ReviewMetabolites2020
Beta Cell Physiological Dynamics and Dysfunctional Transitions in Response to Islet Inflammation in Obesity and Diabetes.
Review in Metabolites, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 54 citations in OpenAlex.
- Improvements in glucose metabolism after high-, but not low-, volume strength exercise in individuals with obesity are associated with baseline insulin resistance: a secondary analysis from a randomized clinical trial.European journal of applied physiology · 2026Trial
- Toll of Chronic Metabolic Acidosis at Molecular, Cellular, and Systemic Levels: A Conceptual Framework to Revisit Type 2 Diabetes (T2D) Pathophysiology.Biomedicines · 2026Review
- Aerobic training and cannabidiol activate the PI3K/AKT/PDX1 axis to ameliorate beta-cell dysfunction in a rat model of diet-induced obesity.Molecular biology reports · 2026Article
- Explainable machine learning model for in-hospital hypoglycemia risk in patients with latent autoimmune diabetes in adults.Frontiers in immunology · 2026Article
- Asthma diagnosis is not associated with reduced beta-cell function in children and adolescents with obesity.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025Article
- Review
- Article
- Cdk5 mediates impaired autophagy by regulating NGF/Sirt1 axis to cause diabetic islet β cell damage.Frontiers in cell and developmental biology · 2025Article
- Article
- Mechanisms and therapeutics of insulin signaling transduction genes in diabetic cardiomyopathy: a comprehensive updated review.Frontiers in endocrinology · 2025Review
- Complement C3 promotes islet β-cell dedifferentiation by activating Wnt/β-catenin pathway.iScience · 2024Article
- Association of polychlorinated biphenyls with vitamin D among rural Chinese adults with normal glycaemia and type 2 diabetes mellitus.Environmental health : a global access science source · 2024Article
- Article
- KSRP improves pancreatic beta cell function and survival.Scientific reports · 2024Article
- Emerging and multifaceted potential contributions of polyphenols in the management of type 2 diabetes mellitus.World journal of diabetes · 2024Review
- Article
- Tripterine Serves a Dual Role in Palmitate-Induced Pancreatic Beta-Cell Lipotoxicity.Doklady. Biochemistry and biophysics · 2023Article
- Peroxisome proliferator-activated receptors as targets to treat metabolic diseases: Focus on the adipose tissue, liver, and pancreas.World journal of gastroenterology · 2023Review
- Denosumab Attenuates Glucolipotoxicity-Induced β-Cell Dysfunction and Apoptosis by Attenuating RANK/RANKL Signals.International journal of molecular sciences · 2023Article
- Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress.World journal of diabetes · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta cells adapt their function to respond to fluctuating glucose concentrations and variable insulin demand. The highly specialized beta cells have well-established endoplasmic reticulum to handle their high metabolic load for insulin biosynthesis and secretion. Beta cell endoplasmic reticulum therefore recognize and remove misfolded proteins thereby limiting their accumulation. Beta cells function optimally when they sense glucose and, in response, biosynthesize and secrete sufficient insulin. Overnutrition drives the pathogenesis of obesity and diabetes, with adverse effects on beta cells. The interleukin signaling system maintains beta cell physiology and plays a role in beta cell inflammation. In pre-diabetes and compromised metabolic states such as obesity, insulin resistance, and glucose intolerance, beta cells biosynthesize and secrete more insulin, i.e., hyperfunction. Obesity is entwined with inflammation, characterized by compensatory hyperinsulinemia, for a defined period, to normalize glycemia. However, with chronic hyperglycemia and diabetes, there is a perpetual high demand for insulin, and beta cells become exhausted resulting in insufficient insulin biosynthesis and secretion, i.e., they hypofunction in response to elevated glycemia. Therefore, beta cell hyperfunction progresses to hypofunction, and may progressively worsen towards failure. Preserving beta cell physiology, through healthy nutrition and lifestyles, and therapies that are aligned with beta cell functional transitions, is key for diabetes prevention and management.
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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.