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Involvement of CD36 in Modulating the Decrease of NPY and AgRP Induced by Acute Palmitic Acid Stimulation in N1E-115
Yan Ma1,2, Xiaoyi Wang3,4, Hongying Yang5
1Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. dezhoumayan@126.com.
Palmitic acid (PA) reduces neuropeptide Y (NPY) and Agouti-related peptide (AgRP) mRNA expression in the central nervous system (CNS). The cluster of differentiation 36 (CD36) protein is involved in this PA-induced reduction.
Area of Science:
- Neuroscience
- Metabolism
- Molecular Biology
Background:
- Central nervous system (CNS) fatty acid sensing is crucial for regulating food intake.
- Palmitic acid (PA), a major dietary long-chain fatty acid (LCFA), influences appetite regulation.
- The role of cluster of differentiation 36 (CD36) in mediating these effects is not fully understood.
Purpose of the Study:
- To investigate the impact of PA on central neuropeptide expression.
- To elucidate the role of CD36 in mediating PA's effects on neuropeptide expression.
Main Methods:
- N1E-115 cells were cultured with PA.
- CD36 inhibition was achieved using sulfosuccinimidyl-oleate (SSO).
- Neuropeptide mRNA expression (NPY, AgRP) and CD36 expression were quantified.
Main Results:
- PA significantly decreased NPY and AgRP mRNA expression within 20 minutes.
- PA upregulated CD36 expression in N1E-115 cells.
- CD36 inhibition with SSO attenuated the PA-induced decrease in NPY and AgRP mRNA levels.
Conclusions:
- CD36 is implicated in the reduction of NPY and AgRP expression induced by PA in the CNS.
- These findings highlight CD36 as a potential mediator in fatty acid-driven appetite regulation.
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