X Li1, L Jiang2, M Yang3, Y Wu3, S Sun3, J Sun3. 1. Department of Endocrinology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China. wdy2003win@163.com. 2. Department of Internal Medicine, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China. 3. Department of Endocrinology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
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.
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.
Entities:
Keywords:
C1q/TNF-related protein-3 (CTRP3); Glucagon-like peptide-1 (GLP-1); Protein kinase A (PKA)
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