الملخص
Generalized bone loss can be considered an extra-articular manifestation of rheumatoid arthritis (RA) that may lead to the occurrence of fractures, resulting in decreased quality of life and increased healthcare costs. The peptide ghrelin has demonstrated to positively affect osteoblasts in vitro and has anti-inflammatory actions, but the studies that correlate ghrelin plasma levels and RA have contradictory results. We aimed to evaluate the correlation between total ghrelin plasma levels, density of ghrelin-immunoreactive cells in the gastric mucosa, and bone mineral density (BMD) in twenty adult women with established RA with 6 months or more of symptoms (mean age of 52.70±11.40 years). Patients with RA presented higher ghrelin-immunoreactive cells density in gastric mucosa (P=0.008) compared with healthy females. There was a positive relationship between femoral neck BMD and gastric ghrelin cell density (P=0.007). However, these same patients presented a negative correlation between plasma ghrelin levels and total femoral BMD (P=0.03). The present results indicate that ghrelin may be involved in bone metabolism of patients with RA. However, the higher density of ghrelin-producing cells in the gastric mucosa of these patients does not seem to induce a corresponding elevation in the plasma levels of this peptide.
الموضوعات
Humans , Female , Adult , Middle Aged , Arthritis, Rheumatoid/metabolism , Bone Density , Endocrine Cells/cytology , Ghrelin/blood , Arthritis, Rheumatoid/physiopathology , Body Mass Index , Bone Density/physiology , Cell Count , Endocrine Cells/metabolism , Femur Neck/anatomy & histology , Gastric Mucosa/metabolism , Gastric Mucosa/pathology , Parietal Cells, Gastric/metabolism , Parietal Cells, Gastric/pathologyالملخص
The stimulation of the oxyntic cell by gastric secretagogues is associated to the activation of oxidative metabolism. The mechanisms of this activation are not exactly known. In the present work, we investigated the possible direct effect of Ca2+ on both oxoglutarate oxidation in rabbit gastric glands and oxoglutarate dehydrogenase activity (OGDH) is isolated gastric mitochondria. Both carbachol and Ca2+ ionophores +(A23187 and ionomycin) significantly stimulated oxoglutarate oxidation in a dose-dependent manner. This effect was only observed in the presence of low substrate concentrations. BAPTA-AM, an intracellular calcium chelator, significantly inhibited the rate of oxoglutarate oxidation. OGDH activity was stimulated by physiological concentrations of Ca2+ in a dose-depentent manner. This effect was reduced by ruthenium red, an inhibitor of mitochondrial Ca2+ uptake, and it was additionally increased by spermine, a stimulant of Ca2+ influx to the mitochondria. Results support the hypothesis that Ca2+ plays a direct role in the activation of oxidative metabolism in the oxyntic cell
الموضوعات
Animals , Rabbits , Ketoglutaric Acids/metabolism , Calcium/physiology , Gastric Mucosa/metabolism , Oxidoreductases/metabolism , Carbachol/pharmacology , Parietal Cells, Gastric , Parietal Cells, Gastric/metabolism , Ionophores/pharmacology , Mitochondria/drug effects , Mitochondria/metabolism , Gastric Mucosa , Gastric Mucosa/enzymologyالملخص
The stimulation of oxyntic cell by gastric secretagogues is associated to the activation of oxidative metabolism. The mechanisms of this activation are not exactly known. In the present work, we investigated the possible direct effect of Ca2+ on both oxoglutarate oxidation in rabbit gastric glands and oxoglutarate dehydrogenase activity (OGDH) in isolated gastric mitochondria. Both carbachol and Ca2+ ionophores (A23187 and ionomycin) significantly stimulated oxoglutarate oxidation in a dose-dependent manner. This effect was only observed in the presence of low substrate concentrations. APTA-AM, an intracellular calcium chelator, significantly inhibited the rate of oxoglutarate oxidation. OGDH activity was stimulated by physiological concentrations of Ca2+ in a dose-dependent manner. This effect was reduced by ruthenium red, an inhibitor of mitochondrial Ca2+ uptake, and it was additionally increased by spermine, a stimulant of Ca2+ influx to the mitochondria. The results support the hypothesis that Ca2+ plays a direct role in the activation of oxidative metabolism in the oxyntic cell
الموضوعات
Animals , Rabbits , Ketoglutaric Acids/metabolism , Calcium/physiology , Gastric Mucosa/metabolism , Oxidoreductases/metabolism , Carbachol/pharmacology , Parietal Cells, Gastric , Parietal Cells, Gastric/metabolism , Ionophores/pharmacology , Mitochondria/drug effects , Mitochondria/metabolism , Gastric Mucosaالملخص
The association of myosin and a filamin-like protein to the F-actin cytoskeleton of parietal cells was studied in the rat gastric mucosa. Myosin and the filamin-like protein were localized by indirect immunofluorescence microscopy while the distribution of actin was established by using FITC-phalloidin. These cytoskeletal proteins, concentrated in the parietal cells, changed their distribution in correlation with the hydrochloric acid (HCl) secretory state of the cells and the appearance of a developed intracellular canaliculus. Thus,in resting parietal cells, actin showed a patchy distribution, delimiting the poorly developed secretory canaliculi, while myosin and the filamin-like protein distributed diffusely over the cytoplasm. In secreting cells, F-actin was concentrated in the cytoplasmic projections filling the canalicular lumen, while myosin and the filamin-like protein were excluded from this region, concentrating in the adjoining cytoplasm. The present results show that myosin and the filamin-like protein change their association with the secretory membranes in relation to the development of the secretory canaliculus of parietal cells. In resting cells, both proteins associate with the endocellular secretory membranes. In secreting cells, the microvillar projections of the canalicular surface formed by these membranes bind F-actin, but exclude myosin and the filamin-like protein