Immunolocalization of AQP5 in resting and stimulated normal labial glands and in Sjogren's syndrome.

OBJECTIVE: In our current work in vivo examination of AQP5 distribution in labial salivary glands following stimulation of secretion has been done in normal individuals and in Sjogren's syndrome patients. SUBJECTS AND METHODS: For this study, we selected 5 patients with primary Sjogren's syndrome (mean age 62,4 + 10,6 SD years) diagnosed in accordance with the European Cooperative Community classification criteria. There were 5 patients (mean age 27 + 2,5 SD years) in the control group. The subcellular distribution of AQP5 in human labial gland biopsies was determined with light and immunoelectron microscopy before and 30 min after administration of oral pilocarpine. RESULTS: In unstimulated control and Sjogren's labial glands AQP5 is about 90% localized in the apical plasma membrane, with only rarely associated gold particles with intracellular membrane structures. We have found no evidence of pilocarpine-induced changes in localization of AQP5 in either healthy individuals or Sjogren's patients. CONCLUSIONS: Our studies indicate that neither Sjogren's syndrome itself, nor muscarinic cholinergic stimulation in vivo caused any significant changes in the distribution of AQP5 in the labial salivary gland cells. This article is protected by copyright. All rights reserved

Neuroendocrine manifestations in Sjogren's syndrome

Sjogren’s Syndrome (SS) is a chronic autoimmune disorder characterized by diminished lacrimal and salivary gland secretion. Female SS patients indicated a central deficiency in three neuroendocrine axes: adrenal, gonadal, and thyroid. At present, it is not clear if any one system plays a primary role in the expresson of the disease. Rather, it is likely that the net effect involves the synergistic and antagonistic effects of multiple hormones. When taken together, adrenal and gonadal steroid hormone deficiency, plus elevated prolactin levels probably greatly facilitate cellular immunity in SS patients

Blood leptin and adiponectin as possible mediators of the relation between fat mass and BMD in perimenopausal women

Fat mass is a predictor of BMD; however, the mechanisms involved remain uncertain. Two adipokines, leptin and adiponectin, were examined as potential mediators of this relation in 80 perimenopausal women. Adiponectin did not exert any effect on BMD, whereas leptin exerted a negative one, with insulin acting as a confounder to this relation. Introduction: Fat mass is an important determinant of bone density, but the mechanism involved in this relation is uncertain. Leptin and adiponectin, as circulating peptides of adipocyte origin, are potential contributors to this relation. We investigated the role of leptin and adiponectin in mediating fat mass effects on the skeleton of perimenopausal women. Materials and Methods: Twenty-five premenopausal and 55 postmenopausal, healthy women (42-68 years old) participated in our study. Lumbar spine BMD (BMDL2-L4) and total body BMC (TBBMC) were measured with DXA, leptin levels with ELISA, and adiponectin levels with radioimmunoassay (RIA). Additionally, body composition analysis was performed, as well as measurements of several hormones. Results: It was shown that serum leptin levels were negatively correlated with BMD (beta = -0.005, p = 0.027) and TBBMC (beta = -14.32, p = 0.013). The above correlation was observed only when serum insulin levels were included, as an independent variable, in the regression analysis model. Adiponectin was not significantly correlated with BMDL2-L4 nor with TBBMC, either in the presence or absence of insulin. Conclusion: Circulating adiponectin does not seem to exert any effect on bone mass. In contrast, circulating leptin showed a negative correlation with bone mass, dependent on serum insulin levels