INFLUENCE OF GASTRIC EMPTYING-RATE AND OF INSULIN RESPONSE ON ORAL GLUCOSE TOLERANCE IN THYROID DISEASE

The calcium-sensing receptor (CaSR) is expressed in various tissues, including the gastrointestinal tract. To investigate the role of gut CaSR on glycemic control, we examined whether single oral administration of CaSR agonist peptides affected the glycemic response in rats. Glucose tolerance tests were performed under oral or duodenal administration of various CaSR agonist peptides (γGlu-Cys, protamine, and poly-d-lysine hydrobromide) in conscious rats. Involvement of CaSR was determined by using a CaSR antagonist. Signaling pathways underlying CaSR agonist-modified glycemia were investigated using gut hormone receptor antagonists. The gastric emptying rate after the administration of CaSR agonist peptides was measured by the phenol red recovery method. Oral and duodenal administration of CaSR agonist peptides attenuated glycemic responses under the oral glucose tolerance test, but the administration of casein did not. The promotive effect on glucose tolerance was weakened by luminal pretreatment with a CaSR antagonist. Treatment with a 5-HT3 receptor antagonist partially diminished the glucose-lowering effect of peptides. Furthermore, the gastric emptying rate was decreased by duodenal administration of CaSR agonist peptides. These results demonstrate that activation of the gut CaSR by peptide agonists promotes glucose tolerance in conscious rats. 5-HT3 receptor and the delayed gastric emptying rate appear to be involved in the glucose-lowering effect of CaSR agonist peptides. Thus, activation of gut CaSR by dietary peptides reduces glycemic responses so that gut CaSR may be a potential target for the improvement of postprandial glycemia.

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Erratum to: Influence of Telmisartan on Insulin Response after Glucose Loading in Obese Patients with Hypertension: ARB Trial of Hypertension in Obese Patients with Hyperinsulinemia Assessed by Oral Glucose Tolerance Test (ATHLETE)

Advances in Therapy ◽

10.1007/s12325-011-0089-y ◽

2012 ◽

Vol 29 (4) ◽

pp. 383-384

Author(s):

Yutaka Mori ◽

Takaaki Tanaka ◽

Kenichi Matsuura ◽

Junichi Yokoyama ◽

Kazunori Utsunomiya

Keyword(s):

Glucose Tolerance ◽

Oral Glucose Tolerance Test ◽

Glucose Tolerance Test ◽

Insulin Response ◽

Tolerance Test ◽

Oral Glucose ◽

Obese Patients ◽

Oral Glucose Tolerance ◽

Glucose Loading

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Effects of dietary supplementation with glucose on gastric emptying of glucose and fructose and oral glucose tolerance in normal subjects

Gastroenterology ◽

10.1016/0016-5085(95)26776-x ◽

1995 ◽

Vol 108 (4) ◽

pp. A616

Keyword(s):

Gastric Emptying ◽

Glucose Tolerance ◽

Dietary Supplementation ◽

Normal Subjects ◽

Oral Glucose ◽

Oral Glucose Tolerance

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Evidence that the oral glucose-tolerance test does not provide a uniform stimulus to pancreatic islets in pregnancy.

Clinical Chemistry ◽

10.1093/clinchem/35.7.1482 ◽

1989 ◽

Vol 35 (7) ◽

pp. 1482-1485 ◽

Cited By ~ 2

Author(s):

E A de Leacy ◽

D M Cowley

Keyword(s):

Glucose Tolerance ◽

Oral Glucose Tolerance Test ◽

Pancreatic Islets ◽

Glucose Tolerance Test ◽

Insulin Response ◽

Tolerance Test ◽

Glucose Absorption ◽

Oral Glucose ◽

Oral Glucose Tolerance ◽

Glucose Load

Abstract Fifty consecutive pregnant patients referred for a glucose-tolerance test were classified on the basis of increasing (n = 20) or decreasing (n = 28) hematocrit after an oral 75-g glucose load. (The hematocrit did not change in the other two patients.) Patients with increasing hematocrit, a response previously seen in patients with the dumping syndrome, showed significantly flatter increases in glucose concentrations in plasma after the load. The mean decrease in the concentration of phosphate in plasma, measured as an index of glucose uptake by cells, was significantly less (P less than 0.05) 2 h after the load in the group with flatter glucose responses, suggesting that the flat response is ascribable to poor glucose absorption rather than to an exaggerated insulin response. These results indicate that the oral glucose-tolerance test stresses the pancreatic islets differently in different pregnant subjects, owing to individual variations in the gastrointestinal handling of the glucose load. Consequently, patients may give a "normal" result who might otherwise become hyperglycemic after normal meals. We suggest that alternative screening procedures be investigated to assess pregnant patients postprandially.

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Meal feeding improves oral glucose tolerance in male rats and causes adaptations in postprandial islet hormone secretion that are independent of plasma incretins or glycemia

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00339.2014 ◽

2014 ◽

Vol 307 (9) ◽

pp. E784-E792 ◽

Cited By ~ 5

Author(s):

Torsten P. ◽

Benedikt A. Aulinger ◽

Eric P. Smith ◽

Deborah L. Drazen ◽

Yve Ulrich-Lai ◽

...

Keyword(s):

Insulin Secretion ◽

Glucose Tolerance ◽

Cell Function ◽

Hormone Secretion ◽

Insulin Response ◽

Male Rats ◽

Oral Glucose ◽

Light Cycle ◽

Oral Glucose Tolerance ◽

Islet Hormone

Meal-fed (MF) rats with access to food for only 4 consecutive hours during the light cycle learn to eat large meals to maintain energy balance. MF animals develop behavioral and endocrine changes that permit glucose tolerance despite increased meal size. We hypothesized that enhanced activity of the enteroinsular axis mediates glucose homeostasis during MF. Cohorts of rats were allocated to MF or ad libitum (AL) regimens for 2–4 wk. Insulin secretion and glucose tolerance were determined after oral carbohydrate and intraperitoneal (ip) and intravenous (iv) glucose. MF rats ate less than AL in the first week but maintained a comparable weight trajectory thereafter. MF rats had decreased glucose excursions after a liquid mixed meal (AUC: MF 75 ± 7, AL 461 ± 28 mmol·l−1·min, P < 0.001), with left-shifted insulin secretion (AUC0–15: MF 31.0 ± 4.9, AL 9.6 ± 4.4 pM·min, P < 0.02), which peaked before a significant rise in blood glucose. Both groups had comparable fasting glucagon levels, but postprandial responses were lower with MF. However, neither intestinal expression of proGIP and proglucagon mRNA nor plasma incretin levels differed between MF and AL groups. There were no differences in the insulin response to ip or iv glucose between MF and AL rats. These findings demonstrate that MF improves oral glucose tolerance and is associated with significant changes in postprandial islet hormone secretion. Because MF enhanced β-cell function during oral but not parenteral carbohydrate administration, and was not accounted for by changes in circulating incretins, these results support a neural mechanism of adaptive insulin secretion.

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