ReviewFrontiers in endocrinology2018
β-Cell Failure or β-Cell Abuse?
Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 57 citations in OpenAlex.
- A Comparison of the Gluco-Regulatory Responses to High-Intensity Interval Exercise and Resistance Exercise.International journal of environmental research and public health · 2021Trial
- Relevance of the KATP channel function for the basal insulin hypersecretion of islets from female NZO mice.Journal of the Endocrine Society · 2026Article
- Association of inflammation with glycemic control, insulin sensitivity, and beta-cell function in diabetic cats.Journal of veterinary internal medicine · 2026Article
- Chestnut-derived ellagitannins (FT50) protect against western diet-induced metabolic dysfunction and preserve beta cell function in mice.Frontiers in endocrinology · 2026Article
- Article
- Human Beta Cell Functional Adaptation and Dysfunction in Insulin Resistance and Its Reversibility.Nephron · 2024Review
- Reactive oxygen species: role in obesity and mitochondrial energy efficiency.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- O304 ameliorates hyperglycemia in mice by dually promoting muscle glucose effectiveness and preserving β-cell function.Communications biology · 2023Article
- Immunotherapy With Low-Dose IL-2/CD25 Prevents β-Cell Dysfunction and Dysglycemia in Prediabetic NOD Mice.Diabetes · 2023Article
- Maternal Western-style diet in nonhuman primates leads to offspring islet adaptations including altered gene expression and insulin hypersecretion.American journal of physiology. Endocrinology and metabolism · 2023Article
- Palmitoylation couples insulin hypersecretion with β cell failure in diabetes.Cell metabolism · 2023Article
- Modeling the progression of Type 2 diabetes with underlying obesity.PLoS computational biology · 2023Article
- Nanocurcumin combined with insulin alleviates diabetic kidney disease through P38/P53 signaling axis.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Understanding islet dysfunction in type 2 diabetes through multidimensional pancreatic phenotyping: The Human Pancreas Analysis Program.Cell metabolism · 2022Review
- Progression from prediabetes to type 2 diabetes mellitus induced by overnutrition.Hormones (Athens, Greece) · 2022Review
- Lipotoxicity in a Vicious Cycle of Pancreatic Beta Cell Exhaustion.Biomedicines · 2022Article
- Pulsatile Basal Insulin Secretion Is Driven by Glycolytic Oscillations.Physiology (Bethesda, Md.) · 2022Review
- The role of selenium in type-2 diabetes mellitus and its metabolic comorbidities.Redox biology · 2022Review
- Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production.Biomolecules · 2022Review
- Age-Related Changes in Lipid and Glucose Levels Associated with Drug Use and Mortality: An Observational Study.Journal of personalized medicine · 2022Article
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
This review is motivated by the need to question dogma that has not yielded significant improvements in outcomes of Type 2 Diabetes treatment: that insulin resistance is the driver of ß-Cell failure and resulting hyperglycemia. We highlight the fact that hyperlipidemia, insulin resistance, and hyperinsulinemia all precede overt diabetes diagnosis and can each induce the other when tested experimentally. New research highlights the importance of high levels of circulating insulin as both a driver of weight gain and insulin resistance. Data from our lab and others document that several nutrients and environmental toxins can stimulate insulin secretion at non-stimulatory glucose in the absence of insulin resistance. This occurs either by direct action on the ß-Cell or by shifting its sensitivity to known secretagogues. We raise the next logical question of whether ß-Cell dysfunction in Type 2 Diabetes is due to impaired function, defined as failure, or if chronic overstimulation of the ß-Cell that exceeds its capacity to synthesize and secrete insulin, defined as abuse, is the main abnormality in Type 2 Diabetes. These questions are important as they have direct implications for how to best prevent and treat Type 2 Diabetes.
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.