Evidence map›Paper›PMID 33241460›Full record

ArticleDiabetologia2021

Altered hormonal and autonomic nerve responses to hypo- and hyperglycaemia are found in overweight and insulin-resistant individuals and may contribute to the development of type 2 diabetes.

Martin H Lundqvist, Kristina Almby, Urban Wiklund, Niclas Abrahamsson, Prasad G Kamble, Maria J Pereira, Jan W Eriksson

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Martin H LundqvistDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-9348-4603
Kristina AlmbyDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-7083-8912
Urban WiklundDepartment of Radiation Sciences, Biomedical Engineering, Umeå University, Umeå, Sweden.ORCID 0000-0002-1313-0934
Niclas AbrahamssonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-5428-8025
Prasad G KambleDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-5627-8904
Maria J PereiraDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-5498-3899
Jan W ErikssonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden. jan.eriksson@medsci.uu.se.ORCID 0000-0002-2639-9481
Uppsala University · SEUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisResults from animal models and some clinical work suggest a role for the central nervous system (CNS) in glucose regulation and type 2 diabetes pathogenesis by modulation of glucoregulatory hormones and the autonomic nervous system (ANS). The aim of this study was to characterise the neuroendocrine response to various glucose concentrations in overweight and insulin-resistant individuals compared with lean individuals.

methodsOverweight/obese (HI, n = 15, BMI ≥27.0 kg/m

resultsDuring hypoglycaemic clamps, there was an elevated cortisol response in HI vs LO (median ΔAUC 12,383 vs 4793 nmol/l × min; p = 0.050) and a significantly elevated adrenocorticotropic hormone (ACTH) response in HI vs LO (median ΔAUC 437.3 vs 162.0 nmol/l × min; p = 0.021). When adjusting for clamp glucose levels, obesity (p = 0.033) and insulin resistance (p = 0.009) were associated with elevated glucagon levels. By contrast, parasympathetic activity was less suppressed in overweight individuals at the last stage of hypoglycaemia compared with euglycaemia (high-frequency power of HRV, p = 0.024). M value was the strongest predictor for the ACTH and P CONCLUSIONS/

interpretationThis study supports the hypothesis that altered responses of insulin-antagonistic hormones and the ANS to glucose fluctuations occur in overweight and insulin-resistant individuals, and that these responses are probably partly mediated by the CNS. Their potential role in development of type 2 diabetes needs to be addressed in future research. Graphical abstract.

Indexed as

Insulin ResistanceAdrenocorticotropic HormoneAdultAutonomic Nervous SystemBiomarkersBlood GlucoseBlood PressureCardiovascular SystemCentral Nervous SystemDiabetes Mellitus, Type 2FemaleGlucagonGlucose Clamp TechniqueHeart RateHormonesHumansAdrenocorticotropic HormoneBiomarkersBlood GlucoseGlucagonHormonesHydrocortisoneACTHCentral nervous systemCortisolDiabetesGlucoregulatory hormonesGlucoseInsulin resistanceObesity

Identifiers

PMID33241460
PMCPMC7864814
OpenAlexW3109061083

What OpenQuestion 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 OpenQuestion graph.