ArticleInternational journal of obesity (2005)2020
Reduced SIRT1 and SIRT2 expression promotes adipogenesis of human visceral adipose stem cells and associates with accumulation of visceral fat in human obesity.
Article in International journal of obesity (2005), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 58 citations in OpenAlex.
- The Sirtuin Network: Linking NADDiabetes/metabolism research and reviews · 2026Review
- Matched Analysis of Circulating and Adipose Tissue SIRT1 Protein Level in Human Obesity.Nutrients · 2026Article
- Isolation of endothelial progenitor cells from human adipose tissue.International journal of obesity (2005) · 2025Article
- Flavonoids inFood science & nutrition · 2025Article
- The impact of decreased SIRT1 levels on pediatric primary hypertension and left ventricular hypertrophy: a case-control study.BMC pediatrics · 2025Article
- Role of sirtuins in obesity and osteoporosis: molecular mechanisms and therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Natural bioactive compounds and their mechanisms of action in the management of obesity: a narrative review.Frontiers in nutrition · 2025Review
- Unveiling the dynamics of acetylation and phosphorylation in SGBS and 3T3-L1 adipogenesis.iScience · 2024Article
- The role of Sirtuin 1 in regulation of fibrotic genes expression in pre-adipocytes.Journal of diabetes and metabolic disorders · 2024Article
- SIRT1 Serum Concentrations in Lipodystrophic Syndromes.International journal of molecular sciences · 2024Article
- SIRT1 safeguards adipogenic differentiation by orchestrating anti-oxidative responses and suppressing cellular senescence.GeroScience · 2024Article
- Deciphering the role of alternative splicing as a potential regulator in fat-tail development of sheep: a comprehensive RNA-seq based study.Scientific reports · 2024Review
- Influence of Polyphenols on Adipose Tissue: Sirtuins as Pivotal Players in the Browning Process.International journal of molecular sciences · 2023Review
- The Role of NAD+, SIRTs Interactions in Stimulating and Counteracting Carcinogenesis.International journal of molecular sciences · 2023Review
- Review
- Management of Obesity and Obesity-Related Disorders: From Stem Cells and Epigenetics to Its Treatment.International journal of molecular sciences · 2023Review
- Article
- Ketogenic Diet Increases Serum and White Adipose Tissue SIRT1 Expression in Mice.International journal of molecular sciences · 2022Article
- Pomegranate Extract Augments Energy Expenditure Counteracting the Metabolic Stress Associated with High-Fat-Diet-Induced Obesity.International journal of molecular sciences · 2022Article
- Progress in Nonalcoholic Fatty Liver Disease: SIRT Family Regulates Mitochondrial Biogenesis.Biomolecules · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesThe histone deacetylases SIRT1 and SIRT2 have been shown to be involved in the differentiation of rodent adipocyte precursors. In light of the differences in gene expression and metabolic function of visceral (V) and subcutaneous (S) adipose tissue (AT) and their resident cells, the aim of this study was to investigate the role of SIRT1 and SIRT2 in the differentiation of adipose stem cells (ASCs) isolated from SAT and VAT biopsies of nondiabetic obese and nonobese individuals.
methodsHuman ASCs were isolated from paired SAT and VAT biopsies obtained from 83 nonobese and 92 obese subjects and were differentiated in vitro. Adipogenesis was evaluated by analyzing the lipid deposition using an image processing software, and gene expression by RT-qPCR. SIRT1 and SIRT2 protein expression was modified by using recombinant adenoviral vectors.
resultsVisceral but not subcutaneous ASCs from obese subjects showed an intrinsic increase in both adipogenesis and lipid accumulation when compared with ASCs from nonobese subjects, and this was associated with reduced SIRT1 and SIRT2 mRNA and protein levels. Moreover, adipose tissue mRNA levels of SIRT1 and SIRT2 showed an inverse correlation with BMI in the visceral but not subcutaneous depot. Overexpression of SIRT1 or SIRT2 in visceral ASCs from obese subjects resulted in inhibition of adipocyte differentiation, whereas knockdown of SIRT1 or SIRT2 in visceral ASCs from nonobese subjects enhanced this process. Changes in SIRT1 or SIRT2 expression and adipocyte differentiation were paralleled by corresponding changes in PPARG, CEBPA, and other genes marking terminal adipocyte differentiation.
conclusionsSIRT1 and SIRT2 modulate the differentiation of human ASC. Reduced expression of SIRT1 and SIRT2 may enhance the differentiation capacity of visceral ASC in human obesity, fostering visceral adipose tissue expansion.
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.