Abstract
The patients with sleep apnea syndrome are exposed to intermittent hypoxia (IH) during sleep. We previously demonstrated the IH-induced up-regulation of the mRNA levels of anorexigenic peptides proopiomelanocortin (POMC), and cocaine- and amphetamine-regulated transcript (CART) in human neuronal cells. Appetite is regulated not only by the central nervous system but also by the peptides from gastrointestinal tract. Here, we investigated the effects of IH on the gene expression(s) of appetite-inhibiting gut hormones. Human enteroendocrine Caco-2 and mouse STC-1 cells were exposed to IH [64 cycles of 5 min hypoxia (1% O2) and 10 min normoxia (21% O2)] or normoxia for 24 h. Real-time RT-PCR revealed that IH significantly increased the mRNA levels of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and neurotensin (NTS) in Caco-2 and STC-1 cells. ELISA showed that the concentrations of PYY, GLP-1, and NTS in the culture medium were significantly increased by IH. The mRNA levels of PYY, GLP-1, and NTS were significantly up-regulated even in normoxia by Trichostatin A (TSA) and were significantly decreased even in IH by 5-azacytidine (5AZC), suggesting that IH increases PYY, GLP-1, and NTS mRNAs via alterations in the chromatin structure in enteroendocrine cells. IH might have an anorexigenic influence on the enteric nervous system.
Highlights
Sleep apnea syndrome (SAS) is a common disorder characterized by repetitive episodes of oxygen desaturation during sleep, the development of daytime sleepiness, and the deterioration of quality of life [1]
Www.mdpi.com/journal/ijms galanin-like peptide (GALP), ghrelin (GHRL), pyroglutamylated RFamide peptide (QRFP), agouti-related peptide (AGRP), neuropeptide Y (NPY), and melanocortin 4 receptor (MC4R) in intermittent hypoxia (IH)-exposed human neuronal cells and demonstrated that IH up-regulated the mRNA levels of anorexigenic peptides in human neuronal cells [4]
IH significantly increased the mRNA. This result indicates that IH-stress up-regulates the mRNA levels of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and NTS, levels of PYY (2.51 fold, p = 0.0003), GLP-1 (4.16 fold, p = 0.0064), and NTS (9.18 fold, p = 0.029) in which are appetite inhibitory hormones, in enteroendocrine cells, suggesting that SAS patients’
Summary
Sleep apnea syndrome (SAS) is a common disorder characterized by repetitive episodes of oxygen desaturation during sleep, the development of daytime sleepiness, and the deterioration of quality of life [1]. The patients with SAS undergo serious recurrent apnea, being exposed to alternating low oxygen pressure and normal oxygen pressure, that is, intermittent hypoxia (IH) [2]. We previously investigated the effect of IH on the regulation of appetite in SAS patients by analyzing the expression(s) of major appetite regulatory neuropeptide and receptor genes such as proopiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), galanin (GAL), galanin-like peptide (GALP), ghrelin (GHRL), pyroglutamylated RFamide peptide (QRFP), agouti-related peptide (AGRP), neuropeptide Y (NPY), Int. J. 2019, 20, 1849; doi:10.3390/ijms20081849 www.mdpi.com/journal/ijms galanin-like peptide (GALP), ghrelin (GHRL), pyroglutamylated RFamide peptide (QRFP), agouti-related peptide (AGRP), neuropeptide Y (NPY), and melanocortin 4 receptor (MC4R) in IH-exposed human neuronal cells and demonstrated that IH up-regulated the mRNA levels of anorexigenic peptides Sci. 2019, 20, 1849; doi:10.3390/ijms20081849 www.mdpi.com/journal/ijms galanin-like peptide (GALP), ghrelin (GHRL), pyroglutamylated RFamide peptide (QRFP), agouti-related peptide (AGRP), neuropeptide Y (NPY), and melanocortin 4 receptor (MC4R) in IH-exposed human neuronal cells and demonstrated that IH up-regulated the mRNA levels of anorexigenic peptides
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