The Effect of LPS and Flagellin on the Process of Lipolysis in Mesenchymal Stromal Cells during Adipogenic Differentiation

Mishra, A.; Tsypandina, E.V.; Gaponov, A. M.; Rumyantsev, S. A.; Шестопалов, А. В.

doi:10.1007/s10517-021-05108-4

Cited by 1 publication

(2 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The study findings suggest that mRNA levels may not be a reliable predictor of HSL activation, and future studies should contemplate analyzing HSL at the protein level to directly measure HSL phosphorylation and localization, both of which are regulated at the post-translational level. 39,40 In contrast to LPS, QCT has been demonstrated to enhance insulin sensitivity, and the study results indicate that it also upregulates the expression of genes (ATGL, HSL) associated with lipolysis. This discrepancy can be elucidated by the hypothesis that free fatty acids resulting from lipolysis may serve as substrates for beta-oxidation, and this process might be stimulated by QCT rather than LPS.…”

Section: Discussionmentioning

confidence: 88%

“…However, the data concerning HSL expression when treated with LPS indicated a slight reduction that was not statistically significant compared to the control group. The study findings suggest that mRNA levels may not be a reliable predictor of HSL activation, and future studies should contemplate analyzing HSL at the protein level to directly measure HSL phosphorylation and localization, both of which are regulated at the post‐translational level 39,40 …”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

The effect of quercetin on adipogenesis, lipolysis, and apoptosis in 3T3‐L1 adipocytes: The role of SIRT1 pathways

Maleki,

Abdizadeh Javazm,

Dastghaib

et al. 2024

Obesity Science & Practice

View full text Add to dashboard Cite

BackgroundLipotoxicity, caused by adipocyte triglyceride over‐accumulation, contributes to obesity‐related comorbidities such as hypertension, type 2 diabetes, coronary heart disease, respiratory dysfunction, and osteoarthritis. This study focuses on determining how sirtuin‐1 (SIRT‐1) mediates quercetin's (QCT) effect on 3T3‐L1 adipocytes. Key aspects of this study include preventing adipogenesis, inducing lipolysis, and stimulating adipocyte apoptosis.Methods3T3‐L1 adipocytes underwent treatment with varying QCT doses, lipopolysaccharide (LPS), and the SIRT‐1 inhibitor EX‐527, followed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide [MTT] assay for cell viability assessment. Furthermore, quantitative real‐time polymerase chain reaction measured mRNA expression levels of adipogenesis markers (fatty acid synthase [FASN] and peroxisome proliferator‐activated receptor gamma [PPARγ]), lipolysis markers (adipose triglyceride lipase [ATGL] and hormone‐sensitive lipase [HSL]), and apoptosis markers (B‐cell lymphoma2 [Bcl‐2], Bcl‐2 Associated ‐X‐protein [BAX] and Caspase‐3).ResultsThe data showed that LPS + QCT significantly reduced cell viability in a dose‐ and time‐dependent manner, unaffected by LPS + QCT + EX‐527. Treatment with LPS + QCT did not affect FASN and PPARγ expression but significantly increased ATGL and HSL mRNA expression compared with LPS alone. Interestingly, EX‐527 reversed the effects of LPS + QCT on lipogenesis and lipolysis markers completely. QCT enhanced apoptosis in a SIRT‐1 independent pattern.ConclusionThe data suggest that QCT suppresses adipogenesis while increasing lipolysis via SIRT‐1. However, QCT's effects on apoptosis appear to be independent of SIRT‐1. These findings provide further evidence for QCT's effects on adipocytes, particularly its interaction with SIRT‐1.

show abstract

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 98%