ReviewF1000Research2020
Recent advances in understanding glucose transport and glucose disposal.
Review in F1000Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Celtis africana (N. L. Burm.) Modulates Glucose Homeostasis and Mitigates Cardiac Tissue Oxidative Injury: Insights From an Ex Vivo Study.Chemistry & biodiversity · 2026Article
- Persimmon carotenoid extract rich in β-cryptoxanthin improves glucose homeostasis and reduces liver damage in high-fat-diet-induced type 2 diabetic and metabolic dysfunction-associated steatotic liver disease mice.Journal of the science of food and agriculture · 2026Article
- The effect of enhanced glycolysis on cardiac aging.GeroScience · 2025Article
- Serum metabolomic responses to aerobic exercise in rats under chronic unpredictable mild stress.Scientific reports · 2022Article
- Current State and Principles of Basal Insulin Therapy in Type 2 Diabetes.Journal of clinical medicine research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deficient glucose transport and glucose disposal are key pathologies leading to impaired glucose tolerance and risk of type 2 diabetes. The cloning and identification of the family of facilitative glucose transporters have helped to identify that underlying mechanisms behind impaired glucose disposal, particularly in muscle and adipose tissue. There is much more than just transporter protein concentration that is needed to regulate whole body glucose uptake and disposal. The purpose of this review is to discuss recent findings in whole body glucose disposal. We hypothesize that impaired glucose uptake and disposal is a consequence of mismatched energy input and energy output. Decreasing the former while increasing the latter is key to normalizing glucose homeostasis.
Indexed as
Identifiers
What OpenQuestion holds
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.