Glucagon Response to Glucose Challenge in Patients with Idiopathic Postprandial Syndrome
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- Kosuda Minami
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Watanabe Kentaro
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Koike Masao
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Morikawa Ai
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Saito Hitoki
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Kohno Genta
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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- Ishihara Hisamitsu
- Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine
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Abstract
<p>Background: Postprandial syndrome is characterized by hunger, weakness, and anxiety neurosis after meals. Although abnormal glucagon response is a suggested mechanism, inaccuracies in conventional glucagon measurement methods have prevented precise analysis. Recently, a more reliable dual-antibody sandwich enzyme-linked immunosorbent assay for glucagon was developed. Methods: We conducted a 75-g oral glucose tolerance test (OGTT) extending to 4 hours in 14 patients with idiopathic postprandial syndrome. In addition to blood glucose and insulin, glucagon concentration was measured with the novel method and analyzed retrospectively. Results: Median (lower quartile, upper quartile) age and body-mass index were 40 years (30, 49) and 24.9 (23.1, 26.2), respectively. The OGTT revealed that one patient had a diabetic pattern, and two were glucose intolerant. Fasting insulin was 7.6 μU/mL (6.8, 8.8) and reached 73.7 μU/mL (54.3, 82.6) at 30 min. Insulin remained elevated until 180 min. Fasting glucagon was 21.1 pg/mL (16.1, 33.8), reached a nadir of 6.9 (3.5, 10.3) at 60 min, one-third the baseline level, and remained suppressed until 180 min. We observed two types of glucagon dynamics: a lower fasting glucagon with further suppression and a normal or higher fasting glucagon with a subsequent large decrease. Conclusions: These data suggest that glucagon suppression is greater in patients with idiopathic postprandial syndrome than in previously studied healthy subjects. The present data will contribute to our understanding and future research of this syndrome.</p>
Journal
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- Journal of Nippon Medical School
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Journal of Nippon Medical School 89 (1), 102-107, 2022-02-25
The Medical Association of Nippon Medical School
