Hyperaminoacidaemia at postprandial levels does not modulate glucose metabolism in type 2 diabetes mellitus

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dc.contributor.author Bassil, M.
dc.contributor.author Burgos, S.
dc.contributor.author Marliss, E.B.
dc.contributor.author Morais, J.A.
dc.contributor.author Chevalier, S.
dc.contributor.author Gougeon, R.
dc.date.accessioned 2015-12-04T09:11:11Z
dc.date.available 2015-12-04T09:11:11Z
dc.date.copyright 2011
dc.date.issued 2015-12-04
dc.identifier.issn 0012-186X en_US
dc.identifier.uri http://hdl.handle.net/10725/2756
dc.description.abstract Aims/hypothesis Hyperaminoacidaemia attenuates glucose disposal during hyperinsulinaemic clamps in healthy lean individuals, an effect thought to be mediated by negative feedback on insulin signalling, downstream of the mammalian target of rapamycin (mTOR) signalling pathway. This has been interpreted as amino acids causing insulin resistance in healthy people, and contributing to it in type 2 diabetes. However, the effect of hyperaminoacidaemia on glucose disposal in type 2 diabetic individuals remains to be determined. Methods Eight obese men with type 2 diabetes underwent a two-step hyperinsulinaemic–hyperglycaemic (8 mmol/l) clamp, first with amino acids at postabsorptive concentrations, followed by postprandial concentrations. Whole-body glucose turnover was assessed using d-[3-3H]glucose. Vastus lateralis biopsies were obtained at baseline and during each step of the clamp to determine the phosphorylation states of AKT, mTOR, ribosomal protein (rp) S6, and insulin receptor substrate (IRS)-1. Results Rates of glucose infusion (1.30 ± 0.19 vs 1.15 ± 0.13 mmol/min), endogenous glucose production (0.48 ± 0.06 vs 0.53 ± 0.05 mmol/min) and disposal (1.24 ± 0.17 vs 1.17 ± 0.14 mmol/min) did not differ between postabsorptive and postprandial amino acid concentrations (p > 0.05). Whereas phosphorylation of AKTSer473, AKTThr308 mTORSer2448 and rpS6Ser235/236 increased (p < 0.05) with elevated amino acids, that of IRS-1Ser636/639 and IRS-1Ser1101 did not change. Conclusions/interpretation Postprandial circulating amino acid concentrations do not worsen the already attenuated glucose disposal in hyperglycaemic type 2 diabetic men, and cell-signalling events are consistent with this. Our results do not support recommendations to restrict dietary protein in type 2 diabetes. en_US
dc.language.iso en en_US
dc.title Hyperaminoacidaemia at postprandial levels does not modulate glucose metabolism in type 2 diabetes mellitus en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SAS en_US
dc.author.idnumber 201102356 en_US
dc.author.woa N/A en_US
dc.author.department Natural Sciences en_US
dc.description.embargo N/A en_US
dc.relation.journal Diabetologia en_US
dc.journal.volume 54 en_US
dc.journal.issue 7 en_US
dc.article.pages 1810-1818 en_US
dc.keywords Glucose disposal en_US
dc.keywords Glucose metabolism en_US
dc.keywords Glucose turnover en_US
dc.keywords Hyperaminoacidaemia en_US
dc.keywords Hyperinsulinaemic clamp en_US
dc.keywords Insulin resistance en_US
dc.keywords Type 2 diabetes en_US
dc.identifier.doi http://dx.doi.org/10.1007/s00125-011-2115-7 en_US
dc.identifier.ctation Bassil, M., Burgos, S., Marliss, E. B., Morais, J. A., Chevalier, S., & Gougeon, R. (2011). Hyperaminoacidaemia at postprandial levels does not modulate glucose metabolism in type 2 diabetes mellitus. Diabetologia, 54(7), 1810-1818. en_US
dc.author.email mbassil@lau.edu.lb
dc.identifier.url http://link.springer.com/article/10.1007/s00125-011-2115-7

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