nystatin-a1 and Diabetes-Mellitus--Type-1

This study investigated the influence of nystatin and fluconazole on virulence properties of Candida albicans.. A total of 108 diabetic patients participated in the study. Eighty-eight patients had clinical oral candidosis. Drug therapy was given at 6 hourly intervals for nystatin or daily with fluconazole for a maximum of 2 weeks. Adhesion of C albicans to buccal epithelial cells was determined by using an autologous adhesion assay prospectively over 6 months. Phospholipase production was estimated by using an agar plate method. The data analysis included a paired Student t test and calculation of correlation coefficients.. Unlike nystatin, treatment with fluconazole reduced the ability of C albicans to colonize the buccal mucosa for up to 8 weeks after the treatment. Patients without clinical signs of oral candidosis had significantly fewer C albicans isolates producing phospholipase than did patients with oral candidosis. Treatment with fluconazole, but not nystatin, reduced the production of phospholipase from C albicans oral isolates in patients with diabetes mellitus.. In addition to being antifungal, fluconazole alters phospholipase production, modifies buccal epithelial cells, and reduces adhesion of C albicans to human buccal epithelial cells for up to 8 weeks posttreatment in diabetic patients with oral candidosis.

Topics: Analysis of Variance; Antifungal Agents; Bacterial Adhesion; Candida albicans; Candidiasis, Oral; Chi-Square Distribution; Diabetes Mellitus, Type 1; Epithelial Cells; Female; Fluconazole; Humans; Male; Middle Aged; Nystatin; Phospholipases; Prospective Studies; Virulence

Topics: Antiporters; Diabetes Mellitus, Type 1; Erythrocyte Membrane; Humans; Individuality; Ionophores; Kinetics; Lithium; Lithium Carbonate; Lithium Chloride; Male; Nystatin; Reference Values; Sodium

The release of insulin from the pancreatic beta cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic beta cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the beta cell has remained controversial. It is reported here that in single beta cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the beta cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.

Topics: Amyloid; Animals; Cell Membrane Permeability; Diabetes Mellitus, Type 1; Glucose; In Vitro Techniques; Insulin; Insulin Secretion; Insulinoma; Islet Amyloid Polypeptide; Islets of Langerhans; Membrane Potentials; Mice; Mice, Inbred C57BL; Nystatin; Pancreatic Neoplasms; Rats; Rats, Sprague-Dawley; Tumor Cells, Cultured