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Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia.
Diabetologia. 1998 Oct; 41(10):1180-6.D

Abstract

The plasma concentrations of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1) are abnormally high after oral glucose in partially gastrectomised subjects with reactive hypoglycaemia, suggesting a causal relationship. Because of the glucose-dependency of its effects, it is impossible to induce hypoglycaemia in normal subjects in the basal state by exogenous GLP-1, regardless of dose. To further assess the role of the incretin hormones in reactive hypoglycaemia, we reproduced the glucose and hormone profiles of the patients with reactive hypoglycaemia in 8 healthy volunteers in 4 separate protocols: 1) i.v. infusion of glucose (25 g) alone, 2) glucose together with i.v. GLP-1 infusion, and 3) and 4) glucose together with i.v. infusion of the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), at two different infusion rates. The plasma glucose, GLP-1 and GIP concentrations (low dose) obtained were comparable with those of the patients. With GLP-1, infusion of a total of 33.4 +/- 1.3 g glucose was required to obtain plasma glucose concentrations similar to those obtained by glucose infusion alone; with low GIP, 28.0 +/- 1.2 g and with high GIP 38.4 +/- 3.5 g. Insulin concentrations increased 10-fold with GLP-1 compared with i.v. glucose alone, but less with high and low GIP. In contrast, C-peptide concentrations were similar after GLP-1 and high GIP. After termination of i.v. glucose the lowest glucose concentrations were 4.5 (3.7-4.9) (median, range) for glucose alone; 2.4 (1.9-2.8) mmol/l with GLP-1; 3.7 (2.6-4.0) with low GIP and 3.3 (2.1-4.2) with high GIP. Thus, the exaggerated GLP-1 response to nutrients in patients with accelerated gastric emptying could be responsible for their high incidence of postprandial reactive hypoglycaemia.

Authors+Show Affiliations

Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, Denmark.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9794105

Citation

Toft-Nielsen, M, et al. "Exaggerated Secretion of Glucagon-like Peptide-1 (GLP-1) Could Cause Reactive Hypoglycaemia." Diabetologia, vol. 41, no. 10, 1998, pp. 1180-6.
Toft-Nielsen M, Madsbad S, Holst JJ. Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia. Diabetologia. 1998;41(10):1180-6.
Toft-Nielsen, M., Madsbad, S., & Holst, J. J. (1998). Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia. Diabetologia, 41(10), 1180-6.
Toft-Nielsen M, Madsbad S, Holst JJ. Exaggerated Secretion of Glucagon-like Peptide-1 (GLP-1) Could Cause Reactive Hypoglycaemia. Diabetologia. 1998;41(10):1180-6. PubMed PMID: 9794105.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia. AU - Toft-Nielsen,M, AU - Madsbad,S, AU - Holst,J J, PY - 1998/10/30/pubmed PY - 1998/10/30/medline PY - 1998/10/30/entrez SP - 1180 EP - 6 JF - Diabetologia JO - Diabetologia VL - 41 IS - 10 N2 - The plasma concentrations of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1) are abnormally high after oral glucose in partially gastrectomised subjects with reactive hypoglycaemia, suggesting a causal relationship. Because of the glucose-dependency of its effects, it is impossible to induce hypoglycaemia in normal subjects in the basal state by exogenous GLP-1, regardless of dose. To further assess the role of the incretin hormones in reactive hypoglycaemia, we reproduced the glucose and hormone profiles of the patients with reactive hypoglycaemia in 8 healthy volunteers in 4 separate protocols: 1) i.v. infusion of glucose (25 g) alone, 2) glucose together with i.v. GLP-1 infusion, and 3) and 4) glucose together with i.v. infusion of the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), at two different infusion rates. The plasma glucose, GLP-1 and GIP concentrations (low dose) obtained were comparable with those of the patients. With GLP-1, infusion of a total of 33.4 +/- 1.3 g glucose was required to obtain plasma glucose concentrations similar to those obtained by glucose infusion alone; with low GIP, 28.0 +/- 1.2 g and with high GIP 38.4 +/- 3.5 g. Insulin concentrations increased 10-fold with GLP-1 compared with i.v. glucose alone, but less with high and low GIP. In contrast, C-peptide concentrations were similar after GLP-1 and high GIP. After termination of i.v. glucose the lowest glucose concentrations were 4.5 (3.7-4.9) (median, range) for glucose alone; 2.4 (1.9-2.8) mmol/l with GLP-1; 3.7 (2.6-4.0) with low GIP and 3.3 (2.1-4.2) with high GIP. Thus, the exaggerated GLP-1 response to nutrients in patients with accelerated gastric emptying could be responsible for their high incidence of postprandial reactive hypoglycaemia. SN - 0012-186X UR - https://www.unboundmedicine.com/medline/citation/9794105/Exaggerated_secretion_of_glucagon_like_peptide_1__GLP_1__could_cause_reactive_hypoglycaemia_ L2 - https://doi.org/10.1007/s001250051049 DB - PRIME DP - Unbound Medicine ER -