Evidence map›Paper›PMID 31114697›Full record

Observational studyBMJ open diabetes research & care2019

Comparison of endothelial function and sympathetic nervous system activity along the glucose continuum in individuals with differing metabolic risk profiles and low dietary sodium intake.

Sara Baqar, Nora E Straznicky, Gavin Lambert, Yee Wen Kong, John B Dixon, George Jerums, Elif Ilhan Ekinci, Elisabeth Lambert

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in BMJ open diabetes research & care, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

7 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Autonomic cardiovascular changes during reactive hyperemia.Clinical physiology and functional imaging · 2026
    Article
  4. Article
  5. Review
  6. ADAM17 cleaves the insulin receptor ectodomain on endothelial cells and causes vascular insulin resistance.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  7. Article
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

8 authors.

Sara BaqarEndocrinology, Austin Health, Heidelberg, Victoria, Australia.ORCID 0000-0002-4921-1349
Nora E StraznickyDepartment of Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Gavin LambertFaculty of Health, Arts and Design, Iverson Health Innovation Research Institute, Swinburne University of Technology, Melbourne, Victoria, Australia.
Yee Wen KongEndocrinology, Austin Health, Heidelberg, Victoria, Australia.
John B DixonVascular and Hypertension, Obesity Research, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
George JerumsDepartment of Endocrinology, Austin Health, Heidelberg, Victoria, Australia.
Elif Ilhan EkinciEndocrinology, Austin Health, Heidelberg, Victoria, Australia.ORCID 0000-0003-2372-395X
Elisabeth LambertFaculty of Health, Arts and Design, Iverson Health Innovation Research Institute, Swinburne University of Technology, Melbourne, Victoria, Australia.ORCID 0000-0002-2232-9048

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLow sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. RESEARCH DESIGN AND

methodsIn this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D-) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile.

resultsMean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D-, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control.

conclusionsIndividuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.

Indexed as

Sodium, DietaryAgedDiabetes Mellitus, Type 2EndotheliumFemaleGlucose IntoleranceGlucose Tolerance TestHumansMaleManometryMiddle AgedRisk FactorsSympathetic Nervous SystemSodium, Dietarycardiovascular diseaseendothelial dysfunctionimpaired glucose tolerancemicroneurographypulse amplitude tonometrysympathetic nervous systemtwenty four hour urinary sodium excretiontype 2 diabetes

Identifiers

PMID31114697
PMCPMC6501854

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.