ArticleFEBS open bio2022
Carbonic anhydrase 3 increases during liver adipogenesis even in pre-obesity, and its inhibitors reduce liver adipose accumulation.
Article in FEBS open bio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Carbonic Anhydrase I and II as Biomarkers and Therapeutic Targets in Human Disease: From Physiology to Clinical Translation.International journal of molecular sciences · 2026Review
- Fragment-Derived Nicotinic Acid Analogues Inhibit hCA III and DownregulateBiomolecules · 2026Article
- Steroidal A/B-ring fusion as a strategy for isoform-selective inhibition of human carbonic anhydrases.RSC advances · 2026Article
- Computational Approaches and Structure-Based Drug Design of CAIs.Sub-cellular biochemistry · 2026Review
- Low-Abundance Proteomics Reveal Pleiotrophin and Fibroblast Growth Factor-21 as Biomarkers of Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Article
- Translational framework linking perfluoroheptanoic acid (PFHpA) exposure to metabolic dysfunction associated steatotic liver disease in adolescents.Communications medicine · 2025Article
- Multi-Target Glitazones for Modulating Peroxisome Proliferator-Activated Receptor-γ, Cyclooxygenase-2, and Carbonic Anhydrases for the Management of Metabolic Dysfunction.ACS pharmacology & translational science · 2025Article
- (Z)-N-(3-([1,1'-biphenyl]-2-yl)-4-heptyl-4-hydroxythiazolidin-2-ylidene)-4-bromobenzamide as carbonic anhydrase inhibitor: exploration of its in vitro and in silico studies.BMC chemistry · 2025Article
- Spaceflight alters host-gut microbiota interactions.NPJ biofilms and microbiomes · 2024Article
- Carbonic Anhydrase 3 is required for cardiac repair post myocardial infarction via Smad7-Smad2/3 signaling pathway.International journal of biological sciences · 2024Article
- Prenylcysteine Oxidase 1 Is a Key Regulator of Adipogenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Anti-obesity carbonic anhydrase inhibitors: challenges and opportunities.Journal of enzyme inhibition and medicinal chemistry · 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The abnormal lipid metabolism in the liver that occurs after high caloric intake is the main cause of nonalcoholic fatty liver disease (NAFLD). Differences between samples from healthy livers and livers from individuals with NAFLD indicate that changes in liver function occur during disease progression. Here, we examined changes in protein expression in a fatty liver model in the early stages of obesity to identify potential alterations in function. The proteins expressed in the liver tissue of pre-obese rats were separated via SDS/PAGE and stained with Coomassie brilliant blue-G250. Peptide mass fingerprinting indicated an increase in the expression of carbonic anhydrase 3 (CA3) relative to controls. Western blotting analysis confirmed the increase in CA3 expression, even in an early fat-accumulation state in which excessive weight gain had not yet occurred. In human hepatoma HepG2 cells, fat accumulation induced with oleic acid also resulted in increased CA3 expression. When the cells were in a state of fat accumulation, treating them with the CA3 inhibitors acetazolamide (ACTZ) or 6-ethoxyzolamide (ETZ) suppressed fat accumulation, but only ETZ somewhat reduced the fat-induced upregulation of CA3 expression. Expression of CA3 was therefore upregulated in response to the consumption of a high-fat diet, even in the absence of an increase in body weight. The suppression of CA3 activity by ACTZ or ETZ reduced fat accumulation in hepatocytes, suggesting that CA3 is involved in the development of fatty liver.
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.