di tale frutto nn sono da ricercarsi nella sinefrina che possiede un blando effetto termogenico (vista la scrsità di BAT nell uomo)ma quanto al contenuto in octopamina che ha effetti simili all'efedrina (b2 agonista) ed agisce sul sistema dopaminergico aumentando il rilascio di dopamina..

La sinefrina riduce a livello sinaptico l'uptake della nora, rendendola più disponibile ad esercitare i suoi effetti: riduzione fame (SNC) e lipolisi, per effetto della stimolazione beta-3, che ripeto non sono presenti solo nel BAT, ma anche nel WAT (vWAT o WAT che sia).
E gli effetti li ha... tant'è che è vietata e l'octopamina no.

L'efedrina ha effetti simili, ma è meno selettiva, agendo su tutti e tre i beta recettori.

[x]

il discorso risiede nella circolazione periferica...negli arti x esempio e molto meno marcata e i recettori sono dormienti..invece nei visceri e molto piu' attivo...x capirci ..pensate di stare a una temperatura di 60g e prendetevi un beta agonista..eccolo che il risultato si acentua come per magia...

Dormienti non mi piace... Di fatti quello che tu definisci "più attivo", negli androidi "dorme" pure. E allora a quel punto, come la mettiamo? Non era più attivo nei visceri?
Che poi si parli di roba esogena che "stravolge" tutto, beh...

E poi un agonista come l'efedrina che, come dicevo, è poco selettivo ed agisce su tutti i beta (quindi anche quelli espressi a livello cardiaco, ad esempio), diventa potenzialmente molto più pericoloso di uno rivolto ai beta-3 che sono presenti solo nel tessuto adiposo...

Che poi un agonista beta-3 non funzioni, i motivi possono essere diversi (polimorfismi, mutazioni, citochine...).

[misterblack79]

Ancora grazie, mister! Posta tutto quello che puoi.

Ascolta, di quella famosa ricerca di Cinti di cui hai messo il link (ricercaitaliana) hai per caso la bibliografia: il testo riporta i riferimenti, ma non la bibliografia...

ieri in laboratorio ho contattato un cardiologo che ha parecchi studi a riguardo,purtroppo è un campo lontano dal mio,il mio è alimentare,cmq sto recuperando roba,ripeto come ben sai si trova solo in inglese,poi appena finito ti posto i link oppure ci daremo un contatto casomai ho del materiale cartaceo

[misterblack79]

Ancora grazie, mister! Posta tutto quello che puoi.

Ascolta, di quella famosa ricerca di Cinti di cui hai messo il link (ricercaitaliana) hai per caso la bibliografia: il testo riporta i riferimenti, ma non la bibliografia...

qui trovi parecchia roba interessante,io mi so fatto un giro disicuro trovi quello che ti interessa...i link degli articoli li trovi sulla destra con il loro collegamento internet

[ct-7b]

La sinefrina riduce a livello sinaptico l'uptake della nora, rendendola più disponibile ad esercitare i suoi effetti: riduzione fame (SNC) e lipolisi, per effetto della stimolazione beta-3, che ripeto non sono presenti solo nel BAT, ma anche nel WAT (vWAT o WAT che sia).
E gli effetti li ha... tant'è che è vietata e l'octopamina no.

L'efedrina ha effetti simili, ma è meno selettiva, agendo su tutti e tre i beta recettori.

la sinefrina nn è vietata....difatti viene usata in sostituzione dellefedrina negli ultimi termogenici...
"Active Components and Pharmacology
The most active components in C. aurantium fruit are
synephrine (also called p-synephrine or oxedrine) and
octopamine. C. aurantium peel also contains flavonoids,
including limonene, hesperidin, neohesperidin, naringin,
and tangaretin. Furanocoumarins are also present (5).
Structurally, the active components in C. aurantium are
closely related to endogenous neurotransmitters and ephedrine
(Fig. 1). Synephrine is structurally similar to
epinephrine, and octopamine is similar in structure to
norepinephrine (they differ only in the number of hydroxyl
groups on the aromatic ring; Ref. 6). Closely related to
synephrine is l-m-synephrine (phenylephrine, neosynephrine).
Phenylephrine is an alpha adrenoreceptor agonist used
in conventional medicine as a nasal decongestant and as a
midriatic agent (7). It will not be discussed here because it is
not present in C. aurantium.
Both synephrine and octopamine are trace endogenous
bioamines widely distributed among plants, bacteria, invertebrates,
and vertebrates, including humans. Octopamine is
found in sympathetic nerves, in the same regions as
norepinephrine, whereas synephrine and m-synephrine are
found only in the adrenal glands (8). A recent study in healthy
men and women detected octopamine in the plasma of all 16
subjects, synephrine in 15 subjects, and tyramine, a precursor
of octopamine and synephrine, in 6 subjects (9). Octopamine
and synephrine, but not tyramine, were detectable in the
platelets of most subjects. In rats, p-octopamine has been
identified in adrenals, heart, spleen, vas deferens, brain, liver,
kidney, large intestine, bladder, and lung (8).
Dopamine beta-hydroxylase converts tyramine into
octopamine; this biosynthesis is enhanced by monoamine
oxidase inhibition (10). Phenylethanolamine N-methyl
transferase catabolizes octopamine into synephrine (9).
Synephrine has alpha-adrenergic effects and activates b-3
(but not b-1 or b-2) adrenoreceptors (9). Octopamine
appears to be a selective b-3 adrenoreceptor agonist (10).
Both synephrine and octopamine appear to inhibit cAMP
production (6).
The functions of endogenous synephrine and octopamine
have not been well delineated. Once termed ‘‘false
neurotransmitters,’’ synephrine, octopamine, and tyramine
may in fact be true neurotransmitters (9). These amines may
affect platelet-mediated signaling events, and may contribute
to the pathophysiology of migraine and other types of
headaches (11).
The compound d,l-m-octopamine has an antidipsogenic
effect on angiotensin II-induced water intake in rats. The
effect is apparently mediated by a-2-adrenoreceptors,
because it is blocked by yohimbine (12). Synephrine had
antidepressant-like effects in a mouse model utilizing
immobility tests, but the effect was not dose-related. No
effect was noted at the lowest (0.3 mg/kg) or highest (30
mg/kg) dose, and the effects of 3 mg/kg and 10 mg/kg were
similar (13). Alpha-1 adrenoreceptors appear to be involved,
because the effects of synephrine were reversed by
administration of the a-1 antagonist prazosin. In a later
study by the same group, S-(þ)-p-synephrine was more
effective than R-()-p-synephrine in reducing immobility in
the tail suspension test (14)."

“Beta-3 adrenoreceptor agonists do have lipolytic effects in the fat cells of rats, hamsters, and dogs, but they are much less active in human fat cells. Octopamine was more potent than synephrine (but far less potent than norepinephrine) for stimulating lipolysis in adipocytes from rats, hamsters, or dogs; however, the effect was not significant in fat cells from guinea pigs or humans (10). Octopamine was fully lipolytic in adipocytes from the garden dormouse and Siberian hamster (25).
In rat cells, activation of lipolysis by octopamine was found to be a specific ß-3 adrenergic effect, and was reversible by administration of a ß-3 adrenoreceptor antagonist (ß-1 and ß-2 receptors did not appear to be activated; Ref. 10). Human fat cells respond only to activation of ß-1 or ß-2 receptors (although low levels of ß-3 adrenergic receptors are also expressed). Only high concentrations of synephrine (0.1–1 mM) significantly stimulated lipolysis in the fat cells of humans, hamsters, and guinea pigs, and the effect was not significant in rats (10).”


Citrus aurantium, an Ingredient of Dietary
Supplements Marketed for Weight Loss:
Current Status of Clinical and Basic
Research
ADRIANE FUGH-BERMAN
1
AND ADAM MYERS
Department of Physiology and Biophysics, Georgetown University,
Washington, District of Columbia 20057

sinefrina ed octopamina sono dei beta3 selettivi inoltre inibiscono la produzione di cAMP e questo nn è il massimo al fine della lipolisi..

Selective activation of beta3-adrenoceptors by octopamine: comparative studies in mammalian fat cells.

Carpene C, Galitzky J, Fontana E, Atgie C, Lafontan M, Berlan M.

Institut National de la Sante et de la Recherche Medicale (INSERM), Unite 317, Institut Federatif de Recherches 31, CHU Rangueil, Toulouse, France. carpene@rangueil.inserm.fr

Numerous synthetic agonists selectively stimulate beta3-adrenoceptors (ARs). The endogenous catecholamines, noradrenaline and adrenaline, however, stimulate all the beta-AR subtypes, and no selective physiological agonist for beta3-ARs has been described so far. The aim of this study was to investigate whether any naturally occurring amine can stimulate selectively beta3-ARs. Since activation of lipolysis is a well-known beta-adrenergic function, the efficacy and potency of various biogenic amines were compared with those of noradrenaline, isoprenaline, and beta3-AR agonists 4-(- inverted question mark[2-hydroxy-(3-chlorophenyl)ethyl]-amino inverted question mark propyl)phenoxyacetate (BRL 37,344) and (R,R)-5-(2- inverted question mark[2-(3-chlorophenyl )-2-hydroxyethyl]-amino propyl)-1,3-benzo-dioxole-2,2-dicarboxylate (CL 316,243) by testing their lipolytic action in white fat cells. Five mammalian species were studied: rat, hamster and dog, in which selective beta-AR agonists act as full lipolytic agents, and guinea-pigs and humans, in which beta3-AR agonists are less potent activators of lipolysis. Several biogenic amines were inefficient (e.g. dopamine, tyramine and beta-phenylethylamine) while others (synephrine, phenylethanolamine, epinine) were partially active in stimulating lipolysis in all species studied. Their actions were inhibited by all the beta-AR antagonists tested, including those selective for beta1- or beta2-ARs. Octopamine was the only amine fully stimulating lipolysis in rat, hamster and dog fat cells, while inefficient in guinea-pig or human fat cells, like the beta3-AR agonists. In rat white fat cells, beta-AR antagonists inhibited the lipolytic effect of octopamine with a relative order of potency very similar to that observed against CL 316,243. Competitive antagonism of octopamine effect resulted in the following apparent pA2 [-log(IC50), where IC50 is the antagonist concentration eliciting half-maximal inhibition] values: 7.77 (bupranolol), 6.48 [3-(2-ethyl-phenoxy)-1[(1 S)-1,2,3,4-tetrahydronaphth-1-ylaminol]-(2S)2-propanol oxalate, SR 59230A, a beta3-selective antagonist], 6.30[erythro-D,L-1(7-lethylindan-4-yloxy)-3-isopropylamino-+ ++butan-2-ol, ICI 118,551, a beta2-selective antagonist] and 4.71 [(+/-)-[2-(3-carbomyl-4-hydroxyphenoxy)-ethylamino]-3-[4-(1- methyl-4-trifluoromethyl-2-imidazolyl)-phenoxy]2-propanolmethane sulphonate, CGP 20712A, a beta1-selective antagonist]. Octopamine had other properties in common with beta3-AR agonists: stimulation of oxygen consumption in rat brown fat cells and very low affinity in displacing [3H]CGP 12,177 binding to [beta1- or beta2-ARs in dog and rat adipocyte membranes. In Chinese hamster ovary (CHO) cells expressing human beta3-ARs, octopamine inhibited [125I]ICYP binding with only twofold less affinity than noradrenaline while it exhibited an affinity around 200-fold lower than noradrenaline in CHO cells expressing human beta1- or beta2-ARs. These data suggest that, among the biogenic amines metabolically related to catecholamines, octopamine can be considered as the most selective for beta3-ARs.


Come vedi i beta3 sono poco espressi nel tessuto adiposo umano.

[DORIAN]

Ho questo stesso studio in italiano...ottimo...ne ho citato le parti che ricordavo in un post predente...

[x]

la sinefrina nn è vietata....difatti viene usata in sostituzione dellefedrina negli ultimi termogenici...
"Active Components and Pharmacology
The most active components in C. aurantium fruit are
synephrine (also called p-synephrine or oxedrine) and
octopamine. C. aurantium peel also contains flavonoids,
including limonene, hesperidin, neohesperidin, naringin,
and tangaretin. Furanocoumarins are also present (5).
Structurally, the active components in C. aurantium are
closely related to endogenous neurotransmitters and ephedrine
(Fig. 1). Synephrine is structurally similar to
epinephrine, and octopamine is similar in structure to
norepinephrine (they differ only in the number of hydroxyl
groups on the aromatic ring; Ref. 6). Closely related to
synephrine is l-m-synephrine (phenylephrine, neosynephrine).
Phenylephrine is an alpha adrenoreceptor agonist used
in conventional medicine as a nasal decongestant and as a
midriatic agent (7). It will not be discussed here because it is
not present in C. aurantium.
Both synephrine and octopamine are trace endogenous
bioamines widely distributed among plants, bacteria, invertebrates,
and vertebrates, including humans. Octopamine is
found in sympathetic nerves, in the same regions as
norepinephrine, whereas synephrine and m-synephrine are
found only in the adrenal glands (8). A recent study in healthy
men and women detected octopamine in the plasma of all 16
subjects, synephrine in 15 subjects, and tyramine, a precursor
of octopamine and synephrine, in 6 subjects (9). Octopamine
and synephrine, but not tyramine, were detectable in the
platelets of most subjects. In rats, p-octopamine has been
identified in adrenals, heart, spleen, vas deferens, brain, liver,
kidney, large intestine, bladder, and lung (8).
Dopamine beta-hydroxylase converts tyramine into
octopamine; this biosynthesis is enhanced by monoamine
oxidase inhibition (10). Phenylethanolamine N-methyl
transferase catabolizes octopamine into synephrine (9).
Synephrine has alpha-adrenergic effects and activates b-3
(but not b-1 or b-2) adrenoreceptors (9). Octopamine
appears to be a selective b-3 adrenoreceptor agonist (10).
Both synephrine and octopamine appear to inhibit cAMP
production (6).
The functions of endogenous synephrine and octopamine
have not been well delineated. Once termed ‘‘false
neurotransmitters,’’ synephrine, octopamine, and tyramine
may in fact be true neurotransmitters (9). These amines may
affect platelet-mediated signaling events, and may contribute
to the pathophysiology of migraine and other types of
headaches (11).
The compound d,l-m-octopamine has an antidipsogenic
effect on angiotensin II-induced water intake in rats. The
effect is apparently mediated by a-2-adrenoreceptors,
because it is blocked by yohimbine (12). Synephrine had
antidepressant-like effects in a mouse model utilizing
immobility tests, but the effect was not dose-related. No
effect was noted at the lowest (0.3 mg/kg) or highest (30
mg/kg) dose, and the effects of 3 mg/kg and 10 mg/kg were
similar (13). Alpha-1 adrenoreceptors appear to be involved,
because the effects of synephrine were reversed by
administration of the a-1 antagonist prazosin. In a later
study by the same group, S-(þ)-p-synephrine was more
effective than R-()-p-synephrine in reducing immobility in
the tail suspension test (14)."

“Beta-3 adrenoreceptor agonists do have lipolytic effects in the fat cells of rats, hamsters, and dogs, but they are much less active in human fat cells. Octopamine was more potent than synephrine (but far less potent than norepinephrine) for stimulating lipolysis in adipocytes from rats, hamsters, or dogs; however, the effect was not significant in fat cells from guinea pigs or humans (10). Octopamine was fully lipolytic in adipocytes from the garden dormouse and Siberian hamster (25).
In rat cells, activation of lipolysis by octopamine was found to be a specific ß-3 adrenergic effect, and was reversible by administration of a ß-3 adrenoreceptor antagonist (ß-1 and ß-2 receptors did not appear to be activated; Ref. 10). Human fat cells respond only to activation of ß-1 or ß-2 receptors (although low levels of ß-3 adrenergic receptors are also expressed). Only high concentrations of synephrine (0.1–1 mM) significantly stimulated lipolysis in the fat cells of humans, hamsters, and guinea pigs, and the effect was not significant in rats (10).”


Citrus aurantium, an Ingredient of Dietary
Supplements Marketed for Weight Loss:
Current Status of Clinical and Basic
Research
ADRIANE FUGH-BERMAN
1
AND ADAM MYERS
Department of Physiology and Biophysics, Georgetown University,
Washington, District of Columbia 20057

sinefrina ed octopamina sono dei beta3 selettivi inoltre inibiscono la produzione di cAMP e questo nn è il massimo al fine della lipolisi..

Selective activation of beta3-adrenoceptors by octopamine: comparative studies in mammalian fat cells.

Carpene C, Galitzky J, Fontana E, Atgie C, Lafontan M, Berlan M.

Institut National de la Sante et de la Recherche Medicale (INSERM), Unite 317, Institut Federatif de Recherches 31, CHU Rangueil, Toulouse, France. carpene@rangueil.inserm.fr

Numerous synthetic agonists selectively stimulate beta3-adrenoceptors (ARs). The endogenous catecholamines, noradrenaline and adrenaline, however, stimulate all the beta-AR subtypes, and no selective physiological agonist for beta3-ARs has been described so far. The aim of this study was to investigate whether any naturally occurring amine can stimulate selectively beta3-ARs. Since activation of lipolysis is a well-known beta-adrenergic function, the efficacy and potency of various biogenic amines were compared with those of noradrenaline, isoprenaline, and beta3-AR agonists 4-(- inverted question mark[2-hydroxy-(3-chlorophenyl)ethyl]-amino inverted question mark propyl)phenoxyacetate (BRL 37,344) and (R,R)-5-(2- inverted question mark[2-(3-chlorophenyl )-2-hydroxyethyl]-amino propyl)-1,3-benzo-dioxole-2,2-dicarboxylate (CL 316,243) by testing their lipolytic action in white fat cells. Five mammalian species were studied: rat, hamster and dog, in which selective beta-AR agonists act as full lipolytic agents, and guinea-pigs and humans, in which beta3-AR agonists are less potent activators of lipolysis. Several biogenic amines were inefficient (e.g. dopamine, tyramine and beta-phenylethylamine) while others (synephrine, phenylethanolamine, epinine) were partially active in stimulating lipolysis in all species studied. Their actions were inhibited by all the beta-AR antagonists tested, including those selective for beta1- or beta2-ARs. Octopamine was the only amine fully stimulating lipolysis in rat, hamster and dog fat cells, while inefficient in guinea-pig or human fat cells, like the beta3-AR agonists. In rat white fat cells, beta-AR antagonists inhibited the lipolytic effect of octopamine with a relative order of potency very similar to that observed against CL 316,243. Competitive antagonism of octopamine effect resulted in the following apparent pA2 [-log(IC50), where IC50 is the antagonist concentration eliciting half-maximal inhibition] values: 7.77 (bupranolol), 6.48 [3-(2-ethyl-phenoxy)-1[(1 S)-1,2,3,4-tetrahydronaphth-1-ylaminol]-(2S)2-propanol oxalate, SR 59230A, a beta3-selective antagonist], 6.30[erythro-D,L-1(7-lethylindan-4-yloxy)-3-isopropylamino-+ ++butan-2-ol, ICI 118,551, a beta2-selective antagonist] and 4.71 [(+/-)-[2-(3-carbomyl-4-hydroxyphenoxy)-ethylamino]-3-[4-(1- methyl-4-trifluoromethyl-2-imidazolyl)-phenoxy]2-propanolmethane sulphonate, CGP 20712A, a beta1-selective antagonist]. Octopamine had other properties in common with beta3-AR agonists: stimulation of oxygen consumption in rat brown fat cells and very low affinity in displacing [3H]CGP 12,177 binding to [beta1- or beta2-ARs in dog and rat adipocyte membranes. In Chinese hamster ovary (CHO) cells expressing human beta3-ARs, octopamine inhibited [125I]ICYP binding with only twofold less affinity than noradrenaline while it exhibited an affinity around 200-fold lower than noradrenaline in CHO cells expressing human beta1- or beta2-ARs. These data suggest that, among the biogenic amines metabolically related to catecholamines, octopamine can be considered as the most selective for beta3-ARs.


Come vedi i beta3 sono poco espressi nel tessuto adiposo umano.

Premesso che in medicina per ogni studio ce n'è almeno uno contrario, quest'ultimo è un pò "vecchiotto"... è del '99... Il caso del maiale della guinea che riporta è stato infatti spiegato successivamente.

Ad ogni modo, tu - e con tu intendo le ricerche di cui sei a conoscenza, chiaramente - sostieni che le catecolamine agirebbero sugli adipociti (parliamo principalmente di bianchi) praticamente solo (o quasi) sugli altri beta, 1 e 2?

[DORIAN]

dagli studi che ho io...sembrerebbe che sia fondametale l'azione sui beta-2.

[misterblack79]

dagli studi che ho io...sembrerebbe che sia fondametale l'azione sui beta-2.

quella credo che sia l'unica cosa sicura...anche io sto avendo riscontro solo di questo fin ora

[ct-7b]

Ad ogni modo, tu - e con tu intendo le ricerche di cui sei a conoscenza, chiaramente - sostieni che le catecolamine agirebbero sugli adipociti (parliamo principalmente di bianchi) praticamente solo (o quasi) sugli altri beta, 1 e 2?

epinefrina e norepinefrina agiscono sia sugli alfa che sui beto, hanno, quindi, proprietà lipolitiche ed anti lipolitiche (nei tessuti con maggior espressione di alfa2 AR)...inoltre aumentano il Camp e ciò è importante per stimolare l'ossidazione degli FFA...
..sinefrina ed octopamina sono beta3 agonisti selettivi (anche se la octopamina ha un blando effetto agonista sugli alfa 2), ma inibiscono il Camp e questo nn è buono a fini lipolitici..

[x]

dagli studi che ho io...sembrerebbe che sia fondametale l'azione sui beta-2.

Sì, ma qual'è la presenza degli altri beta negli adipociti (WAT e/o BAT)? Non mi riferisco al rapporto con gli alpha, ma ai soli beta.

Inoltre, il meccanismo lipolitico degli altri beta negli adipociti dovrebbe essere uguale a quello del beta-3:
(AC ---> cAMP---> PKA ---> HSL ---> LIPOLISI)

ma nelle altre cellule (ad es. quelle cardiache) il legame NE-beta recettore che cascata attiverà?

[ct-7b]

Sì, ma qual'è la presenza degli altri beta negli adipociti (WAT e/o BAT)? Non mi riferisco al rapporto con gli alpha, ma ai soli beta.

Inoltre, il meccanismo lipolitico degli altri beta negli adipociti dovrebbe essere uguale a quello del beta-3:
(AC ---> cAMP---> PKA ---> HSL ---> LIPOLISI)

ma nelle altre cellule (ad es. quelle cardiache) il legame NE-beta recettore che cascata attiverà?

mi pare di averti postato un link sul tutto il sistema adrenegico....
..

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=bnchm.TOC&depth=10

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=bnchm.section.890

[x]

mi pare di averti postato un link sul tutto il sistema adrenegico....
..

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=bnchm.TOC&depth=10

http://www.ncbi.nlm.nih.gov/books/bv...hm.section.890

Ho letto il lavoro, ma non ho trovato riferimenti al tessuto adiposo (se non li ho visti io, mi scuso):
b1-Adrenergic receptors predominate in the heart and in the cerebral cortex, whereas b2-adrenergic receptors predominate in the lung and cerebellum.


Torno dunque a chiedere: qual’è la presenza degli altri beta negli adipociti?

Inoltre, da queste zone (cuore, cervello, polmoni), l’effetto sulla lipolisi dovrebbe essere indiretto (aumento frequenza cardica o respiratoria, ad esempio), giusto?


Mi interessa poi capire una cosa.
Voi dite che potrebbero essere altri recettori beta (soprattutto i beta-2, mi pare di aver capito) a mediare la lipolisi negli adipociti. Ma se i beta-3 non sono così tanto espressi nell’uomo, perché nelle popolazioni in cui si è manifestata una mutazione del gene che codifica per tale recettore si presentano in maniera devastante l’obesità ed il NIDDM (attribuiti entrambi al polimorfismo del gene)? Gli effetti mancanti dei beta-3 non dovrebbero essere prontamente svolti dai beta-2?

[ct-7b]

Mi interessa poi capire una cosa.
Voi dite che potrebbero essere altri recettori beta (soprattutto i beta-2, mi pare di aver capito) a mediare la lipolisi negli adipociti. Ma se i beta-3 non sono così tanto espressi nell’uomo, perché nelle popolazioni in cui si è manifestata una mutazione del gene che codifica per tale recettore si presentano in maniera devastante l’obesità ed il NIDDM (attribuiti entrambi al polimorfismo del gene)? Gli effetti mancanti dei beta-3 non dovrebbero essere prontamente svolti dai beta-2?

ti ripeto, dagli studi che ho postato qualche pagina prima, nell'uomo i beta 3 sono poco espressi....nn ho trovato alcuno studio che mostrasse l'utilità di un beta3 agonista nell'uomo.....
...ho anche dato uno sguardo alla tua bibliografia, imho stai sbagliando, il 90% degli studi che hai ricercato sono condotti sugli animali...
..posta lo studio su questa mutazione genica....