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Cited by 145Diabetes Management and ResearchPancreatic function and diabetesDiabetes and associated disorders

Correlation Between Minimal Secretory Capacity of Pancreatic β-Cells and Stability of Diabetic Control

Fukuda, Masahiro, Tanaka, Akira, Tahara, Yasuhiro, Ikegami, Hiroshi, Yamamoto, Yoshihiro, Kumahara, Yuichi, Shima, Kenji·1988·Diabetes
DOI 10.2337/diab.37.1.81
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Abstract

The significance of the minimal secretory capacity of pancreatic β-cells for the stability of the plasma glucose level was studied in 20 patients with insulin-dependent diabetes mellitus. Changes in plasma concentrations of major counterregulatory hormones in response to hypoglycemia were also investigated in these patients to clarify their contribution to diabetic brittleness. β-Cell function was evaluated on the basis of elevation of plasma C-peptide immunoreactivity (CPR) during the intravenous glucagon test with a highly sensitive assay for plasma CPR that could detect as little as 0.03 ng/ml. After stimulation with glucagon, a significant increase in plasma CPR was observed in 10 of the patients whose β-cell function had been evaluated as completely depleted by a conventional assay for plasma CPR. A clear inverse correlation was found between the secretory capacity of pancreatic β-cells measured in this way and the degree of glycemic instability (r = −.74, P < .01). Infusion of insulin at a rate of 0.15 U.kg−1.h−1 for 60 min caused a continuous decrease in the plasma glucose level, resulting in neuroglycopenia in 7 of the 10 CPR nonresponders but only 2 of the CPR responders. During insulin-induced hypoglycemia, plasma glucagon immunoreactivity did not increase in the CPR nonresponders but increased significantly in the CPR responders. A positive correlation was found between the minimal residual β-cell capacity and the responsiveness of α-cells to hypoglycemia (r = .65, P < .01).In contrast to the difference in the responses of their pancreatic α-cells to hypoglycemia, the two groups showed more or less the same responses of plasma epinephrine, norepinephrine, growth hormone, and cortisol to hypoglycemia. Total lack of insulinogenic reserve inevitably results in loss of automatic regulation of the circulating insulin level and seems to be a major factor in causing hyperlability of diabetic control. The lack of β-cell function may be related causally to pancreatic α-cell dysfunction, which also contributes in part to metabolic variability in brittle diabetes.

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Authors
Fukuda, M., Tanaka, A., Tahara, Y., Ikegami, H., Yamamoto, Y., Kumahara, Y., & Shima, K.
Affiliations
  • The University of Osaka (JP)
  • Tokushima University (JP)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
1988-01-01
Volume
37
Issue
1
Pages
81-88
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.37.1.81
OpenAlex
W2074943120
Cited by
145
References
0
Citations by year
2025: 2 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 7 · 2014: 4 · 2013: 5 · 2012: 5
FWCI
1.77
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
type 1 diabetes, beta-cell function, residual beta-cell function, glycemic variability, hypoglycemia, glucagon stimulation test, C-peptide, alpha-cell dysfunction, counterregulatory hormones, glucagon, neuroglycopenia, insulin-induced hypoglycemia
MeSH terms
Adult, Blood Glucose, C-Peptide, Diabetes Mellitus, Type 1, Epinephrine, Female, Glucagon, Humans, Hydrocortisone, Insulin, Islets of Langerhans, Kinetics, Male, Middle Aged, Norepinephrine, Growth Hormone

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