ArticleDiabetes2016
Sorcin Links Pancreatic β-Cell Lipotoxicity to ER Ca2+ Stores.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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Who cites it
37 citing papers in PubMed, 69 citations in OpenAlex.
- Long-Timescale Molecular Dynamics Reveal a Coordination-Biased Conformational Selection Mechanism for Sorcin Activation.bioRxiv : the preprint server for biology · 2026Article
- Vitamin K as an Endocrine Modulator: Mechanistic Links to Glucose Metabolism and Beyond.Nutrients · 2026Review
- Sorcin: mechanisms of action in cancer hallmarks, drug resistance and opportunities in therapeutics.Medical oncology (Northwood, London, England) · 2024Review
- Sorcin can trigger pancreatic cancer-associated new-onset diabetes through the secretion of inflammatory cytokines such as serpin E1 and CCL5.Experimental & molecular medicine · 2024Article
- Review
- Disrupted Endoplasmic Reticulum CaBiology · 2024Review
- Mechanism of Obesity-Related Lipotoxicity and Clinical Perspective.Advances in experimental medicine and biology · 2024Review
- Association between serum PCSK9 and coronary heart disease in patients with type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2023Article
- Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes.Experimental & molecular medicine · 2023Review
- Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways.Cellular and molecular life sciences : CMLS · 2023Article
- FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity.Cell metabolism · 2023Article
- FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity.bioRxiv : the preprint server for biology · 2023Article
- LDL Promotes Disorders in β-Cell Cholesterol Metabolism, Implications on Insulin Cellular Communication Mediated by EVs.Metabolites · 2022Article
- Hypoglycemic Effect of Electroacupuncture at ST25 Through Neural Regulation of the Pancreatic Intrinsic Nervous System.Molecular neurobiology · 2022Article
- Lipid-Induced Adaptations of the Pancreatic Beta-Cell to Glucotoxic Conditions Sustain Insulin Secretion.International journal of molecular sciences · 2021Review
- Lipotoxicity and β-Cell Failure in Type 2 Diabetes: Oxidative Stress Linked to NADPH Oxidase and ER Stress.Cells · 2021Review
- Article
- The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021Review
- Sorcin is an early marker of neurodegeneration, CaCell death & disease · 2020Article
- Potential positive and negative consequences of ZnT8 inhibition.The Journal of endocrinology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 8 institutions in 6 countries.
Funding
Abstract
Preserving β-cell function during the development of obesity and insulin resistance would limit the worldwide epidemic of type 2 diabetes. Endoplasmic reticulum (ER) calcium (Ca(2+)) depletion induced by saturated free fatty acids and cytokines causes β-cell ER stress and apoptosis, but the molecular mechanisms behind these phenomena are still poorly understood. Here, we demonstrate that palmitate-induced sorcin downregulation and subsequent increases in glucose-6-phosphatase catalytic subunit-2 (G6PC2) levels contribute to lipotoxicity. Sorcin is a calcium sensor protein involved in maintaining ER Ca(2+) by inhibiting ryanodine receptor activity and playing a role in terminating Ca(2+)-induced Ca(2+) release. G6PC2, a genome-wide association study gene associated with fasting blood glucose, is a negative regulator of glucose-stimulated insulin secretion (GSIS). High-fat feeding in mice and chronic exposure of human islets to palmitate decreases endogenous sorcin expression while levels of G6PC2 mRNA increase. Sorcin-null mice are glucose intolerant, with markedly impaired GSIS and increased expression of G6pc2 Under high-fat diet, mice overexpressing sorcin in the β-cell display improved glucose tolerance, fasting blood glucose, and GSIS, whereas G6PC2 levels are decreased and cytosolic and ER Ca(2+) are increased in transgenic islets. Sorcin may thus provide a target for intervention in type 2 diabetes.
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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.