ArticleFrontiers in endocrinology2023
Induction of remission in diabetes by lowering blood glucose.
Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled 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.
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, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.
- Clinical parameters and emerging biomarkers of partial remission in pediatric type 1 diabetes: a systematic review.Frontiers in endocrinology · 2026Pooled it
- Effect of dietary carbohydrate intake on glycaemic control and insulin resistance in type 2 diabetes: A systematic review and meta-analysis.Asia Pacific journal of clinical nutrition · 2025Pooled it
- Effects of insulin and exenatide therapy on glycemic control and β-cell function in patients newly diagnosed with type 2 diabetes and severe hyperglycemia.Journal of the Chinese Medical Association : JCMA · 2026Trial
- Genetic Risk Phenotypes for Type 2 Diabetes Differ with Ancestry in US Adults with Diabetes and Overweight/Obesity.Archives of medical research · 2025Article
- Metabolic interventions as adjunctive therapies to insulin in type 1 diabetes: Current clinical landscape and perspectives.Diabetes, obesity & metabolism · 2025Review
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 1 institution in 1 country.
Funding
Abstract
As diabetes continues to grow as major health problem, there has been great progress in understanding the important role of pancreatic beta-cells in its pathogenesis. Diabetes develops when the normal interplay between insulin secretion and the insulin sensitivity of target tissues is disrupted. With type 2 diabetes (T2D), glucose levels start to rise when beta-cells are unable to meet the demands of insulin resistance. For type 1 diabetes (T1D) glucose levels rise as beta-cells are killed off by autoimmunity. In both cases the increased glucose levels have a toxic effect on beta-cells. This process, called glucose toxicity, has a major inhibitory effect on insulin secretion. This beta-cell dysfunction can be reversed by therapies that reduce glucose levels. Thus, it is becoming increasingly apparent that an opportunity exists to produce a complete or partial remission for T2D, both of which will provide health benefit.
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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.