ArticleThe Journal of clinical endocrinology and metabolism2000
Lack of suppression of glucagon contributes to postprandial hyperglycemia in subjects with type 2 diabetes mellitus.
Article in The Journal of clinical endocrinology and metabolism, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00716170 (The Role of GIP, GLP-1 and GLP-2 in Type 2 Diabetic Hyperglucagonemia), which is not on this map. Cited by 152 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
The Role of GIP, GLP-1 and GLP-2 in Type 2 Diabetic Hyperglucagonemia
Who cites it
152 citing papers in PubMed, 368 citations in OpenAlex.
- Hepatic steatosis in humans is associated with preserved glucagon action on amino acid metabolism.The Journal of clinical investigation · 2026Trial
- Tirzepatide Improved Markers of Islet Cell Function and Insulin Sensitivity in People With T2D (SURPASS-2).The Journal of clinical endocrinology and metabolism · 2024Trial
- Insulin secretion and action and the response of endogenous glucose production to a lack of glucagon suppression in nondiabetic subjects.American journal of physiology. Endocrinology and metabolism · 2021Trial
- Diabetes-associated genetic variation in TCF7L2 alters pulsatile insulin secretion in humans.JCI insight · 2020Trial
- Greater early postprandial suppression of endogenous glucose production and higher initial glucose disappearance is achieved with fast-acting insulin aspart compared with insulin aspart.Diabetes, obesity & metabolism · 2018Trial
- Effect of Glycemic Control on Chylomicron Metabolism and Correlation between Postprandial Metabolism of Plasma Glucose and Chylomicron in Patients with Type 2 Diabetes Treated with Basal-bolus Insulin Therapy with or without Vildagliptin.Journal of atherosclerosis and thrombosis · 2017Trial
- Improving Effect of the Acute Administration of Dietary Fiber-Enriched Cereals on Blood Glucose Levels and Gut Hormone Secretion.Journal of Korean medical science · 2016Trial
- Dipeptidyl peptidase-4 inhibition by vildagliptin and the effect on insulin secretion and action in response to meal ingestion in type 2 diabetes.Diabetes care · 2009Trial
- Acute high-protein feeding induces hepatic amino acid accumulation in diabetic male mice prior to transcriptional adaptation.Physiological reports · 2026Article
- Increased Early Postprandial Glucagon Concentrations in Humans With Newly Diagnosed Type 2 Diabetes and Steatotic Liver Disease.Diabetes care · 2026Article
- Article
- Liver fibrosis and type 2 diabetes modulate postprandial incretin and glucagon responses in fatty liver disease.Journal of physiology and biochemistry · 2026Article
- Gut Peptide Alterations in Type 2 Diabetes and Obesity: A Narrative Review.Current obesity reports · 2026Review
- Article
- Prolonged Somatostatin Receptor 2 Antagonism Enhances Glucagon Response to Hypoglycemia in Male Diabetic Rats.Endocrinology · 2026Article
- Efficacy of Dual Glucagon and GLP-1 Agonists as New Treatments for Type II Diabetes.Mini reviews in medicinal chemistry · 2026Review
- Evaluation of distinct and similar pathological features between diabetes and Alzheimer's disease.EXCLI journal · 2026Review
- Modeling the effect of glucagon on endogenous glucose production in healthy individuals under meal-like conditions.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2025Observational
- Glucagon in metabolic disease: a mini-review of emerging multi-organ roles beyond glycemic control.Frontiers in endocrinology · 2025Review
92 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We tested the hypothesis that a lack of suppression of glucagon causes postprandial hyperglycemia in subjects with type 2 diabetes. Nine diabetic subjects ingested 50 g glucose on two occasions. On both occasions, somatostatin was infused at a rate of 4.3 nmol/kg x min, and insulin was infused in a diabetic insulin profile. On one occasion, glucagon was also infused at a rate of 1.25 ng/kg x min to maintain portal glucagon concentrations constant (nonsuppressed study day). On the other occasion, glucagon infusion was delayed by 2 h to create a transient decrease in glucagon (suppressed study day). Glucagon concentrations on the suppressed study day fell to about 70 ng/L during the first 2 h, rising thereafter to approximately 120 ng/L. In contrast, glucagon concentrations on the nonsuppressed study day remained constant at about 120 ng/L throughout. The decrease in glucagon resulted in substantially lower (P < 0.001) glucose concentrations on the suppressed compared with the nonsuppressed study days (9.2+/-0.7 vs. 10.9+/-0.8 mmol/L) and a lower (P < 0.001) rate of release of [14C]glucose from glycogen (labeled by infusing [1-14C]galactose). On the other hand, flux through the hepatic UDP-glucose pool (and, by implication, glycogen synthesis), measured using the acetaminophen glucuronide method, did not differ on the two occasions. We conclude that lack of suppression of glucagon contributes to postprandial hyperglycemia in subjects with type 2 diabetes at least in part by accelerating glycogenolysis. These data suggest that agents that antagonize glucagon action or secretion are likely to be of value in the treatment of patients with type 2 diabetes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.