Evidence map›Paper›PMID 22664956›Full record

ArticleDiabetes2012

Neuroadrenergic dysfunction along the diabetes continuum: a comparative study in obese metabolic syndrome subjects.

Nora E Straznicky, Mariee T Grima, Carolina I Sari, Nina Eikelis, Elisabeth A Lambert, Paul J Nestel, Murray D Esler, John B Dixon, Reena Chopra, Alan J Tilbrook and 2 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. A Need to Preserve Ejection Fraction during Heart Failure.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Phenotyping autonomic neuropathy using principal component analysis.Autonomic neuroscience : basic & clinical · 2023
    Article
  12. Article
  13. The denervation or activation of renal sympathetic nerve and renal blood flow.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2023
    Review
  14. Article
  15. Review
  16. Role of the arterial baroreflex in the sympathetic response to hyperinsulinemia in adult humans.American journal of physiology. Endocrinology and metabolism · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Nora E StraznickyLaboratory of Human Neurotransmitters, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia. nora.straznicky@bakeridi.edu.au
Mariee T Grima
Carolina I Sari
Nina Eikelis
Elisabeth A Lambert
Paul J Nestel
Murray D Esler
John B Dixon
Reena Chopra
Alan J Tilbrook
Markus P Schlaich
Gavin W Lambert
Baker Heart and Diabetes Institute · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroadrenergic function in type 2 diabetic (T2D) patients without neuropathy is poorly characterized. We therefore compared sympathetic nervous system activity at rest and during an oral glucose tolerance test in obese metabolic syndrome (MetS) subjects classified as glucose intolerant (impaired glucose tolerance [IGT]; n = 17) or treatment-naive T2D (n = 17). Untreated subjects, matched for age (mean 59 ± 1 year), sex, BMI (32.4 ± 0.6 kg/m(2)), and family history of diabetes were studied. We measured resting muscle sympathetic nerve activity (MSNA) by microneurography, whole-body norepinephrine kinetics by isotope dilution, insulin sensitivity by euglycemic-hyperinsulinemic clamp (steady-state glucose utilization adjusted for fat-free mass and steady-state insulin concentration [M/I]), and MetS components. T2D subjects had higher resting MSNA burst incidence (67 ± 4 versus 55 ± 3 bursts per 100 heartbeats; P = 0.05) and arterial norepinephrine levels (264 ± 33 versus 167 ± 16 pg/mL; P = 0.02), lower plasma norepinephrine clearance (by 17%; P = 0.03), and reduced neuronal reuptake compared with IGT subjects (by 46%; P = 0.04). Moreover, norepinephrine spillover responses to glucose ingestion were blunted in T2D subjects. The M/I value independently predicted whole-body norepinephrine spillover (r = -0.47; P = 0.008), whereas fasting insulin level related to neuronal norepinephrine reuptake (r = -0.35, P = 0.047). These findings demonstrate that progression to T2D is associated with increased central sympathetic drive, blunted sympathetic responsiveness, and altered norepinephrine disposition.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2FemaleGlucose IntoleranceHumansInsulin ResistanceMaleMetabolic SyndromeMiddle AgedNorepinephrineObesitySympathetic Nervous SystemBlood GlucoseNorepinephrine

Identifiers

PMID22664956
PMCPMC3447913
OpenAlexW2130172549

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.