ArticleDiabetes2016
Impact of Perturbed Pancreatic β-Cell Cholesterol Homeostasis on Adipose Tissue and Skeletal Muscle Metabolism.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 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
15 citing papers in PubMed, 30 citations in OpenAlex.
- Dual modulation of lipid and glucose metabolism by a nutraceutical combination in patients at cardiometabolic risk: results from a multicenter randomized controlled trial.Cardiovascular diabetology · 2025 · on this mapTrial
- Understanding the link between lipid and ocular disorders for effective therapy.Archives of medical science : AMS · 2026Article
- High-density lipoprotein in diabetes: Structural and functional relevance.Journal of diabetes investigation · 2024Review
- Effect of insulin insufficiency on ultrastructure and function in skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2024Article
- Identification of structural motifs critical for human G6PC2 function informed by sequence analysis and an AlphaFold2-predicted model.Bioscience reports · 2024Article
- Effect of Triglyceride-Glucose Indices and Circulating PCSK9-Associated Cardiovascular Risk in STEMI Patients with Primary Percutaneous Coronary Artery Disease: A Prospective Cohort Study.Journal of inflammation research · 2023Article
- Regulation of cholesterol homeostasis in health and diseases: from mechanisms to targeted therapeutics.Signal transduction and targeted therapy · 2022Review
- HDL and Diabetes.Advances in experimental medicine and biology · 2022Article
- High Density Lipoproteins and Diabetes.Cells · 2021Review
- Role of High-Density Lipoproteins in Cholesterol Homeostasis and Glycemic Control.Journal of the American Heart Association · 2020Review
- ABCA1 variants rs2230806 (R219K), rs4149313 (M8831I), and rs9282541 (R230C) are associated with susceptibility to coronary heart disease.Journal of clinical laboratory analysis · 2019Article
- Trials and Tribulations of CETP Inhibitors.Circulation research · 2018Review
- Single-cell transcriptomics of East-Asian pancreatic islets cells.Scientific reports · 2017Article
- Macrophage functions in lean and obese adipose tissue.Metabolism: clinical and experimental · 2017Review
- Lessons from basic pancreatic beta cell research in type-2 diabetes and vascular complications.Diabetology international · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Elevated pancreatic β-cell cholesterol levels impair insulin secretion and reduce plasma insulin levels. This study establishes that low plasma insulin levels have a detrimental effect on two major insulin target tissues: adipose tissue and skeletal muscle. Mice with increased β-cell cholesterol levels were generated by conditional deletion of the ATP-binding cassette transporters, ABCA1 and ABCG1, in β-cells (β-DKO mice). Insulin secretion was impaired in these mice under basal and high-glucose conditions, and glucose disposal was shifted from skeletal muscle to adipose tissue. The β-DKO mice also had increased body fat and adipose tissue macrophage content, elevated plasma interleukin-6 and MCP-1 levels, and decreased skeletal muscle mass. They were not, however, insulin resistant. The adipose tissue expansion and reduced skeletal muscle mass, but not the systemic inflammation or increased adipose tissue macrophage content, were reversed when plasma insulin levels were normalized by insulin supplementation. These studies identify a mechanism by which perturbation of β-cell cholesterol homeostasis and impaired insulin secretion increase adiposity, reduce skeletal muscle mass, and cause systemic inflammation. They further identify β-cell dysfunction as a potential therapeutic target in people at increased risk of developing 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.