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Increased postprandial GIP and glucagon responses, but unaltered GLP-1 response after intervention with steroid hormone, relative physical inactivity, and high-calorie diet in healthy subjects.
J Clin Endocrinol Metab. 2011 Feb; 96(2):447-53.JC

Abstract

OBJECTIVE

Increased postprandial glucose-dependent insulinotropic polypeptide (GIP) and glucagon responses and reduced postprandial glucagon-like peptide-1 (GLP-1) responses have been observed in some patients with type 2 diabetes mellitus. The causality of these pathophysiological traits is unknown. We aimed to determine the impact of insulin resistance and reduced glucose tolerance on postprandial GIP, GLP-1, and glucagon responses in healthy subjects.

RESEARCH DESIGN AND METHODS

A 4-h 2200 KJ-liquid meal test was performed in 10 healthy Caucasian males without family history of diabetes [age, 24 ± 3 yr (mean ± sd); body mass index, 24 ± 2 kg/m(2); fasting plasma glucose, 4.9 ± 0.3 mm; hemoglobin A(1)c, 5.4 ± 0.1%] before and after intervention using high-calorie diet, relative physical inactivity, and administration of prednisolone (37.5 mg/d) for 12 d.

RESULTS

The intervention resulted in insulin resistance according to the homeostatic model assessment [1.1 ± 0.3 vs. 2.3 (mean ± SEM) ± 1.3; P = 0.02] and increased postprandial glucose excursions [area under curve (AUC), 51 ± 28 vs. 161 ± 32 mm · 4 h; P = 0.045], fasting plasma insulin (36 ± 3 vs. 61 ± 6 pm; P = 0.02), and postprandial insulin responses (AUC, 22 ± 6 vs. 43 ± 13 nm · 4 h; P = 0.03). This disruption of glucose homeostasis had no impact on postprandial GLP-1 responses (AUC, 1.5 ± 0.7 vs. 2.0 ± 0.5 nm · 4 h; P = 0.56), but resulted in exaggerated postprandial GIP (6.2 ± 1.0 vs. 10.0 ± 1.3 nm · 4 h; P = 0.003) and glucagon responses (1.6 ± 1.5 vs. 2.4 ± 3.2; P = 0.007).

CONCLUSIONS

These data suggest that increased postprandial GIP and glucagon responses may occur as a consequence of insulin resistance and/or reduced glucose tolerance. Our data suggest that acute disruption of glucose homeostasis does not result in reduced postprandial GLP-1 responses as observed in some individuals with type 2 diabetes mellitus.

Authors+Show Affiliations

Department of Clinical Physiology, Glostrup Hospital, University of Copenhagen, Nordre Ringvej 57, DK-2600 Glostrup, Denmark. kbaggehansen@dadlnet.dkNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

21047927

Citation

Hansen, Katrine B., et al. "Increased Postprandial GIP and Glucagon Responses, but Unaltered GLP-1 Response After Intervention With Steroid Hormone, Relative Physical Inactivity, and High-calorie Diet in Healthy Subjects." The Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 2, 2011, pp. 447-53.
Hansen KB, Vilsbøll T, Bagger JI, et al. Increased postprandial GIP and glucagon responses, but unaltered GLP-1 response after intervention with steroid hormone, relative physical inactivity, and high-calorie diet in healthy subjects. J Clin Endocrinol Metab. 2011;96(2):447-53.
Hansen, K. B., Vilsbøll, T., Bagger, J. I., Holst, J. J., & Knop, F. K. (2011). Increased postprandial GIP and glucagon responses, but unaltered GLP-1 response after intervention with steroid hormone, relative physical inactivity, and high-calorie diet in healthy subjects. The Journal of Clinical Endocrinology and Metabolism, 96(2), 447-53. https://doi.org/10.1210/jc.2010-1605
Hansen KB, et al. Increased Postprandial GIP and Glucagon Responses, but Unaltered GLP-1 Response After Intervention With Steroid Hormone, Relative Physical Inactivity, and High-calorie Diet in Healthy Subjects. J Clin Endocrinol Metab. 2011;96(2):447-53. PubMed PMID: 21047927.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased postprandial GIP and glucagon responses, but unaltered GLP-1 response after intervention with steroid hormone, relative physical inactivity, and high-calorie diet in healthy subjects. AU - Hansen,Katrine B, AU - Vilsbøll,Tina, AU - Bagger,Jonatan I, AU - Holst,Jens J, AU - Knop,Filip K, Y1 - 2010/11/03/ PY - 2010/11/5/entrez PY - 2010/11/5/pubmed PY - 2011/3/22/medline SP - 447 EP - 53 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 96 IS - 2 N2 - OBJECTIVE: Increased postprandial glucose-dependent insulinotropic polypeptide (GIP) and glucagon responses and reduced postprandial glucagon-like peptide-1 (GLP-1) responses have been observed in some patients with type 2 diabetes mellitus. The causality of these pathophysiological traits is unknown. We aimed to determine the impact of insulin resistance and reduced glucose tolerance on postprandial GIP, GLP-1, and glucagon responses in healthy subjects. RESEARCH DESIGN AND METHODS: A 4-h 2200 KJ-liquid meal test was performed in 10 healthy Caucasian males without family history of diabetes [age, 24 ± 3 yr (mean ± sd); body mass index, 24 ± 2 kg/m(2); fasting plasma glucose, 4.9 ± 0.3 mm; hemoglobin A(1)c, 5.4 ± 0.1%] before and after intervention using high-calorie diet, relative physical inactivity, and administration of prednisolone (37.5 mg/d) for 12 d. RESULTS: The intervention resulted in insulin resistance according to the homeostatic model assessment [1.1 ± 0.3 vs. 2.3 (mean ± SEM) ± 1.3; P = 0.02] and increased postprandial glucose excursions [area under curve (AUC), 51 ± 28 vs. 161 ± 32 mm · 4 h; P = 0.045], fasting plasma insulin (36 ± 3 vs. 61 ± 6 pm; P = 0.02), and postprandial insulin responses (AUC, 22 ± 6 vs. 43 ± 13 nm · 4 h; P = 0.03). This disruption of glucose homeostasis had no impact on postprandial GLP-1 responses (AUC, 1.5 ± 0.7 vs. 2.0 ± 0.5 nm · 4 h; P = 0.56), but resulted in exaggerated postprandial GIP (6.2 ± 1.0 vs. 10.0 ± 1.3 nm · 4 h; P = 0.003) and glucagon responses (1.6 ± 1.5 vs. 2.4 ± 3.2; P = 0.007). CONCLUSIONS: These data suggest that increased postprandial GIP and glucagon responses may occur as a consequence of insulin resistance and/or reduced glucose tolerance. Our data suggest that acute disruption of glucose homeostasis does not result in reduced postprandial GLP-1 responses as observed in some individuals with type 2 diabetes mellitus. SN - 1945-7197 UR - https://www.unboundmedicine.com/medline/citation/21047927/Increased_postprandial_GIP_and_glucagon_responses_but_unaltered_GLP_1_response_after_intervention_with_steroid_hormone_relative_physical_inactivity_and_high_calorie_diet_in_healthy_subjects_ DB - PRIME DP - Unbound Medicine ER -