Cited by 353Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes Management and Research

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Glucose-Dependent Insulinotropic Polypeptide

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Christensen, Mikkel, Vedtofte, Louise, Holst, Jens J., Vilsbøll, Tina, Knop, Filip K.·2011·Diabetes

DOI 10.2337/db11-0979PMC PMC3219957

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Abstract

OBJECTIVE: To evaluate the glucose dependency of glucose-dependent insulinotropic polypeptide (GIP) effects on insulin and glucagon release in 10 healthy male subjects ([means ± SEM] aged 23 ± 1 years, BMI 23 ± 1 kg/m2, and HbA1c 5.5 ± 0.1%). RESEARCH DESIGN AND METHODS: Saline or physiological doses of GIP were administered intravenously (randomized and double blinded) during 90 min of insulin-induced hypoglycemia, euglycemia, or hyperglycemia. RESULTS: During hypoglycemia, GIP infusion caused greater glucagon responses during the first 30 min compared with saline (76 ± 17 vs. 28 ± 16 pmol/L per 30 min, P < 0.008), with similar peak levels of glucagon reached after 60 min. During euglycemia, GIP infusion elicited larger glucagon responses (62 ± 18 vs. −11 ± 8 pmol/L per 90 min, P < 0.005). During hyperglycemia, comparable suppression of plasma glucagon (−461 ± 81 vs. −371 ± 50 pmol/L per 90 min, P = 0.26) was observed with GIP and saline infusions. In addition, during hyperglycemia, GIP more than doubled the insulin secretion rate (P < 0.0001). CONCLUSIONS: In healthy subjects, GIP has no effect on glucagon responses during hyperglycemia while strongly potentiating insulin secretion. In contrast, GIP increases glucagon levels during fasting and hypoglycemic conditions, where it has little or no effect on insulin secretion. Thus, GIP seems to be a physiological bifunctional blood glucose stabilizer with diverging glucose-dependent effects on the two main pancreatic glucoregulatory hormones.

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Authors: Christensen, M., Vedtofte, L., Holst, J. J., Vilsbøll, T., & Knop, F. K.
Affiliations: University of Copenhagen (DK)
Gentofte Hospital (DK)
Corresponding author: Christensen, Mikkel
ORCID: Christensen, Mikkel
Vedtofte, Louise
Holst, Jens J.
Vilsbøll, Tina
Knop, Filip K.
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2011-11-13
Volume: 60
Issue: 12
Pages: 3103-3109
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/db11-0979
PMC: PMC3219957
OpenAlex: W2414002317
Cited by: 353
References: 37
Citations by year: 2026: 20 · 2025: 31 · 2024: 31 · 2023: 22 · 2022: 36 · 2021: 31 · 2020: 21 · 2019: 32 · 2018: 29 · 2017: 15 · 2016: 20 · 2015: 16 · 2014: 21 · 2013: 17 · 2012: 8
FWCI: 15.40
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/3.0/ (vor, 3575 d)
Locations: Diabetes (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Funders: Novo Nordisk Fonden
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Keywords: glucose-dependent insulinotropic polypeptide, glucagon secretion, insulin secretion, glucose dependence, hypoglycemia, hyperglycemia, normoglycemia, pancreatic hormone regulation, glucose homeostasis
MeSH terms: Insulin Secretion, Adult, Blood Glucose, Gastric Inhibitory Polypeptide, Glucagon, Humans, Hyperglycemia, Hypoglycemia, Injections, Intraventricular, Insulin, Male, Young Adult

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