ArticleAdipocyte2013
Regulation of alternative splicing in obesity and weight loss.
Article in Adipocyte, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Altered splicing factor and alternative splicing events in a mouse model of diet- and polychlorinated biphenyl-induced liver disease.Environmental toxicology and pharmacology · 2023Article
- Deletion of the Brain-Specific α and δ Isoforms of Adapter Protein SH2B1 Protects Mice From Obesity.Diabetes · 2021Article
- Identification and characterization of adipose surface epitopes.The Biochemical journal · 2020Review
- Observational
- Dysregulation of the Splicing Machinery Is Associated to the Development of Nonalcoholic Fatty Liver Disease.The Journal of clinical endocrinology and metabolism · 2019Article
- Regulation of alternative splicing in obesity-induced hypertension.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Palmitate- and C6 ceramide-inducedNutrition & metabolism · 2018Article
- Roles of silent information regulator 1-serine/arginine-rich splicing factor 10-lipin 1 axis in the pathogenesis of alcohol fatty liver disease.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Global Gene Expression Profiling in Omental Adipose Tissue of Morbidly Obese Diabetic African Americans.Journal of endocrinology and metabolism · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative splicing (AS) is a mechanism by which multiple mRNA transcripts are generated from a single gene. According to recent reports approximately 95-100% of human multi-exon genes undergo AS. This increases the amount of functionally different protein isoforms, and in some cases leads to metabolic diseases. Herein we provide a brief overview of the basic aspects of splicing regulation in obesity and insulin resistance with specific examples. In addition, we review our recent findings demonstrating that weight loss regulates AS of TCF7L2 gene in both liver and adipose tissue, and that this splicing associates with changes in fatty acid and glucose metabolism. Future studies using global analysis of transcript variants and splicing regulators are needed for exploring the association of AS with metabolic alterations in obesity and type 2 diabetes (T2D). Understanding of the molecular mechanisms behind the aberrantly spliced transcripts may also provide opportunities for new diagnostic approaches.
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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.