Effect of ghrelin on duodenal migrating myoelectric complex in rats with chronic renal failure / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of ghrelin on duodenal migrating myoelectric complex (MMC) in rats with chronic renal failure (CRF).</p><p><b>METHODS</b>Thirty healthy male SD rats were randomly assigned into sham-operated group (n=6) and CRF group (n=24), and the latter group was divided into 4 subgroups according to ghrelin doses administered with or without pretreatment with the receptor antagonist D-Lys(3)-GHRP-6. After a 18-h fasting, the rats with or without pretreatment with D-Lys(3)-GHRP-6 were given subcutaneous injections of ghrelin at different doses to observe the changes in duodenal MMC recorded using a multi lead physiological recording system.</p><p><b>RESULTS</b>Ghrelin significantly increased the MMC cycle duration and dose-dependently enhanced the frequency, amplitude and percentage of phase III MMC cycle. This effect was inhibited by the pretreatment with ghrelin receptor antagonist D-Lys(3)-GHRP-6.</p><p><b>CONCLUSION</b>Ghrelin can promote gastrointestinal motilities of rats with CRF, and the receptor of ghrelin can regulate the activity of MMC.</p>

Effects of linoleic acid on intracellular calcium concentration in primarily cultured rat pancreatic β-cells and underlying mechanism / 生理学报

In this study, we investigated the mechanism of linoleic acid-stimulated increase in intracellular calcium concentration ([Ca(2+)](i)) in pancreatic islet β-cells. Pancreatic islet cells were primarily isolated from rats and cultured for the experiments. The cells were loaded with Fluo-3/AM, the indicator of [Ca(2+)](i), and the intensity of Fluo-3 was measured using confocal microscope. The islet β-cells were identified by immunocytochemical staining with insulin antibody after recording. The drugs were given by perfusion system. The results showed that linoleic acid (20 μmol/L) stimulated [Ca(2+)](i) increase with the first peak increase and the following plateau increase. Linoleic acid-stimulated [Ca(2+)](i) increase was partly inhibited by removal of extracellular calcium and by transient receptor potential (TRP) channel blocker, La(3+), and it was totally blocked by exhaustion of intracellular calcium stores and inhibition of phospholipase C. It is concluded that linoleic acid stimulates [Ca(2+)](i) increase in islet β-cells through both extracellular calcium influx via TRP channels and calcium release from intracellular calcium stores.