Esophageal and Gastric Dysmotilities are Associated with Altered Glucose Homeostasis and Plasma Levels of Incretins and Leptin

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The Review of Diabetic Studies,2016,13,1,79-90.
Published:May 2016
Type:Original Article
Author(s) affiliations:

Rebecka Hammersjö1, Bodil Roth1, Peter Höglund2, and Bodil Ohlsson1

1Department of Clinical Sciences, Division of Internal Medicine, Skåne University Hospital, Malmö, Lund University, Lund, SWEDEN.

2Department of Laboratory Medicine, Division of Clinical Chemistry and Pharmacology, Skåne University Hospital, Lund, Lund University, Lund, SWEDEN. 


Background: Gastrointestinal complications in diabetes may affect glucose and endocrine homeostasis. Glucosedependent insulinotropic peptide (GIP), glucagon-like peptide- 1 (GLP-1), and leptin regulate glucose homeostasis, food intake, and gastric emptying. Aim: The aim was to investigate associations between diabetes complications and glucose homeostasis and plasma levels of GIP, GLP-1, and leptin. Methods: Sixteen diabetes patients (seven men) were examined with gastric emptying scintigraphy and 72-h continuous subcutaneous glucose monitoring, 14 with the deep-breathing test, and 12 with esophageal manometry. A fiber-rich breakfast was given during the second day of glucose registration. Blood samples were taken 10 min and right before a fat-rich breakfast, as well as 10, 20, 30, 45, 60, 90, 120, 150, and 180 min afterwards. 20 healthy volunteers acted as controls. Plasma was analyzed regarding GIP, GLP- 1, and leptin by Luminex. Results: Gastroparesis lowered maximal concentration (c-max) (p = 0.003) and total area under the curve (tAUC) (p = 0.019) of glucose levels as well as d-min (p = 0.043) of leptin levels. It tended to lower baseline (p = 0.073), c-max (p = 0.066), change from baseline (dmax) (p = 0.073), and tAUC (p = 0.093) of GLP-1 concentrations. Esophageal dysmotility tended to lower tAUC of glucose levels (p = 0.063), and c-min (p = 0.065) and tAUC (p = 0.063) of leptin levels. Diabetes patients had a higher baseline concentration of glucose (p = 0.013), GIP (p = 0.023), and leptin (p = 0.019) compared with healthy subjects. Conclusion: Gastric and esophageal dysmotility are associated with both lesser increases in postprandial glucose elevations and decreased postprandial changes in GLP-1 and leptin.