AI Article Synopsis
- The study aimed to understand how epicardial adipocytes change their characteristics during the development of coronary atherosclerosis, focusing on potential molecular mechanisms.
- The experiment involved 30 male rabbits divided into two groups: one group was fed a high-fat diet to induce atherosclerosis, while the control group received normal food.
- Results showed a decrease in essential fat-burning markers (UCP-1 and PPARγ) and an increase in leptin, indicating a shift in adipose tissue phenotype; IL-6 was identified as a key factor in this conversion through the JAK-STAT3 signaling pathway.
Article Abstract
Objective: To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis.
Methods: A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food.
Results: At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05).
Conclusion: During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656752 | PMC |
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