ReviewJournal of physiology and biochemistry2000
Nutrient toxicity in pancreatic beta-cell dysfunction.
Review in Journal of physiology and biochemistry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 26 citations in OpenAlex.
- Silencing the FABP3 gene in insulin-secreting cells reduces fatty acid uptake and protects against lipotoxicity.Acta diabetologica · 2024Article
- Chemical Compounds and Ambient Factors Affecting Pancreatic Alpha-Cells Mass and Function: What Evidence?International journal of environmental research and public health · 2022Review
- Coloured Rice Phenolic Extracts Increase Expression of Genes Associated with Insulin Secretion in Rat Pancreatic Insulinoma β-cells.International journal of molecular sciences · 2020Article
- Metabolic responses and "omics" technologies for elucidating the effects of heat stress in dairy cows.International journal of biometeorology · 2017Review
- Anthocyanins-rich extract of wild Chinese blueberry protects glucolipotoxicity-induced INS832/13 β-cell against dysfunction and death.Journal of food science and technology · 2015Article
- Adipocyte gene expression is altered in formerly obese mice and as a function of diet composition.The Journal of nutrition · 2008Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nutrients, such as glucose and fatty acids, have a dual effect on pancreatic beta-cell function. Acute administration of high glucose concentrations to pancreatic beta-cells stimulates insulin secretion. In addition, short term exposure of this cell type to dietary fatty acids potentiates glucose-induced insulin release. On the other hand, long-term exposure to these nutrients causes impaired insulin secretion, characterized by elevated exocytosis at low concentrations of glucose and no response when glucose increases in the extracellular medium. In addition, other phenotypic changes are observed in these conditions. One major step in linking these phenotypic changes to the diabetic pathology has been the recognition of both glucose and fatty acids as key modulators of beta-cell gene expression. This could explain the adaptative response of the cell to sustained nutrient concentration. Once this phase is exhausted, the beta-cell becomes progressively unresponsive to glucose and this alteration is accompanied by the irreversible induction of apoptotic programs. The aim of this review is to present actual data concerning the development of the toxicity to the main nutrients glucose and fatty acids in the pancreatic beta-cell and to find a possible link to the development of type 2 diabetes.
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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.