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Nutrition Research Newsletter, Feb, 2001
Subjects with type 2 diabetes have either normal or slightly elevated fasting glucagon concentrations that fail to decrease appropriately after food ingestion. In a paper recently published in the Journal of Clinical Endocrinology and Metabolism, the researchers tested the hypothesis that a lack of suppression of glucagons causes postprandial hyperglycemia in subjects with type 2 diabetes.
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Nine otherwise healthy subjects (55 [ or -] 8 yr of age, 7 men) with type 2 diabetes were studied on two occasions. On each occasion, the subjects ingested 50 g glucose. A low dose of somatostatin was infused on both occasions to inhibit glucagons and insulin secretion. Identical amounts of insulin were infused in a pattern that created a typical postprandial diabetic insulin profile to insure that insulin concentrations were equal on both occasions. On one occasion glucagon was infused at a constant rate throughout the experiment, and on the other occasion the glucagons infused was delayed for 2 h, creating a transient decrease in plasma glucagon immediately following glucose ingestion, mimicking the pattern normally observed in nondiabetic subjects.
In the current experiments a lack of glucagons suppression led to an approximately 1.5-2 [micro]mol/L increment in postprandial glucose concentrations. Glucose concentrations were higher despite the fact that higher C peptide concentrations were also higher on the nonsuppressed study day.
The findings of this study demonstrate that lack of suppression of glucagons worsens glucose tolerance in subjects with type 2 diabetes mellitus. The researchers previously demonstrated the same finding in patients with type 1 diabetes mellitus. Taken together, these data indicate than inappropriately elevated glucagon concentrations can substantially increase postprandial glucose concentrations in both insulin-sensitive and insulin-resistant patients.
P. Shah, A. Vella, A. Basu, R. Basu, W. Schwenk, R. Rizza. Lack of Suppression of Glucagon Contributes to Postprandial Hyperglycemia in Subjects with Type 2 Diabetes Mellitus. J Clin Endocrinol Metab 85(11):4053-4059 (Nov 2000) [Correspondence: Robert A. Rizza, MD, Endocrine Research Unit, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. E-mail: rizza.robert@mayo.edu].
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