ReviewBiochimie2017
Nutrient regulation of pancreatic β-cell proliferation.
Review in Biochimie, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- ETV5 regulates proliferation and cell cycle genes in the INS-1 (832/13) cell line independently of the concentration of secreted insulin.FEBS open bio · 2023Article
- Noncanonical CDK4 signaling rescues diabetes in a mouse model by promoting β cell differentiation.The Journal of clinical investigation · 2023Article
- Repurposing Pitavastatin and L-Glutamine: Replenishing β-Cells in Hyperlipidemic Type 2 Diabetes Mouse Model.Life (Basel, Switzerland) · 2023Article
- Hyperinsulinemic Compensation for Insulin Resistance Occurs Independent of Elevated Glycemia in Male Dogs.Endocrinology · 2021Article
- Discovery of ciliary G protein-coupled receptors regulating pancreatic islet insulin and glucagon secretion.Genes & development · 2021Article
- Targeting β-cell dedifferentiation and transdifferentiation: opportunities and challenges.Endocrine connections · 2021Review
- MicroRNA Sequences Modulated by Beta Cell Lipid Metabolism: Implications for Type 2 Diabetes Mellitus.Biology · 2021Review
- Article
- Article
- Fatty acid transport protein-2 regulates glycemic control and diabetic kidney disease progression.JCI insight · 2020Article
- Connecting pancreatic islet lipid metabolism with insulin secretion and the development of type 2 diabetes.Annals of the New York Academy of Sciences · 2020Review
- VEGF-B ablation in pancreatic β-cells upregulates insulin expression without affecting glucose homeostasis or islet lipid uptake.Scientific reports · 2020Article
- Article
- Effects of Nutrient Intake during Pregnancy and Lactation on the Endocrine Pancreas of the Offspring.Nutrients · 2019Review
- The relevance of AMP-activated protein kinase in insulin-secreting β cells: a potential target for improving β cell function?Journal of physiology and biochemistry · 2019Review
- The autonomic nervous system regulates pancreatic β-cell proliferation in adult male rats.American journal of physiology. Endocrinology and metabolism · 2019Article
- Anti-Diabetic Effects and Mechanisms of Dietary Polysaccharides.Molecules (Basel, Switzerland) · 2019Review
- Fatty Acid-Induced Lipotoxicity in Pancreatic Beta-Cells During Development of Type 2 Diabetes.Frontiers in endocrinology · 2018Review
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 1 institution in 1 country.
Funding
Abstract
Excess consumption of energy-dense foods combined with a sedentary lifestyle is driving an obesity epidemic. Although obesity is closely associated with insulin resistance, most individuals meet the insulin demand by increasing their functional β-cell mass. Those who eventually develop type 2 diabetes are distinguished by a failure in this compensatory process. Although a causal role of insulin resistance in compensatory β-cell responses has received considerable experimental support, precisely how the β cell senses changes in the metabolic environment is still unknown. As metabolism of glucose, lipids and amino acids is profoundly altered in obesity, it is not surprising that these nutrients are conspicuous among the factors proposed to contribute. In this review we summarise our understanding of the role of nutrients, in particular glucose, fatty acids and amino acids in β-cell compensation with a particular emphasis on their relation to insulin resistance-induced factors and their underlying mechanism of action. Finally, we describe the concept of epigenetic programming and review recent studies illustrating how the status of the β cell epigenome is a product of its nutrient environment, and how metabolic programming of the β cell contributes to diabetes risk.
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.