Abstract
Blockade of the neuropeptide Y Y2 receptor with the potent antagonist BIIE0246 regulates gene expression levels in the lipid metabolic pathways in human hepatoma cell line HepG2
Highlights
Neuropeptide Y (NPY) is originally isolated from porcine brain [1] and generally known to stimulate appetite through hypothalamic NPY Y1 receptor as shown in our review [2]
Effect of BIIE0246 on mRNA levels of HDL metabolic regulators assessed by real-time RT-PCR
BIIE0246 appeared to decrease cholesterol ester transfer protein (CETP), scavenger receptor-B1 (SR-B1) and hepatic lipase mRNA expression levels, the differences were not statistically significant among cells added by none, 100nM NPY alone, 1 μM BIIE0246 alone, and 100nM NPY plus 1 μM BIIE0246 (n=4, representative results of 3 repeated experiments) (Figure 2)
Summary
Neuropeptide Y (NPY) is originally isolated from porcine brain [1] and generally known to stimulate appetite through hypothalamic NPY Y1 receptor as shown in our review [2]. Stress stimulates cortisol secretion from adrenal cortex and NPY release from sympathetic nerve terminal, especially with concomitant excess food intake. NPY Y2 receptor (Y2R) is involved in visceral obesity induced by stress with high caloric diet in mice [3]. We have previously examined the association between 5’-flanking region of Y2R gene single nucleotide polymorphism (SNP) s and metabolic traits and reported the significant association between these SNPs and plasma HDL-cholesterol levels in healthy subjects [4]. Quantity and quality of HDL is being considered important. Despite these evidences, plasma low levels of HDL-cholesterol are still an important risk factor for cardiovascular disorders
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