Evidence map›Paper›PMID 32045582›Full record

ArticleMetabolism: clinical and experimental2020

Fasting glucagon concentrations are associated with longitudinal decline of β-cell function in non-diabetic humans.

Jon D Adams, Chiara Dalla Man, Marcello C Laurenti, M Daniela Hurtado Andrade, Claudio Cobelli, Robert A Rizza, Kent R Bailey, Adrian Vella

Open access · greenAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2025
    Observational
  4. Article
  5. Article
  6. Diabetes-associated Genetic Variation inJournal of the Endocrine Society · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. The Role of Glucagon in Glycemic Variability in Type 1 Diabetes: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Review
  12. Assessment of individual and standardized glucagon kinetics in healthy humans.American journal of physiology. Endocrinology and metabolism · 2021
    Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Jon D AdamsDivision of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA.
Chiara Dalla ManDepartment of Information Engineering, University of Padua, Padua, Italy.
Marcello C LaurentiDivision of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA.
M Daniela Hurtado AndradeDivision of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA.
Claudio CobelliDepartment of Information Engineering, University of Padua, Padua, Italy.
Robert A RizzaDivision of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA.
Kent R BaileyBiomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, MN, USA.
Adrian VellaDivision of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA. Electronic address: vella.adrian@mayo.edu.
Mayo Clinic in Arizona · USMayo Clinic · USUniversity of Padua · IT

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
DIABETES AND METABOLISMT32DK007352 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1986 to 2026
$9.4M
The regulation of fasting glucose metabolism in people with and without prediabetesR01DK078646 · NIDDK · MAYO CLINIC ROCHESTER · PI Adrian Vella · 2007 to 2026
$8.7M
Glucagon suppression and diabetes-associated variation in TCF7L2R01DK116231 · NIDDK · MAYO CLINIC ROCHESTER · PI Adrian Vella · 2017 to 2026
$5.4M
NIDDK NIH HHS R01 DK078646NIDDK NIH HHS R01 DK116231NIDDK NIH HHS T32 DK007352
6 · The paper itself

Abstract

purposeAbnormal glucagon concentrations are a feature of prediabetes but it is uncertain if α-cell dysfunction contributes to a longitudinal decline in β-cell function. We therefore sought to determine if a decline in β-cell function is associated with a higher nadir glucagon in the postprandial period or with higher fasting glucagon.

methodsThis was a longitudinal study in which 73 non-diabetic subjects were studied on 2 occasions 6.6 ± 0.3 years apart using a 2-hour, 7-sample oral glucose tolerance test. Disposition Index (DI) was calculated using the oral minimal model applied to the measurements of glucose, insulin, C-peptide concentrations during the studies. We subsequently examined the relationship of glucagon concentrations at baseline with change in DI (used as a measure of β-cell function) after adjusting for changes in weight and the baseline value of DI.

resultsAfter adjusting for covariates, nadir postprandial glucagon concentrations were not associated with changes in β-cell function as quantified by DI. On the other hand, fasting glucagon concentrations during the baseline study were inversely correlated with longitudinal changes in DI.

conclusionsDefects in α-cell function, manifest as elevated fasting glucagon, are associated with a subsequent decline in β-cell function. It remains to be ascertained if abnormal α-cell function contributes directly to loss of β-cell secretory capacity in the pathogenesis of type 2 diabetes.

Indexed as

AdultBlood GlucoseC-PeptideFastingFemaleGlucagonGlucose Tolerance TestHumansInsulinInsulin-Secreting CellsLongitudinal StudiesMaleMiddle AgedPancreasPostprandial PeriodPrediabetic StateBlood GlucoseC-PeptideGlucagonInsulinGlucagonInsulin actionPrediabetesα-Cell functionβ-Cell function

Identifiers

PMID32045582
PMCPMC7093233
OpenAlexW3005335922

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.