Evidence mapPaperPMID 37708362Full record

ArticleThe Journal of clinical endocrinology and metabolism2024

Regulation of the Cortisol Axis, Glucagon, and Growth Hormone by Glucose Is Altered in Prediabetes and Type 2 Diabetes.

Martin H Lundqvist, Maria J Pereira, Kristina Almby, Susanne Hetty, Jan W Eriksson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
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  8. Review
  9. β-Cells: So Sensitive.Diabetes · 2025
    Article
  10. Glycemic Management in Adults With Diabetes During Illness.Clinical diabetes : a publication of the American Diabetes Association · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Martin H LundqvistClinical Diabetology and Metabolism, Department of Medical Sciences, Uppsala University, 751 85 Uppsala, Sweden.ORCID 0000-0001-9348-4603
Maria J PereiraClinical Diabetology and Metabolism, Department of Medical Sciences, Uppsala University, 751 85 Uppsala, Sweden.ORCID 0000-0001-5498-3899
Kristina AlmbyClinical Diabetology and Metabolism, Department of Medical Sciences, Uppsala University, 751 85 Uppsala, Sweden.ORCID 0000-0002-7083-8912
Susanne HettyClinical Diabetology and Metabolism, Department of Medical Sciences, Uppsala University, 751 85 Uppsala, Sweden.ORCID 0000-0002-0964-6700
Jan W ErikssonClinical Diabetology and Metabolism, Department of Medical Sciences, Uppsala University, 751 85 Uppsala, Sweden.ORCID 0000-0002-2639-9481
Uppsala University · SE

Funding

Agnes och Mac Rudbergs Stiftelse, HORIZON EUROPE Marie-Sklodowska Curie ITN TREATMENT H2020-MSCA-ITN-721236Diabetesfonden DIA2021-661Novo Nordisk Fonden NNF20OC0063864P.O. Zetterlings stiftelseStiftelsen Familjen Ernfors Fondthe governmental strategic research program Excellence of Diabetes Research in SwedenUppsala University Hospital ALF grants
6 · The paper itself

Abstract

contextInsulin-antagonistic, counter-regulatory hormones have been implicated in the development of type 2 diabetes (T2D).

objectiveIn this cross-sectional study, we investigated whether glucose-dependent regulation of such hormones differ in individuals with T2D, prediabetes (PD), and normoglycemia (NG).

methodsFifty-four individuals with or without T2D underwent one hyperinsulinemic-normoglycemic-hypoglycemic and one hyperglycemic clamp with repeated hormonal measurements. Participants with T2D (n = 19) were compared with a group-matched (age, sex, BMI) subset of participants without diabetes (ND, n = 17), and also with participants with PD (n = 18) and NG (n = 17).

resultsIn T2D vs ND, glucagon levels were higher and less suppressed during the hyperglycemic clamp whereas growth hormone (GH) levels were lower during hypoglycemia (P < .05). Augmented ACTH response to hypoglycemia was present in PD vs NG (P < .05), with no further elevation in T2D. In contrast, glucagon and GH alterations were more marked in T2D vs PD (P < .05).In the full cohort (n = 54), augmented responses of glucagon, cortisol, and ACTH and attenuated responses of GH correlated with adiposity, dysglycemia, and insulin resistance. In multilinear regressions, insulin resistance was the strongest predictor of elevated hypoglycemic responses of glucagon, cortisol, and ACTH. Conversely, fasting glucose and HbA1c were the strongest predictors of low GH levels during hypoglycemia and elevated, i.e. less suppressed glucagon levels during hyperglycemia, respectively. Notably, adiposity measures were also strongly associated with the responses above.

conclusionsAltered counter-regulatory hormonal responses to glucose variations are observed at different stages of T2D development and may contribute to its progression by promoting insulin resistance and dysglycemia.

Indexed as

Diabetes Mellitus, Type 2Human Growth HormoneHypoglycemiaInsulin ResistancePrediabetic StateAdrenocorticotropic HormoneBlood GlucoseCross-Sectional StudiesGlucagonGlucoseGrowth HormoneHumansHydrocortisoneHypoglycemic AgentsInsulinAdrenocorticotropic HormoneBlood GlucoseGlucagonGlucoseGrowth HormoneHuman Growth HormoneHydrocortisoneHypoglycemic AgentsInsulinACTHcortisolcounter-regulatory hormonesglucagoninsulin resistancetype 2 diabetes

Identifiers

PMID37708362
PMCPMC10795937
OpenAlexW4386726960

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.