Masako Kaji1, Masahiro Nomura, Yoshiyuki Tamura, Susumu Ito. 1. Department of Digestive and Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
Abstract
BACKGROUND: Detailed information concerning the influence of insulin resistance on gastrointestinal motility are not available. METHODS: The relationship between insulin resistance and gastric motility and emptying, and changes in gastric motility with changes in blood glucose level were investigated using electrogastrography (EGG) and external ultrasonography in 20 non-diabetic subjects. The homeostasis model assessment ratio (HOMA-R) was used as an index of insulin resistance. The cut off value for HOMA-R was set at 1.7. Subjects with HOMA-R > or = 1.7 were the high HOMA-R group, and HOMA-R < 1.7 were the normal HOMA-R group. In the EGG data, a Fast Fourier Transform (FFT) analysis was performed, and the mean peak power was compared among brady-, normal-, and tachy-gastria. RESULTS: In the fasting state, the ratios of brady-gastria in EGG and HOMA-R were significantly positively correlated, and the ratios of normal-gastria and HOMA-R were significantly negatively correlated. When glucose was intravenously administered, the ratio of normal-gastria was significantly decreased and the ratio of brady-gastria was significantly increased in subjects with a high HOMA-R. In a gastric emptying test by external ultrasonography, gastric emptying activity was significantly decreased in subjects with a high HOMA-R. CONCLUSIONS: We conclude that insulin resistance induces abnormal gastric motility. Though abnormal gastric motility is related to HOMA-R, the findings herein suggest that incretin, showing insulin resistance, or an adipocyokine might be related to the differences in EGG in both groups. The relation between abnormal gastric motility and other serum parameters (incretin, adipocyokine, etc) would contribute to a better understanding of this process.
BACKGROUND: Detailed information concerning the influence of insulin resistance on gastrointestinal motility are not available. METHODS: The relationship between insulin resistance and gastric motility and emptying, and changes in gastric motility with changes in blood glucose level were investigated using electrogastrography (EGG) and external ultrasonography in 20 non-diabetic subjects. The homeostasis model assessment ratio (HOMA-R) was used as an index of insulin resistance. The cut off value for HOMA-R was set at 1.7. Subjects with HOMA-R > or = 1.7 were the high HOMA-R group, and HOMA-R < 1.7 were the normal HOMA-R group. In the EGG data, a Fast Fourier Transform (FFT) analysis was performed, and the mean peak power was compared among brady-, normal-, and tachy-gastria. RESULTS: In the fasting state, the ratios of brady-gastria in EGG and HOMA-R were significantly positively correlated, and the ratios of normal-gastria and HOMA-R were significantly negatively correlated. When glucose was intravenously administered, the ratio of normal-gastria was significantly decreased and the ratio of brady-gastria was significantly increased in subjects with a high HOMA-R. In a gastric emptying test by external ultrasonography, gastric emptying activity was significantly decreased in subjects with a high HOMA-R. CONCLUSIONS: We conclude that insulin resistance induces abnormal gastric motility. Though abnormal gastric motility is related to HOMA-R, the findings herein suggest that incretin, showing insulin resistance, or an adipocyokine might be related to the differences in EGG in both groups. The relation between abnormal gastric motility and other serum parameters (incretin, adipocyokine, etc) would contribute to a better understanding of this process.