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GLP-1 receptor agonist increases the expression of CTRP3, a novel adipokine, in 3T3-L1 adipocytes through PKA signal pathway.
J Endocrinol Invest · 2015
Last updated 2026-05-28A study found that treating 3T3-L1 fat cells with 2.5 or 5.0 nmol/l of the GLP-1 drug Exendin-4 for 8 hours significantly increased the cells' production of CTRP3, a protein linked to metabolism. The increase was blocked when researchers used a GLP-1 blocker or a protein kinase A (PKA) blocker, suggesting the effect depends on the PKA signaling pathway.
AI summary of the abstract below.
| Journal | J Endocrinol Invest, 2015 |
|---|---|
| Citations | 19 |
| Relative citation ratio | 0.74 |
| NIH percentile | 40 |
| Molecules | — |
| Conditions studied | Obesity, Type 2 Diabetes |
Abstract
OBJECTIVE: To investigate the effects of Exendin-4 (Ex-4), a glucagon-like peptide-1 (GLP-1) receptor agonist, on the expression of C1q/TNF-related protein-3 (CTRP3), a novel adipokine, in 3T3-L1 adipocytes. The role of protein kinase A (PKA) signal pathway in the effects was also investigated.
METHODS: The mRNA and protein expressions of CTRP3 in 3T3-L1 adiocytes were detected by real-time polymerase chain reaction and western blot, respectively. Exendin-fragment 9-39 (Ex-9), a specific GLP-1 receptor antagonist, and H89, a selective antagonist of PKA, were used to confirm the signal pathway of Ex-4 on CTRP3.
RESULTS: 2.5 or 5.0 nmol/l Ex-4 treatment for 8 h increased the expressions of CTRP3 mRNA and protein as well as PKA protein in 3T3-L1 adipocytes significantly, while Ex-9 or H89 blocked the up-regulation of CTRP3 expression induced by Ex-4 completely.
CONCLUSION: GLP-1 receptor agonist increases the expression of CTRP3 mRNA and protein in 3T3-L1 adipocytes via PKA signal pathway.
Verbatim abstract via PubMed 25149084 ↗