Somatostatin receptor ligands suppressed proliferation and lipogenesis in 3T3-L1 preadipocytes.
Zhe ZhaoFengying GongLian DuanXiaorui LvHaijie WuYan TangHuijuan ZhuXiaoguang ChenPublished in: Basic & clinical pharmacology & toxicology (2022)
Somatostatin and its analogues, known as somatostatin receptor ligands (SRLs), have been reported to attenuate weight gain in some clinical settings. However, their direct effects on preadipocytes are barely investigated. Therefore, this study aimed to evaluate the influence of SRLs on preadipocytes and to further explore the potential mechanisms. Cell Counting Kit-8 assay, Oil Red O staining, triglyceride contents measurements, quantitative polymerase chain reaction (qPCR) and western blot were used to investigate the effects of SRLs on preadipocytes. We found that three SRLs (octreotide, TT232 and pasireotide) inhibited cell viability after 8-48 h but not 4 h. Further western blot results showed that they significantly suppressed activation of PI3K/Akt pathway. Besides, lipid accumulation was also significantly inhibited by these SRLs. Moreover, mRNA levels of some critical adipogenic markers, including Pparg, Cebpa, Fasn, Fabp4, Acaca and Lpl, were downregulated by the treatments of all these SRLs. Consistently, the protein expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα) and fatty acid synthase (FAS) was also suppressed by SRLs. SRLs inhibit the proliferation and lipogenesis in preadipocytes. Their inhibitory effects on cell proliferation may be mediated by the downregulated PI3K/Akt pathway, and the suppressive actions on lipogenesis may be related to the decreased PPARγ and C/EBPα expression.
Keyphrases
- binding protein
- fatty acid
- weight gain
- neuroendocrine tumors
- cell proliferation
- signaling pathway
- body mass index
- south africa
- insulin resistance
- birth weight
- molecular docking
- cell therapy
- type diabetes
- poor prognosis
- high fat diet induced
- cell cycle
- risk assessment
- metabolic syndrome
- pi k akt
- transcription factor
- adipose tissue
- physical activity
- high throughput
- mass spectrometry
- bone marrow
- long non coding rna
- drug induced
- skeletal muscle