Assessment of Glycometabolism Impairment and Glucose Variability Using Flash Glucose Monitoring System in Patients With Adrenal Diseases

Abstract

Background: This study aimed to investigate the characteristics and extent of glycometabolism impairment in patients with adrenal diseases, including Cushing syndrome, primary aldosteronism, pheochromocytoma, and nonfunctional adrenal incidentaloma. Methods: This study enrolled thirty-two patients with adrenal diseases as adrenal disease groups and eight healthy individuals as healthy controls. Blood glucose levels were indicated by glucose concentration in interstitial fluid, which was documented using flash glucose monitoring system. According to flash glucose monitoring system data, parameters representing general blood glucose alterations, within-day and day-today glucose variability, and glucose-target-rate were calculated. Furthermore, blood glucose levels at nocturnal, fasting, and postprandial periods were analyzed. Besides, islet b-cell function and insulin resistance were assessed.

Association of Aldosterone, Renin, and Aldosterone to Renin Ratio with Metabolic Profile in Primary Aldosteronism

“…Based on FGMS recording data, parameters of GV and glucose target rate were calculated by referring to a previously published paper. 18 The normal range of the sensor glucose was set as 3.9–7.8 mmol/L. GV parameters from general, within-day, and day-to-day levels were calculated: 24-hour mean glucose (24hMG) and glucose variable coefficient (CV) representing general GV, standard deviation of sensor glucose (SD) and mean amplitude of glucose excursion (MAGE) indicating within-day GV, along with mean of daily difference (MODD) and area of interquartile range (IQR) representing day-to-day GV.…”

The role of counterinsular hormones in the regulation of glucose homeostasis and the pathogenesis of type 2 diabetes mellitus in COPD

“…Роль КИГ с пози-ции пульмонологии исследована фрагментарно и отражена лишь в единичных работах, а имеющиеся данные противоречивы. При этом предполагается, что они играют далеко не последнюю роль, если учесть то, что гиперпродукция КИГ, как это наблюдается при ряде эндокринопатий, способствует повышению сахара в крови и развитию сахарного диабета [5][6][7][8][9]. Выраженная гипергликемия, особенно в условиях нарушения так называемой «пластичности» β-клеток (способности их массы адаптироваться к потребностям организма в инсулине), неблагоприятно воздействует на инсулярный аппарат, еще больше подавляя выработку инсулина [10].…”