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The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype.
J Clin Endocrinol Metab. 2003 Oct; 88(10):4897-903.JC

Abstract

The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. We studied (six in each group): 1) patients with diabetes mellitus secondary to chronic pancreatitis; 2) lean type 2 diabetic patients (body mass index < 25 kg/m(2)); 3) patients with latent autoimmune diabetes in adults; 4) diabetic patients with mutations in the HNF-1alpha gene [maturity-onset diabetes of the young (MODY)3]; and 5) newly diagnosed type 1 diabetic patients. All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes.

Authors+Show Affiliations

Department of Internal Medicine F, Gentofte Hospital, DK-2900 Hellerup, Denmark. tivi@gentoftehosp.kbhamt.dkNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14557471

Citation

Vilsbøll, T, et al. "The Pathophysiology of Diabetes Involves a Defective Amplification of the Late-phase Insulin Response to Glucose By Glucose-dependent Insulinotropic Polypeptide-regardless of Etiology and Phenotype." The Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 10, 2003, pp. 4897-903.
Vilsbøll T, Knop FK, Krarup T, et al. The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. J Clin Endocrinol Metab. 2003;88(10):4897-903.
Vilsbøll, T., Knop, F. K., Krarup, T., Johansen, A., Madsbad, S., Larsen, S., Hansen, T., Pedersen, O., & Holst, J. J. (2003). The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. The Journal of Clinical Endocrinology and Metabolism, 88(10), 4897-903.
Vilsbøll T, et al. The Pathophysiology of Diabetes Involves a Defective Amplification of the Late-phase Insulin Response to Glucose By Glucose-dependent Insulinotropic Polypeptide-regardless of Etiology and Phenotype. J Clin Endocrinol Metab. 2003;88(10):4897-903. PubMed PMID: 14557471.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide-regardless of etiology and phenotype. AU - Vilsbøll,T, AU - Knop,F K, AU - Krarup,T, AU - Johansen,A, AU - Madsbad,S, AU - Larsen,S, AU - Hansen,T, AU - Pedersen,O, AU - Holst,J J, PY - 2003/10/15/pubmed PY - 2003/11/13/medline PY - 2003/10/15/entrez SP - 4897 EP - 903 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 88 IS - 10 N2 - The effect of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1), is preserved in typical middle-aged, obese, insulin-resistant type 2 diabetic patients, whereas a defective amplification of the so-called late-phase plasma insulin response (20-120 min) to glucose by the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is seen in these patients. The aim of the present investigation was to evaluate plasma insulin and C-peptide responses to GLP-1 and GIP in five groups of diabetic patients with etiology and phenotype distinct from the obese type 2 diabetic patients. We studied (six in each group): 1) patients with diabetes mellitus secondary to chronic pancreatitis; 2) lean type 2 diabetic patients (body mass index < 25 kg/m(2)); 3) patients with latent autoimmune diabetes in adults; 4) diabetic patients with mutations in the HNF-1alpha gene [maturity-onset diabetes of the young (MODY)3]; and 5) newly diagnosed type 1 diabetic patients. All participants underwent three hyperglycemic clamps (2 h, 15 mM) with continuous infusion of saline, 1 pmol GLP-1 (7-36)amide/kg body weight.min or 4 pmol GIP pmol/kg body weight.min. The early-phase (0-20 min) plasma insulin response tended to be enhanced by both GIP and GLP-1, compared with glucose alone, in all five groups. In contrast, the late-phase (20-120 min) plasma insulin response to GIP was attenuated, compared with the plasma insulin response to GLP-1, in all five groups. Significantly higher glucose infusion rates were required during the late phase of the GLP-1 stimulation, compared with the GIP stimulation. In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/14557471/The_pathophysiology_of_diabetes_involves_a_defective_amplification_of_the_late_phase_insulin_response_to_glucose_by_glucose_dependent_insulinotropic_polypeptide_regardless_of_etiology_and_phenotype_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2003-030738 DB - PRIME DP - Unbound Medicine ER -