Insulin and glucose sensitivity, insulin secretion and beta-cell distribution in endocrine pancreas of the fruit bat Artibeus lituratus.

The fruit bat Artibeus lituratus absorbs large amounts of glucose in short periods of time and maintains normoglycemia even after a prolonged starvation period. Based on these data, we aimed to investigate various aspects related with glucose homeostasis analyzing: blood glucose and insulin levels, intraperitoneal glucose and insulin tolerance tests (ipGTT and ipITT), glucose-stimulated insulin secretion (2.8, 5.6 or 8.3 mmol/L glucose) in pancreas fragments, cellular distribution of beta cells, and the amount of pAkt/Akt in the pectoral muscle and liver. Blood glucose levels were higher in fed bats (6.88+/-0.5 mmol/L) than fasted bats (4.0+/-0.8 mmol/L), whereas insulin levels were similar in both conditions. The values of the area-under-the curve obtained from ipGTT were significantly higher when bats received 2 (5.5-fold) or 3g/kg glucose (7.5-fold) b.w compared to control (saline). These bats also exhibited a significant decrease of blood glucose values after insulin administration during the ipITT. Insulin secretion from fragments of pancreas under physiological concentrations of glucose (5.6 or 8.3 mmol/L) was similar but higher than in 2.8 mmol/L glucose 1.8- and 2.0-fold, respectively. These bats showed a marked beta-cell distribution along the pancreas, and the pancreatic beta cells are not exclusively located at the central part of the islet. The insulin-induced Akt phosphorylation was more pronounced in the pectoral muscle, compared to liver. The high sensitivity to glucose and insulin, the proper insulin response to glucose, and the presence of an apparent large beta-cell population could represent benefits for the management of high influx of glucose from a carbohydrate-rich meal, which permits appropriate glucose utilization.

The adaptive compensations in endocrine pancreas from glucocorticoid-treated rats are reversible after the interruption of treatment.

AIM: Glucocorticoid administration induces insulin resistance (IR) and enhances islet mass and insulin secretion in rodents and humans. Here, we analysed whether these effects are still present after the interruption of dexamethasone treatment. METHODS: Adult Wistar rats were distributed into CTL (daily injection of saline for five consecutive days), DEX (daily injection of 1 mg kg(-1) body wt of dexamethasone for five consecutive days) and DEX(10) (5 days of dexamethasone treatment, followed by a period of 10 days without dexamethasone). RESULTS: In vivo experiments indicated that the marked hyperinsulinemia found in DEX rats during fasting and fed states was normalized in the DEX(10) group. Furthermore, the IR and glucose intolerance observed in DEX were restored in DEX(10) rats. Islets from DEX rats secreted more insulin in response to increasing concentrations of glucose and other metabolic and non-metabolic stimuli, compared with that in the CTL group. The insulin secretion for the most compounds studied returned to CTL values in DEX(10) islets. Increased insulin secretion correlated well with the augmentation in ß-cell proliferation and mass in DEX rats, and these morphological alterations were normalized in islets from DEX(10) rats. In parallel, the increased levels of proteins involved in ß-cell proliferation such as Cd2 and Cdk4 observed in DEX islets were also normalized in DEX(10) islets. CONCLUSION: These data strongly support the view that almost all the morphophysiological alterations induced by dexamethasone in the endocrine pancreas are reverted after discontinuation of the treatment. This information is important, considering the frequent use of glucocorticoids in humans.