ReviewDiabetes2021
What Regulates Basal Insulin Secretion and Causes Hyperinsulinemia?
Review in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 55 citations in OpenAlex.
- Nutrient and non-nutrient regulators of insulin secretion.Nature reviews. Endocrinology · 2026Review
- Persistent organic pollutant concentrations in human pancreas correlate with markers of beta cell dysfunction.Nature communications · 2026Article
- Physical Activity, Metabolic Dysfunction, and the Kynurenine Pathway in Endometriosis and Polycystic Ovary Syndrome: A Literature Review.Biomolecules · 2026Review
- Hypothesis: Nutrient Off-Loading and Ectopic Fat Reduction Reverse Insulin Resistance and Improve Cardiovascular Outcomes in Type 2 Diabetes-A Narrative Review.International journal of molecular sciences · 2026Review
- A shared stress-inflammation signalling architecture underlying chronic disease and multimorbidity.Frontiers in immunology · 2026Review
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Organelle-specific crosstalk between calcium and redox signaling in pancreatic β-cells in physiology and type 2 diabetes.Frontiers in network physiology · 2026Review
- GLP-1 receptor agonists and cancer: current clinical evidence and translational opportunities for preclinical research.The Journal of clinical investigation · 2025Review
- GLP-1 receptor agonist protects glucose-stimulated insulin secretion in pancreatic β-cells against lipotoxicity via PPARδ/UCP2 pathway.Cellular and molecular life sciences : CMLS · 2025Article
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells.Cell reports · 2025Article
- Renalase inhibition defends against acute and chronic β cell stress by regulating cell metabolism.Molecular metabolism · 2025Article
- Consensus on the key characteristics of metabolism disruptors.Nature reviews. Endocrinology · 2025Review
- An antireductant approach ameliorates misfolded proinsulin-induced hyperglycemia and glucose intolerance in male Akita mice.GeroScience · 2025Article
- The Causal Role of Ectopic Fat Deposition in the Pathogenesis of Metabolic Syndrome.International journal of molecular sciences · 2024Review
- Calorie restriction increases insulin sensitivity to promote beta cell homeostasis and longevity in mice.Nature communications · 2024Article
- Advances and counterpoints in type 2 diabetes. What is ready for translation into real-world practice, ahead of the guidelines.BMC medicine · 2024Review
- Beta-Hydroxybutyrate Promotes Basal Insulin Secretion While Decreasing Glucagon Secretion in Mouse and Human Islets.Endocrinology · 2024Article
- Aging and "Age-Related" Diseases - What Is the Relation?Aging and disease · 2024Review
- Article
- Obesogens: a unifying theory for the global rise in obesity.International journal of obesity (2005) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We hypothesize that basal hyperinsulinemia is synergistically mediated by an interplay between increased oxidative stress and excess lipid in the form of reactive oxygen species (ROS) and long-chain acyl-CoA esters (LC-CoA). In addition, ROS production may increase in response to inflammatory cytokines and certain exogenous environmental toxins that mislead β-cells into perceiving nutrient excess when none exists. Thus, basal hyperinsulinemia is envisioned as an adaptation to sustained real or perceived nutrient excess that only manifests as a disease when the excess demand can no longer be met by an overworked β-cell. In this article we will present a testable hypothetical mechanism to explain the role of lipids and ROS in basal hyperinsulinemia and how they differ from glucose-stimulated insulin secretion (GSIS). The model centers on redox regulation, via ROS, and
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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.