Cited by 49Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes Management and Research

Abnormal Response of Pancreatic Glucagon to Glycemic Changes in Diabetes Mellitus

OHNEDA, AKIRA, WANTANABE, KIYOSHI, HORIGOME, KEN, SAKAI, TAKEAKI, KAI, YUKIHIRO, OIKAWA, SHIN-ICHI·1978·The Journal of Clinical Endocrinology & Metabolism

Abstract

In order to determine pancreatic alpha cell function in diabetes mellitus, plasma glucagon responses to either an oral glucose load or insulin-induced hypoglycemia were investigated. Plasma glucagon in 6 normal control subjects fell significantly after the administration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in patients with diabetes mellitus. In the group with severe diabetes, whose fasting blood glucose exceeded 200 mg/100 ml, the plasma glucagon level rose after glucose administration instead of decreasing. In 6 patients with diabetes mellitus, plasma glucagon did not decrease but rather increased during a glucose tolerance test which was performed after treatment with insulin and/or diet. In 6 control subjects, there was a remarkable rise of plasma glucagon in response to insulin-induced hypoglycemia. In contrast, no significant rise in plasma glucagon was demonstrated in 19 diabetic subjects undergoing intravenous insulin test. Seven patients, in whom an insulin test was repeated after treatment with insulin, sulfonylurea, or diet had a small rise in peak plasma glucagon and an increase in the integrated area under the glucagon response curve. It is concluded that the abnormal glucagon response to changes in blood glucose might be a primary defect in diabetes mellitus.

Integrity signals

Registry

Crossref · 10.1210/jcem-46-3-504

Cites

8 of 8 references verified0 citation errors · 0 not checkable

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  • A similar regulation of human alpha-cells may explain why diabetic patients with hyperglycemia display paradoxical hyperglucagonemia and why a further glucose challenge has been found to stimulate glucagon release.

    “A similar regulation of human ␣-cells may explain why diabetic patients with hyperglycemia display paradoxical hyperglucagonemia and why a further glucose challenge has been found to stimulate glucagon release (9 -11).”

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Authors
OHNEDA, A., WANTANABE, K., HORIGOME, K., SAKAI, T., KAI, Y., & OIKAWA, S.-I.
Affiliations
Tohoku University (JP)
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
1978-03
Volume
46
Issue
3
Pages
504-510
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2101993026
Cited by
49
References
8
Citations by year
2026: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2018: 4 · 2016: 2 · 2014: 5 · 2013: 2 · 2012: 3
FWCI
1.46
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & 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
glucagon, diabetes mellitus, alpha cells, glucagon secretion, insulin-induced hypoglycemia, oral glucose tolerance, insulin assay, sulfonylureas, insulin therapy, glycemic regulation
MeSH terms
Adult, Blood Glucose, Diabetes Mellitus, Glucagon, Glucose Tolerance Test, Humans, Insulin, Pancreas

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