Metabolic remodeling triggered by salivation and diabetes in major salivary glands.

The metabolic profile of major salivary glands was evaluated by 13 C nuclear magnetic resonance isotopomer analysis (13 C NMR-IA) following the infusion of [U-13 C]glucose in order to define the true metabolic character of submandibular (SM) and parotid (PA) glands at rest and during salivary stimulation, and to determine the metabolic remodeling driven by diabetes. In healthy conditions, the SM gland is characterized at rest by a glycolytic metabolic profile and extensive pyruvate cycling. On the contrary, the PA gland, although also dominated by glycolysis, also possesses significant Krebs' cycle activity and does not sustain extensive pyruvate cycling. Under stimulation, both glands increase their glycolytic and Krebs' cycle fluxes, but the metabolic coupling between the two pathways is further compromised to account for the much increased biosynthetic anaplerotic fluxes. In diabetes, the responsiveness of the PA gland to a salivary stimulus is seriously hindered, mostly as a result of the incapacity to burst glycolytic activity and also an inability to improve the Krebs' cycle flux to compensate. The Krebs' cycle activity in the SM gland is also consistently compromised, but the glycolytic flux in this gland is more resilient. This diabetes-induced metabolic remodeling in SM and PA salivary glands illustrates the metabolic need to sustain adequate saliva production, and identifies glycolytic and oxidative pathways as key players in the metabolic dynamism of salivary glands.

Physical, chemical, and immunohistochemical investigation of the damage to salivary glands in a model of intoxication with aluminium citrate.

Aluminum absorption leads to deposits in several tissues. In this study, we have investigated, to our knowledge for the first time, aluminum deposition in the salivary glands in addition to the resultant cellular changes in the parotid and submandibular salivary glands in a model of chronic intoxication with aluminum citrate in rats. Aluminum deposits were observed in the parotid and submandibular glands. Immunohistochemical evaluation of cytokeratin-18 revealed a decreased expression in the parotid gland with no changes in the submandibular gland. A decreased expression of α-smooth muscle actin was observed in the myoepithelial cells of both glands. The expression of metallothionein I and II (MT-I/II), a group of metal-binding proteins, which are useful indicators for detecting physiological responses to metal exposure, was higher in both glands. In conclusion, we have shown that at a certain time and quantity of dosage, aluminum citrate promotes aluminum deposition in the parotid and submandibular glands, leads to an increased expression of MT-I/II in both the glands, damages the cytoskeleton of the myoepithelial cells in both glands, and damages the cytoskeleton of the acinar/ductal cells of the parotid glands, with the submandibular glands showing resistance to the toxicity of the latter.

Salivary analysis of patients with chronic renal failure undergoing hemodialysis.

This study evaluated the flow rate and composition of whole saliva in patients with chronic renal failure undergoing hemodialysis. In the group on dialysis (RG) (n = 15), saliva was collected just prior to hemodialysis CT1) and at completion (T2), while in the healthy subjects (HG)(n = 15) saliva was collected at the same time of day as the pre-dialysis. Saliva samples were analyzed by inductively coupled argon plasma with atomic emission spectrometry. Significant differences were found in the flow rate, potassium, magnesium and phosphorus concentrations at the RG-T1 and HG (p < 0.05). Sodium concentration at RG-T1 and RG-T2 were higher than HG (p < 0.05). Total protein concentration was higher at RG-T1 than at the other two analyses. Salivary peroxidase activity at RG-T1 and RG-T2 was lower than at HG. Our findings suggest that in patients with chronic renal failure, the saliva is altered. Hemodialysis, however, seems to help control saliva composition and flow rate.

[Non-neoplastic enlargement of salivary glands: clinico-histologic analysis]. / Agrandamiento no neoplásico de glándulas salivales. Análisis clínico-histológico.

We carried out a retrospective study on non-neoplastic enlargement of the salivary glands at the Oral Histopathology Diagnostic Center of the Autonomous Metropolitan University at Xochimilco (UAM-Xochimilco) in Mexico during a period of 24 years (1979-2003). From 5,625 biopsies received and analyzed, a total of 461 (8.2%) were non-neoplastic enlargement of the salivary glands; for each case, we registered demographic data as well as clinic characteristics. These lesions were characterized as a heterogeneous group of pathologic entities among which we included local, obstructive, infectious, and immunopathologic lesions. The most frequent lesion was the extravasation cyst in 341 (74%) cases, followed by chronic sialoadenitis and Sjögren's syndrome with 54 (11.7%) and 41 (8.8%) cases, respectively, and at a lesser percentage mucous retention cyst, sialosis, benign lymphoepithelial lesions and those related with sialolytes. Females were affected more frequently; mean age was second to third life decades. These lesions were most frequently localized on inferior labial mucosa.

Changes in glucose metabolism in submandibular salivary glands of rats after isoproterenol or incisor-tooth amputation.

Rats were injected daily with isoproterenol (2 mg/kg of body wt) for up to five days, or their incisor teeth were amputated on every other day for up to five amputations. The animals were subdivided in two subgroups killed 12 or 24 h after the first or last intervention. At 12 h all enzymes except hexokinase (HK) and pyruvate kinase (PFK) showed decreased activities after isoproterenol. After incisor amputation, only increased HK and PFK activities were observed. With both procedures, there is activation of beta-adrenergic receptors but results show that different biochemical events take place, suggesting different mechanisms.