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Cited by 25Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes Management and Research

Acute hyperglycemia alters the ability of the normal β-cell to sense and respond to glucose

Meyer, Jürgen, Sturis, Jeppe, Katschinski, Martin, Arnold, Rudolf, Göke, Burkhard, Byrne, Maria M.·2002·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.00427.2001
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Abstract

Impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) are associated with an impaired ability of the beta-cell to sense and respond to small changes in plasma glucose. The aim of this study was to establish whether acute hyperglycemia per se plays a role in inducing this defect in beta-cell response. Seven healthy volunteers with no family history of NIDDM were studied on two occasions during a 12-h oscillatory glucose infusion with a periodicity of 144 min. Once, low-dose glucose was infused at a mean rate of 6 mg x kg(-1) x min(-1) and amplitude 33% above and below the mean rate, and, once, high-dose glucose was infused at 12 mg x kg(-1) x min(-1) and amplitude 16% above and below the mean rate. Mean glucose levels were significantly higher during the high-dose compared with the low-dose glucose infusion [9.5 +/- 0.8 vs. 6.8 +/- 0.2 mM (P < 0.01)], resulting in increased mean insulin secretion rates [ISRs; 469.1 +/- 43.8 vs. 268.4 +/- 29 pmol/min (P < 0.001)] and mean insulin levels [213.6 +/- 46 vs. 67.9 +/- 10.9 pmol/l (P < 0.008)]. Spectral analysis evaluates the regularity of oscillations in glucose, insulin secretion, and insulin at a predetermined frequency. Spectral power for glucose, ISR, and insulin was reduced during the high-dose glucose infusion [11.8 +/- 1.4 to 7.0 +/- 1.6 (P < 0.02), 7.6 +/- 1.5 to 3.2 +/- 0.5 (P < 0.04), and 10.5 +/- 1.6 to 4.6 +/- 0.7 (P < 0.01), respectively]. In conclusion, short-term infusion of high-dose glucose to obtain glucose levels similar to those previously seen in IGT subjects results in reduced spectral power for glucose, ISR, and insulin. The reduction in spectral power previously observed for ISR in IGT or NIDDM subjects may be due partly to hyperglycemia.

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Crossref · 10.1152/ajpendo.00427.2001

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Authors
Meyer, J., Sturis, J., Katschinski, M., Arnold, R., Göke, B., & Byrne, M. M.
Affiliations
  • Philipps University of Marburg (DE)
  • Novo Nordisk (Denmark) (DK)
  • Ludwig-Maximilians-Universität München (DE)
ORCID
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2002-04-01
Volume
282
Issue
4
Pages
E917-E922
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.00427.2001
OpenAlex
W2133286965
Cited by
25
References
35
Citations by year
2026: 1 · 2023: 1 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 2
FWCI
1.59
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › 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
acute hyperglycemia, beta-cell insulin secretion, impaired glucose tolerance, type 2 diabetes, insulin secretion rate, spectral power, healthy volunteers
MeSH terms
Insulin Secretion, Adult, Blood Glucose, Glucose, Humans, Hyperglycemia, Infusions, Intravenous, Insulin, Islets of Langerhans, Kinetics, Male, Periodicity, Glucose Intolerance

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