Evidence map›Paper›PMID 26922582›Full record

Trial reportJournal of diabetes and its complications

The antioxidant N-Acetylcysteine does not improve glucose tolerance or β-cell function in type 2 diabetes.

Magdalena A Szkudlinska, Anize D von Frankenberg, Kristina M Utzschneider

Registry-linked trialOpen access · greenAbstract readClinical TrialComparative Study
In one paragraph

Trial report in Journal of diabetes and its complications. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01394510 (Effect of Anti-oxidants on Beta-cell Function in Humans), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 16% 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.

NCT01394510 nacompletednot on this map

Effect of Anti-oxidants on Beta-cell Function in Humans

TypeinterventionalSponsorUtzschneider, Kristina, M.D.Ran2011 to 2015Enrolled13ConditionsType 2 Diabetes, Oxidative StressArmsN-acetylcysteine
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Oxidative Stress, Endothelial Dysfunction, andAntioxidants & redox signaling · 2024
    Review
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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

3 authors at 2 institutions in 2 countries.

Magdalena A SzkudlinskaDivision of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System and University of Washington, Seattle, WA. Electronic address: magda3@u.washington.edu.
Anize D von FrankenbergPost-Graduate Endocrinology Program, School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. Electronic address: anize.frankenberg@gmail.com.
Kristina M UtzschneiderDivision of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System and University of Washington, Seattle, WA. Electronic address: kutzschn@u.washington.edu.
University of Washington · USUniversidade Federal do Rio Grande do Sul · BR

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Nutrition, Obesity and Atherosclerosis Training ProgramT32HL007028 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1985 to 2026
$6.4M
NHLBI NIH HHS T32 HL007028NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30DK017047
6 · The paper itself

Abstract

unlabelledHyperglycemia induces oxidative stress and thereby may exacerbate β-cell dysfunction in type 2 diabetes (T2DM). Notably, glutathione (GSH), synthesized from N-Acetylcysteine (NAC), neutralizes reactive oxygen species within cells and is low in individuals with diabetes.

aimDetermine if NAC supplementation improves β-cell function and glucose tolerance by decreasing oxidative stress in T2DM.

methodsThirteen subjects (6M/7F) with T2DM (duration: 0-13 years, median: 2 years), treated with diet/exercise alone (n=7) or metformin (n=6), underwent a 2-h oral glucose tolerance test (OGTT) at baseline, after 2 weeks supplementation with 600 mg NAC orally twice daily, and again after 2 weeks supplementation with 1200 mg NAC twice daily. The following measurements were made: fasting glucose and fructosamine for glycemic control, incremental AUC glucose (0-120 min) for glucose tolerance, and Δ insulin/Δ glucose (0-30 min) for the early insulin response to glucose. Fasting erythrocyte GSH and GSSG (oxidized glutathione) levels, plasma thiobarbituric acid reactive substances (TBARS), and urine F2α isoprostanes were measured to assess oxidative status.

resultsSubjects were middle aged (mean ± SEM: 53.9 ± 3.2 years), obese (BMI 37.3 ± 2.8 kg/m(2)), and relatively well-controlled (HbA1c 6.7 ± 0.3%, 50 mmol/mol). Glycemic control, glucose tolerance, insulin release, and oxidative markers did not change with either dose of NAC.

conclusionsBased on the lack of any short-term benefit from NAC supplementation on markers of glucose metabolism, β-cell response, and oxidative status, it is unlikely to be a valuable therapeutic approach for treatment of type 2 diabetes.

Indexed as

Dietary SupplementsAcetylcysteineAntioxidantsBiomarkersBody Mass IndexCombined Modality TherapyDiabetes Mellitus, Type 2F2-IsoprostanesFructosamineGlucose Tolerance TestGlycated HemoglobinHumansHyperglycemiaInsulinInsulin-Secreting CellsInsulin SecretionAcetylcysteineAntioxidantsBiomarkersF2-IsoprostanesFructosamineGlycated Hemoglobinhemoglobin A1c protein, humanInsulinAntioxidantN-AcetylcysteineOxidative stressSupplementβ-cell function

Identifiers

PMID26922582
PMCPMC4834245
OpenAlexW2272878535

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.