Heterogeneous expression of melatonin receptor MT1 mRNA in the rat intestine under control and fasting conditions

被引:39
作者
Sotak, Matus
Mrnka, Libor
Pacha, Jiri
机构
[1] Acad Sci Czech Republ, Inst Physiol, CR-14220 Prague, Czech Republic
[2] Charles Univ Prague, Fac Sci, Prague, Czech Republic
关键词
circadian; fasting; gastrointestinal tract; melatonin; MT1; undernutrition;
D O I
10.1111/j.1600-079X.2006.00355.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Melatonin is found in mammalian central nervous system and various peripheral tissues including gastrointestinal tract (GIT) where it participates in the regulation of intestinal motility, blood flow, immunomodulation, ion transport, cell proliferation and scavenging of free radicals. Some of these effects are achieved via melatonin binding to specific receptors, MT1 and MT2. As no thorough study on the expression of these receptors in the GIT has yet been done, the aim of this study was to determine the MT1 mRNA expression in the rat intestine under both control and fasting conditions. Our results suggest that MT1 mRNA is present in epithelial as well as subepithelial layer, with higher expression in the latter in all intestinal segments studied. The highest signal of the MT1 transcript along the rostro-caudal intestinal axis was found both in epithelial and subepithelial layers of the duodenum. Nevertheless, duodenal MT1 mRNA expression did not reach the level found in pituitary gland. In a 12:12-hr light:dark cycle a MT1 receptor expression in the subepithelial layer of rat distal colon did not manifest a significant diurnal rhythm. Short-term fasting increased the expression of MT1 transcript in the subepithelial layer of both the small and large intestine. During long-term fasting the increase persisted only in distal colon while a return to control levels was observed in small intestinal segments. In conclusion we demonstrated heterogeneous expression of MT1 receptor in the rat intestine and showed that its expression is up-regulated by nutritional deprivation.
引用
收藏
页码:183 / 188
页数:6
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