Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener
Article first published online: 25 SEP 2011
© 2011 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd
Journal of Diabetes Investigation
Volume 3, Issue 2, pages 156–163, April 2012
How to Cite
Sakurai, K., Lee, E. Y., Morita, A., Kimura, S., Kawamura, H., Kasamatsu, A., Shiiba, M., Yabe, D., Yokote, K. and Miki, T. (2012), Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. Journal of Diabetes Investigation, 3: 156–163. doi: 10.1111/j.2040-1124.2011.00163.x
- Issue published online: 27 MAR 2012
- Article first published online: 25 SEP 2011
- Received 24 February 2011; revised 21 July 2011; accepted 9 August 2011
- Apolipoprotein B-48;
- Glucagon-like peptide-1
Aims/Introduction: Oral ingestion of carbohydrate triggers secretion of glucagon-like peptide (GLP)-1, which inhibits the postprandial rise in blood glucose levels. However, the mechanism of carbohydrate-induced GLP-1 secretion from enteroendocrine L cells remains unclear. In the present study, GLP-1 secretion was examined by meal tolerance tests of healthy Japanese volunteers.
Materials and Methods: Twenty-one healthy Japanese men participated in the study. The meal tolerance test was performed with modified nutrient compositions, with or without pretreatment with the α-glucosidase inhibitor acarbose, or with substitution of sucrose with an equivalent dose of sweeteners in the meal. Blood concentrations of glucose, insulin, GLP-1, and apolipoprotein (Apo) B-48 were measured.
Results: GLP-1 secretion started concomitant with the increase in blood glucose levels 10 min after meal ingestion. Insulin secretion started at 5 min, before the increase in blood glucose levels, reflecting the contribution of direct nutrient stimulation on the former parameter and neural regulation in the latter. Carbohydrate retention in the gut lumen induced by acarbose pretreatment extended postprandial GLP-1 secretion and negated the increase in serum ApoB-48 levels. GLP-1 secretion was markedly decreased by a reduction in the amount of sucrose in the meal and was not restored by an equivalent dose of sweeteners used to compensate for the sweet taste.
Conclusions: The results indicate that direct stimulation of L cells with sugar, but not sweetener, is required for carbohydrate-induced GLP-1 secretion. In addition, inhibition of digestion of dietary carbohydrate by α-glucosidase inhibitors may prevent postprandial hyperglycemia by increasing GLP-1 secretion and by inhibiting glucose absorption. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00163.x, 2011)