期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/ijms22031431
关键词
p-Coumaric acid; AMPK; leptin signaling; glucose homeostasis; HFD-induced obesity
资金
- Tan Tao University (TTU) Foundation for Science and Technology Development [TTU.RS.19.305.024]
- Vietnam National Foundation for Science and Technology Development (NAFOSTED) [NAFOSTED 108.05-2019.01]
- National Research Foundation (NRF), Korea [2020M3E5E2038221]
- National Research Foundation of Korea [2020M3E5E2038221] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
p-Coumaric acid potentially activates peripheral AMPK and improves glucose metabolism, while showing inhibitory effects on central AMPK activity. This differential effect enhances hypothalamic leptin sensitivity and improves whole-body glucose homeostasis.
AMP-activated protein kinase (AMPK) plays a crucial role in the regulation of energy homeostasis in both peripheral metabolic organs and the central nervous system. Recent studies indicated that p-Coumaric acid (CA), a hydroxycinnamic phenolic acid, potentially activated the peripheral AMPK pathway to exert beneficial effects on glucose metabolism in vitro. However, CA's actions on central AMPK activity and whole-body glucose homeostasis have not yet been investigated. Here, we reported that CA exhibited different effects on peripheral and central AMPK activation both in vitro and in vivo. Specifically, while CA treatment promoted hepatic AMPK activation, it showed an inhibitory effect on hypothalamic AMPK activity possibly by activating the S6 kinase. Furthermore, CA treatment enhanced hypothalamic leptin sensitivity, resulting in increased proopiomelanocortin (POMC) expression, decreased agouti-related peptide (AgRP) expression, and reduced daily food intake. Overall, CA treatment improved blood glucose control, glucose tolerance, and insulin sensitivity. Together, these results suggested that CA treatment enhanced hypothalamic leptin signaling and whole-body glucose homeostasis, possibly via its differential effects on AMPK activation.
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