Evidence map›Paper›PMID 37498479›Full record

Observational studyGeroScience2023

Basal autophagic flux measured in blood correlates positively with age in adults at increased risk of type 2 diabetes.

Julien Bensalem, Xiao Tong Teong, Kathryn J Hattersley, Leanne K Hein, Célia Fourrier, Kai Liu, Amy T Hutchison, Leonie K Heilbronn, Timothy J Sargeant

Open access · greenAbstract readObservational Study
In one paragraph

Observational study in GeroScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Links Between Autophagy and Healthy Aging.Journal of molecular biology · 2026
    Review
  5. Article
  6. Article
  7. Cell-Type-Specific Autophagy in Human Leukocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Article
  9. Monitoring Autophagy in Human Aging: Key Cell Models and Insights.Frontiers in bioscience (Landmark edition) · 2025
    Review
  10. Article
  11. Review
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

9 authors at 1 institution in 1 country.

Julien BensalemLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0003-3873-4627
Xiao Tong TeongLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0002-1387-0975
Kathryn J HattersleyLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.
Leanne K HeinLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0001-5887-7858
Célia FourrierLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0003-1505-1559
Kai LiuLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0003-3633-1226
Amy T HutchisonLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0002-6393-3671
Leonie K HeilbronnLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.ORCID 0000-0003-2106-7303
Timothy J SargeantLifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia. Tim.Sargeant@sahmri.com.ORCID 0000-0003-1254-4390
South Australian Health and Medical Research Institute · AU

Funding

Diabetes Australia Y21G-SARTNational Health and Medical Research Council 2002608
6 · The paper itself

Abstract

Preclinical data show that autophagy delays age-related disease. It has been postulated that age-related disease is-at least in part-caused by an age-related decline in autophagy. However, autophagic flux has never been measured in humans across a spectrum of aging in a physiologically relevant context. To address this critical gap in knowledge, the objective of this cross-sectional observational study was to measure basal autophagic flux in whole blood taken from people at elevated risk of developing type 2 diabetes and correlate it with chronological age. During this study, 119 people were recruited and five people were excluded during sample analysis such that 114 people were included in the final analysis. Basal autophagic flux measured in blood and correlations with parameters such as age, body weight, fat mass, AUSDRISK score, blood pressure, glycated hemoglobin HbA1c, blood glucose and insulin, blood lipids, high-sensitivity C-reactive protein, plasma protein carbonylation, and plasma β-hexosaminidase activity were analysed. Despite general consensus in the literature that autophagy decreases with age, we found that basal autophagic flux increased with age in this human cohort. This is the first study to report measurement of basal autophagic flux in a human cohort and its correlation with age. This increase in basal autophagy could represent a stress response to age-related damage. These data are significant not only for their novelty but also because they will inform future clinical studies and show that measurement of basal autophagic flux in a human cohort is feasible.

Indexed as

Diabetes Mellitus, Type 2AutophagyBlood GlucoseCross-Sectional StudiesHumansBlood GlucoseAgingAutophagyCell biologyDiabetesHuman

Identifiers

PMID37498479
PMCPMC10643809
OpenAlexW4385294957

What OpenQuestion holds

Textmetadata
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.