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Cited by 132Pancreatic function and diabetesDiabetes Management and ResearchDiabetes Treatment and Management

Lack of control by glucose of ultradian insulin secretory oscillations in impaired glucose tolerance and in non-insulin-dependent diabetes mellitus.

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O'Meara, N M, Sturis, J, Van Cauter, E, Polonsky, K S·1993·Journal of Clinical Investigation
DOI 10.1172/jci116560PMC PMC293585
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Abstract

Normal subjects demonstrate the presence of ultradian oscillations (period 80-150 min) in insulin secretion rate (ISR) tightly coupled to glucose oscillations of similar period. These oscillations appear to be a function of the feedback loop linking glucose and insulin. The present study was undertaken to determine whether the control by glucose of the ultradian oscillations in insulin secretion is altered in impaired glucose tolerance IGT and in non-insulin-dependent diabetes mellitus (NIDDM). Patients with NIDDM (n = 7), IGT (n = 4), and matched nondiabetic controls (n = 5) were studied under three separate protocols that involved administration of glucose at either a constant rate of 6 mg/kg per min for 28 h or in one of two oscillatory patterns at the same overall mean rate. The amplitude of the oscillations was 33% above and below the mean infusion rate, and their respective periods were 144 min (slow oscillatory infusion) or 96 min (rapid oscillatory infusion). Insulin, C-peptide, and glucose were sampled at 10-min intervals during the last 24 h of each study. ISRs were calculated by deconvolution of C-peptide levels. Analysis of the data showed that (a) the tight temporal coupling between glucose and ISR in the nondiabetic controls was impaired in the IGT and NIDDM groups as demonstrated by pulse analysis, cross-correlation analysis, and spectral analysis; (b) the absolute amplitude of the ISR pulses progressively declined with the transition from obesity to IGT to NIDDM; and (c) the absolute amplitude of the ISR oscillations failed to increase appropriately with increasing absolute amplitude of glucose oscillations in the IGT and NIDDM subjects compared with the control group. In conclusion, the present study demonstrates that important dynamic properties of the feedback loop linking insulin secretion and glucose are disrupted not only in established NIDDM but also in conditions where glucose tolerance is only minimally impaired. Further studies are needed to determine how early in the course of beta-cell dysfunction this lack of control by glucose of the ultradian oscillations in insulin secretion occurs and to define more precisely if this phenomenon plays a pathogenetic role in the onset of hyperglycemia in genetically susceptible individuals.

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  • The predicted slow ultradian oscillations agree with previously reported 80-150 min ultradian oscillations of glucose and insulin measured in healthy subjects.

    “This result agrees with previously reported ultradian oscillations (80-150 min period) of glucose and insulin measured in healthy subjects, where the origin of these slow ultradian oscillations was first hypothesized ( 51 ).”

    From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [51]

    The Introduction reports 80–150-minute insulin-secretion oscillations in normal subjects, tightly coupled to glucose oscillations of similar period. It also discusses the insulin–glucose feedback mechanism as a possible origin, but attributes that view to earlier references (12, 13); this paper does not support the claim that the origin was first hypothesized here. (LLM, conf=0.84)

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  • Studies in high-risk subjects have shown reductions in the later second-phase insulin response to intravenous glucose, glucose potentiation of insulin release, pulsatile insulin secretion, oscillatory insulin release, and the ability of an oscillating glucose infusion to induce oscillations in insulin secretion.

    “Studies in subjects at high risk including first degree relatives of subjects with Type 2 diabetes [121, 122], women with a history of gestational diabetes [100] or polycystic ovarian disease [96] and subjects with IGT [123, 124] have shown reductions in the later (second-phase) insulin response to intravenous glucose [121], in glucose potentiation of insulin release [123], in pulsatile insulin”

    From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [124]

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Authors
O'Meara, N. M., Sturis, J., Van Cauter, E., & Polonsky, K. S.
Affiliations
University of Chicago (US)
ORCID
Sturis, J
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1993-07-01
Volume
92
Issue
1
Pages
262-271
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci116560
PMC
PMC293585
OpenAlex
W2129565951
Cited by
132
References
53
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 4 · 2014: 2 · 2013: 2 · 2012: 5
FWCI
7.66
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01dk013941-20)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 13941, DK-31842, DK 20595)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
insulin secretion rate, impaired glucose tolerance, type 2 diabetes, C-peptide, glucose oscillations, beta-cell dysfunction, obesity
MeSH terms
Insulin Secretion, C-Peptide, Diabetes Mellitus, Type 2, Female, Glucose, Humans, Insulin, Islets of Langerhans, Male, Periodicity, Spectrum Analysis

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