Evidence map›Paper›PMID 38905209›Full record

ArticleDiabetes care2024

Glucose Load Following Prolonged Fasting Increases Oxidative Stress- Linked Response in Individuals With Diabetic Complications.

Ekaterina von Rauchhaupt, Claus Rodemer, Elisabeth Kliemank, Ruben Bulkescher, Marta Campos, Stefan Kopf, Thomas Fleming, Stephan Herzig, Peter P Nawroth, Julia Szendroedi and 2 more

Abstract read
In one paragraph

Article in Diabetes care, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–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.

  1. Total saponins fromJournal of ginseng research · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

12 authors.

Ekaterina von RauchhauptDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Claus RodemerDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Elisabeth KliemankDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Ruben BulkescherDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Marta CamposDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Stefan KopfDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Thomas FlemingDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.ORCID 0000-0002-6455-3769
Stephan HerzigGerman Center for Diabetes Research, München-Neuherberg, Germany.
Peter P NawrothDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Julia SzendroediDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Johanna ZemvaDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.
Alba SulajDepartment of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine I), University Hospital of Heidelberg, Heidelberg, Germany.ORCID 0000-0002-6051-6696

Funding

Deutsche Diabetes Gesellschaft (DDG)Deutsche Forschungsgemeinschaft (DFG) 236360313â€"SFB 1118German Center for Diabetes Research (DZD) 82DZD07C2GMedizinischen Fakultät Heidelberg, Universität Heidelberg Friedrich-Fischer-Estate
6 · The paper itself

Abstract

objectiveProlonged catabolic states in type 2 diabetes (T2D), exacerbated by excess substrate flux and hyperglycemia, can challenge metabolic flexibility and antioxidative capacity. We investigated cellular responses to glucose load after prolonged fasting in T2D. RESEARCH DESIGN AND

methodsGlucose-tolerant individuals (CON, n = 10) and individuals with T2D with (T2D+, n = 10) and without (T2D-, n = 10) diabetes complications underwent oral glucose tolerance test before and after a 5-day fasting-mimicking diet. Peripheral blood mononuclear cell (PBMC) resistance to ex vivo dicarbonyl methylglyoxal (MG) exposure after glucose load was assessed. Markers of dicarbonyl detoxification, oxidative stress, and mitochondrial biogenesis were analyzed by quantitative PCR, with mitochondrial complex protein expression assessed by Western blotting.

resultsT2D+ exhibited decreased PBMC resistance against MG, while T2D- resistance remained unchanged, and CON improved postglucose load and fasting (-19.0% vs. -1.7% vs. 12.6%; all P = 0.017). T2D+ showed increased expression in dicarbonyl detoxification (mRNA glyoxalase-1, all P = 0.039), oxidative stress (mRNA glutathione-disulfide-reductase, all P = 0.006), and mitochondrial complex V protein (all P = 0.004) compared with T2D- and CON postglucose load and fasting. Citrate synthase activity remained unchanged, indicating no change in mitochondrial number. Mitochondrial biogenesis increased in T2D- compared with CON postglucose load and fasting (mRNA HspA9, P = 0.032). T2D-, compared with CON, exhibited increased oxidative stress postfasting, but not postglucose load, with increased mRNA expression in antioxidant defenses (mRNA forkhead box O4, P = 0.036, and glutathione-peroxidase-2, P = 0.034), and compared with T2D+ (glutathione-peroxidase-2, P = 0.04).

conclusionsThese findings suggest increased susceptibility to glucose-induced oxidative stress in individuals with diabetes complications after prolonged fasting and might help in diet interventions for diabetes management.

Indexed as

Diabetes Mellitus, Type 2FastingOxidative StressAdultAgedBlood GlucoseDiabetes ComplicationsFemaleGlucoseGlucose Tolerance TestHumansLeukocytes, MononuclearMaleMiddle AgedBlood GlucoseGlucose

Identifiers

PMID38905209
PMCPMC11362116

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.