Glutamine reduces postprandial glycemia and augments the glucagon-like peptide-1 response in type 2 diabetes patients
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Glutamine reduces postprandial glycemia and augments the glucagon-like peptide-1 response in type 2 diabetes patients. / Samocha-Bonet, Dorit; Wong, Olivia; Synnott, Emma-Leigh; Piyaratna, Naomi; Douglas, Ashley; Gribble, Fiona M; Holst, Jens Juul; Chisholm, Donald J; Greenfield, Jerry R.
In: Journal of Nutrition, Vol. 141, No. 7, 07.2011, p. 1233-1238.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Glutamine reduces postprandial glycemia and augments the glucagon-like peptide-1 response in type 2 diabetes patients
AU - Samocha-Bonet, Dorit
AU - Wong, Olivia
AU - Synnott, Emma-Leigh
AU - Piyaratna, Naomi
AU - Douglas, Ashley
AU - Gribble, Fiona M
AU - Holst, Jens Juul
AU - Chisholm, Donald J
AU - Greenfield, Jerry R
PY - 2011/7
Y1 - 2011/7
N2 - Impaired glucagon-like peptide (GLP-1) secretion or response may contribute to ineffective insulin release in type 2 diabetes. The conditionally essential amino acid glutamine stimulates GLP-1 secretion in vitro and in vivo. In a randomized, crossover study, we evaluated the effect of oral glutamine, with or without sitagliptin (SIT), on postprandial glycemia and GLP-1 concentration in 15 type 2 diabetes patients (glycated hemoglobin 6.5 ± 0.6%). Participants ingested a low-fat meal (5% fat) after receiving either water (control), 30 g l-glutamine (Gln-30), 15 g L-glutamine (Gln-15), 100 mg SIT, or 100 mg SIT and 15 g L-glutamine (SIT+Gln-15). Studies were conducted 1-2 wk apart. Blood was collected at baseline and postprandially for 180 min for measurement of circulating glucose, insulin, C-peptide, glucagon, and total and active GLP-1. Gln-30 and SIT+Gln-15 reduced the early (t = 0-60 min) postprandial glycemic response compared with control. All Gln treatments enhanced the postprandial insulin response from t = 60-180 min but had no effect on the C-peptide response compared with control. The postprandial glucagon concentration was increased by Gln-30 and Gln-15 compared with control, but the insulin:glucagon ratio was not affected by any treatment. In contrast to Gln-30, which tended to increase the total GLP-1 AUC, SIT tended to decrease the total GLP-1 AUC relative to control (both P = 0.03). Gln-30 and SIT increased the active GLP-1 AUC compared with control (P = 0.008 and P = 0.01, respectively). In summary, Gln-30 decreased the early postprandial glucose response, enhanced late postprandial insulinemia, and augmented postprandial active GLP-1 responses compared with control. These findings suggest that glutamine may be a novel agent for stimulating GLP-1 concentration and limiting postprandial glycemia in type 2 diabetes.
AB - Impaired glucagon-like peptide (GLP-1) secretion or response may contribute to ineffective insulin release in type 2 diabetes. The conditionally essential amino acid glutamine stimulates GLP-1 secretion in vitro and in vivo. In a randomized, crossover study, we evaluated the effect of oral glutamine, with or without sitagliptin (SIT), on postprandial glycemia and GLP-1 concentration in 15 type 2 diabetes patients (glycated hemoglobin 6.5 ± 0.6%). Participants ingested a low-fat meal (5% fat) after receiving either water (control), 30 g l-glutamine (Gln-30), 15 g L-glutamine (Gln-15), 100 mg SIT, or 100 mg SIT and 15 g L-glutamine (SIT+Gln-15). Studies were conducted 1-2 wk apart. Blood was collected at baseline and postprandially for 180 min for measurement of circulating glucose, insulin, C-peptide, glucagon, and total and active GLP-1. Gln-30 and SIT+Gln-15 reduced the early (t = 0-60 min) postprandial glycemic response compared with control. All Gln treatments enhanced the postprandial insulin response from t = 60-180 min but had no effect on the C-peptide response compared with control. The postprandial glucagon concentration was increased by Gln-30 and Gln-15 compared with control, but the insulin:glucagon ratio was not affected by any treatment. In contrast to Gln-30, which tended to increase the total GLP-1 AUC, SIT tended to decrease the total GLP-1 AUC relative to control (both P = 0.03). Gln-30 and SIT increased the active GLP-1 AUC compared with control (P = 0.008 and P = 0.01, respectively). In summary, Gln-30 decreased the early postprandial glucose response, enhanced late postprandial insulinemia, and augmented postprandial active GLP-1 responses compared with control. These findings suggest that glutamine may be a novel agent for stimulating GLP-1 concentration and limiting postprandial glycemia in type 2 diabetes.
KW - Administration, Oral
KW - Aged
KW - Blood Glucose
KW - C-Peptide
KW - Cross-Over Studies
KW - Diabetes Mellitus, Type 2
KW - Female
KW - Gastric Emptying
KW - Glucagon
KW - Glucagon-Like Peptide 1
KW - Glutamine
KW - Humans
KW - Hyperglycemia
KW - Insulin
KW - Male
KW - Middle Aged
KW - Postprandial Period
KW - Pyrazines
KW - Triazoles
U2 - 10.3945/jn.111.139824
DO - 10.3945/jn.111.139824
M3 - Journal article
C2 - 21593352
VL - 141
SP - 1233
EP - 1238
JO - Journal of Nutrition
JF - Journal of Nutrition
SN - 0022-3166
IS - 7
ER -
ID: 38531687