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Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener.

Sakurai K, Lee EY, Morita A, Kimura S, Kawamura H, Kasamatsu A, Shiiba M, Yabe D, Yokote K, Miki T - J Diabetes Investig (2012)

Bottom Line: 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.   The results indicate that direct stimulation of L cells with sugar, but not sweetener, is required for carbohydrate-induced GLP-1 secretion.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Cell Biology and Medicine ; Department of Diabetes, Metabolism and Endocrinology.

ABSTRACT

Unlabelled: 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).

No MeSH data available.


Related in: MedlinePlus

 Changes in (a) plasma glucose and (b) serum insulin after of a meal tolerance test with either a low glycemic index (GI) meal (○), a high‐GI meal (•), or sucrose (△). Data are the mean ± SE.
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f1:  Changes in (a) plasma glucose and (b) serum insulin after of a meal tolerance test with either a low glycemic index (GI) meal (○), a high‐GI meal (•), or sucrose (△). Data are the mean ± SE.

Mentions: To evaluate the effects of nutrient components on glucose and insulin responses, the subjects (n = 3) were fed a low‐GI meal composed of chicken cream soup and a biscuit (41.7 g carbohydrate in a total of 365 kcal) and changes in plasma glucose and serum insulin were monitored (Figure 1). As expected, plasma glucose levels showed only a slight increase up to 15 min after meal intake. To increase the plasma glucose upsurge and the consequent rise in insulin secretion, we modified the meal by adding 50 g sucrose (high‐GI meal; Figure 1). Ingestion of the high‐GI meal induced a significant increase in plasma glucose as soon as 10 min after the meal and serum insulin was also markedly increased. To determine whether the added sucrose was responsible for the early rise in plasma glucose and serum insulin, we measured these parameters again after loading with 50 g sucrose alone (Figure 1). The shift in plasma glucose was almost identical to that seen after the high‐GI meal tolerance test, even though insulin secretion up to 15 min after the high‐GI meal was higher than that after sucrose alone. Similarly, plasma intact GLP‐1 levels after the high‐GI meal and sucrose alone did not differ up to 15 min after the meal (data not shown), indicating that the sucrose in the high‐GI meal plays a central role in eliciting early phase GLP‐1 secretion. Because there was only a small increase in plasma glucose and serum insulin levels in the early phase (up to 15 min) after ingestion of the low‐GI meal (Figure 1), we used the high‐GI meal to assess GLP‐1 secretion.


Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener.

Sakurai K, Lee EY, Morita A, Kimura S, Kawamura H, Kasamatsu A, Shiiba M, Yabe D, Yokote K, Miki T - J Diabetes Investig (2012)

 Changes in (a) plasma glucose and (b) serum insulin after of a meal tolerance test with either a low glycemic index (GI) meal (○), a high‐GI meal (•), or sucrose (△). Data are the mean ± SE.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020733&req=5

f1:  Changes in (a) plasma glucose and (b) serum insulin after of a meal tolerance test with either a low glycemic index (GI) meal (○), a high‐GI meal (•), or sucrose (△). Data are the mean ± SE.
Mentions: To evaluate the effects of nutrient components on glucose and insulin responses, the subjects (n = 3) were fed a low‐GI meal composed of chicken cream soup and a biscuit (41.7 g carbohydrate in a total of 365 kcal) and changes in plasma glucose and serum insulin were monitored (Figure 1). As expected, plasma glucose levels showed only a slight increase up to 15 min after meal intake. To increase the plasma glucose upsurge and the consequent rise in insulin secretion, we modified the meal by adding 50 g sucrose (high‐GI meal; Figure 1). Ingestion of the high‐GI meal induced a significant increase in plasma glucose as soon as 10 min after the meal and serum insulin was also markedly increased. To determine whether the added sucrose was responsible for the early rise in plasma glucose and serum insulin, we measured these parameters again after loading with 50 g sucrose alone (Figure 1). The shift in plasma glucose was almost identical to that seen after the high‐GI meal tolerance test, even though insulin secretion up to 15 min after the high‐GI meal was higher than that after sucrose alone. Similarly, plasma intact GLP‐1 levels after the high‐GI meal and sucrose alone did not differ up to 15 min after the meal (data not shown), indicating that the sucrose in the high‐GI meal plays a central role in eliciting early phase GLP‐1 secretion. Because there was only a small increase in plasma glucose and serum insulin levels in the early phase (up to 15 min) after ingestion of the low‐GI meal (Figure 1), we used the high‐GI meal to assess GLP‐1 secretion.

Bottom Line: 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.   The results indicate that direct stimulation of L cells with sugar, but not sweetener, is required for carbohydrate-induced GLP-1 secretion.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Cell Biology and Medicine ; Department of Diabetes, Metabolism and Endocrinology.

ABSTRACT

Unlabelled: 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).

No MeSH data available.


Related in: MedlinePlus