ArticleIn vitro cellular & developmental biology. Animal2026
The differential expression of lipocalin-2 in pig tissues and its molecular mechanism of regulating cell viability, differentiation, adipogenesis, and glycometabolism in porcine intramuscular preadipocytes.
Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Lipocalin-2 (LCN-2) is an adipocytokine secreted mainly by adipose tissue. Increasing evidences suggest that LCN-2 is an inflammatory factor associated with insulin resistance, obesity, and its complications. The precise mechanism of the development of obesity-related disorders induced by LCN-2 is not very clear. This study evaluated the expression of LCN-2 in pig tissues and its molecular mechanism of regulating preadipocyte differentiation in porcine intramuscular preadipocytes. LCN-2 expression in tissues of Tongcheng pigs, intramuscular adipose tissue of Tongcheng pigs (fat type) and Landrace pigs (lean type) in embryonic stage and growth stage, and adipocyte differentiation-induced porcine intramuscular preadipocytes was detected using reverse transcription polymerase chain reaction (qRT-PCR). After LCN-2 treatment, cell viability was measured by the methyl thiazolyl tetrazolium (MTT) method, mRNA expression of CCAAT/enhancer binding protein-ɑ (C/EBPɑ), adipocyte determination and differentiation factor-1 (ADD1), fatty acid desaturase (FAD), fatty acid synthase (FAS), and glucose transporter (GLUT) 1,4 was determined by qRT-PCR, protein expression of LCN-2 and peroxisome proliferator-activated receptor-γ (PPARγ) was analyzed by Western blot. Results of qRT-PCR indicated that LCN-2 showed significantly higher expression in high-intramuscular fat (IMF) pigs compared to low-IMF pigs (P < 0.05). LCN-2 expression in porcine intramuscular preadipocytes was significantly upregulated after adipocytic differentiation induction (P < 0.05). Silencing of LCN-2 with LCN-2 siRNA (siLCN-2) inhibited cell viability, lipid droplets, protein expression of PPARγ, and mRNA expression of C/EBPa, ADD1, FAD, FAS, and GLUT 1,4. siLCN-2 treated cells also showed a lower content of triglyceride and release of glucose. Moreover, LCN-2-induced downregulation of cell viability, adipocytic differentiation, adipogenesis, and glycometabolism of porcine intramuscular preadipocytes was partially blocked by the PPARγ inhibitor (GW9662). It is indicated that LCN-2 silencing suppresses cell viability, adipocytic differentiation and adipogenesis, glycometabolism, and fat deposition of porcine intramuscular preadipocytes through suppression of the PPARγ signaling pathway.
Indexed as
Identifiers
41845028What 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.