Originariamente Scritto da marco78
Visualizza Messaggio
Castellino P, Luzi L, Simonson DC, Haymond M, DeFronzo RA.
Division of Endocrinology/Diabetes, Yale University School of Medicine, New Haven, Connecticut 06510.
We examined the effect of insulin and plasma amino acid concentrations on leucine kinetics in 15 healthy volunteers (age 22 +/- 2 yr) using the euglycemic insulin clamp technique and an infusion of [1-14C]leucine. Four different experimental conditions were examined: (a) study one, high insulin with reduced plasma amino acid concentrations; (b) study two, high insulin with maintenance of basal plasma amino acid concentrations; (c) study three, high insulin with elevated plasma amino acid concentrations; and (d) study four, basal insulin with elevated plasma amino acid concentrations. Data were analyzed using both the plasma leucine and alpha-ketoisocaproate (the alpha-ketoacid of leucine) specific activities. In study one total leucine flux, leucine oxidation, and nonoxidative leucine disposal (an index of whole body protein synthesis) all decreased (P less than 0.01) regardless of the isotope model utilized. In study two leucine flux did not change, while leucine oxidation increased (P less than 0.01) and nonoxidative leucine disposal was maintained at the basal rate; endogenous leucine flux (an index of whole body protein degradation) decreased (P less than 0.01). In study three total leucine flux, leucine oxidation, and nonoxidative leucine disposal all increased significantly (P less than 0.01). In study four total leucine flux, leucine oxidation, and nonoxidative leucine disposal all increased (P less than 0.001), while endogenous leucine flux decreased (P less than 0.001). We conclude that: (a) hyperinsulinemia alone decreases plasma leucine concentration and inhibits endogenous leucine flux (protein breakdown), leucine oxidation, and nonoxidative leucine disposal (protein synthesis); (b) hyperaminoacidemia, whether in combination with hyperinsulinemia or with maintained basal insulin levels decreases endogenous leucine flux and stimulates both leucine oxidation and nonoxidative leucine disposal.
Come vedi nn cambia nulla tra l'iperinsulinemia ed un livello normale di insulina se la disponibilità di aminoacidi è mantenuta positiva
Differential effects of hyperinsulinemia and hyperaminoacidemia on leucine-carbon metabolism in vivo. Evidence for distinct mechanisms in regulation of net amino acid deposition.
Tessari P, Inchiostro S, Biolo G, Trevisan R, Fantin G, Marescotti MC, Iori E, Tiengo A, Crepaldi G.
The effects of physiologic hyperinsulinemia and hyperaminoacidemia, alone or in combination, on leucine kinetics in vivo were studied in postabsorptive healthy subjects with primed-constant infusions of L-[4,5-3H]leucine and [1-14C]alpha-ketoisocaproate (KIC) under euglycemic conditions. Hyperinsulinemia (approximately 100 microU/ml) decreased (P less than 0.05 vs. baseline) steady state Leucine + KIC rates of appearance (Ra) from proteolysis, KIC (approximately leucine-carbon) oxidation, and nonoxidized leucine-carbon flux (leucine----protein). Hyperaminoacidemia (plasma leucine, 210 mumol/liter), with either basal hormone replacement or combined to hyperinsulinemia, resulted in comparable increases in leucine + KIC Ra, KIC oxidation, and leucine----protein (P less than 0.05 vs. baseline). However, endogenous leucine + KIC Ra was suppressed only with the combined infusion. Therefore, on the basis of leucine kinetic data, hyperinsulinemia and hyperaminoacidemia stimulated net protein anabolism in vivo by different mechanisms. Hyperinsulinemia decreased proteolysis but did not stimulate leucine----protein. Hyperaminoacidemia per se stimulated leucine----protein but did not suppress endogenous proteolysis. When combined, they had a cumulative effect on net leucine deposition into body protein.
Bene, questo è ciò di cui ti parlavo....
l'iperinsulinemia nn è anabolica, ma anticatabolica, blocca la proteolisi...
iperaminoacidemia è anabolica (aumenta l'utilizzao della leucina a scopo proteogenico), ma nn anticatabolica (nn inibisce la proteolisi)....l'unione dei 2 fattori potrebbe darci il massimo anabolismo tissutale. Ciò però ci riporta aal primo studio, dove nn abbiamo aluna differenza nel flusso della leucina tra un clamp iperinsulinemico o uno normoinsulinemico se rimane costante ed alta la disponibilità di aminoacidi...
..l'insulina, di per se, nn è anabolica....la ricerca di un clamp iperinsulinemico è solo una boiata...e nn porta ad alcun effetto positivo.....solo la totale inibizione della lipolisi e se si sta in ipercalorica, un aumento delle scorte di adipe..
poi riguardo all'azione dell'insulina su IGF-1..
L' IGF-1 è un ormone pepetidico rilasciato dall'epatocito sotto stimolo di insulina + GH....l'iperinsulinemia (cerca tutti gli studi che vuoi, ne ho una marea) blocca il rilascio di GH.....indi...nada IGF-1
l'insulina è anabolica sul tessuto adiposo ed anticatabolica sul tessuto muscolare.....
....poi potete credere ciò che volete, ma vi consiglierei di provare, sia in massa che definizione, di buttare via destrosio e compagnia bella nel post e farvi solo un bel pasto completo....nell'immediato post wo solo siero pro....dopo carbo+grassi+proteine....noterete dei miglioramenti nella composizione corporea..
Commenta