Abstract
Central nervous system (CNS) fatty acid sensing plays an important role in the regulation of food intake, and palmitic acid (PA) is the most important long chain fatty acid (LCFA) in the mammalian diet. To explore the effect of PA on central neuropeptide expression and the role of the cluster of the differentiation of 36 (CD36) in the process, N1E-115 cells were cultured with PA in the presence or absence of sulfosuccinimidyl-oleate (SSO), a CD36 inhibitor. Results showed that 10 μmol/L PA significantly reduced NPY and AgRP mRNA expression after 20 min of exposure, while the expression of CD36 was upregulated. The presence of SSO significantly attenuated the decrease of NPY and AgRP expression that was induced by PA alone, although no notable effect on PA- induced CD36 gene expression was observed. In conclusion, our study suggests the involvement of CD36 in the PA-induced decrease of NPY and AgRP in N1E-115 cells.
Highlights
The central nervous system (CNS) plays an essential role in the regulation of mammalian appetite control and energy expenditure, integrating signals from gastrointestinal afferents and circulating nutrient-related factors to alter behavior and neuroendocrine function [1]
The molecular mechanism involved in this fatty acids (FA) sensing by the Central nervous system (CNS) remains unclear, but it is widely accepted that anorexigenic proopiomelanocortin (POMC)-expressing neurons and orexigenic agouti-related protein (AgRP)/neuropeptide Y (NPY)-expressing neurons are involved in the process [5]
To determine the effect of palmitic acid (PA) treatment on NPY, AgRP, and POMC gene expression, N1E-115 cells were treated with 10 μmol/L PA for 0, 10, 20, 30 min, 1, 2, and 4 h, respectively
Summary
The central nervous system (CNS) plays an essential role in the regulation of mammalian appetite control and energy expenditure, integrating signals from gastrointestinal afferents and circulating nutrient-related factors to alter behavior and neuroendocrine function [1]. A growing body of evidence suggests that CNS lipid sensing regulates energy balance through insulin secretion and action, adipose deposition, and food intake, etc. The molecular mechanism involved in this FA sensing by the CNS remains unclear, but it is widely accepted that anorexigenic proopiomelanocortin (POMC)-expressing neurons and orexigenic agouti-related protein (AgRP)/neuropeptide Y (NPY)-expressing neurons are involved in the process [5]. It has been demonstrated that the selective ablation of NPY/AgRP neurons from adult mice causes marked reduction of feeding and body weight [6,7]. The cellular activation of AgRP neurons, which are largely overlapped with NPY neurons in the arcuate nucleus [8], induces acute and robust food intake [9,10]. Research has suggested that NPY/AgRP neurons are the principal inducer of feeding
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