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.

This study investigated how proteins of the insulin signaling cascade could modulate insulin resistance after dexamethasone (Dexa) treatment and aerobic training. Rats were distributed into 4 groups: sedentary control (SC), sedentary+Dexa (SD), trained control (TC), and trained+Dexa (TD), and underwent aerobic training for 70 days or remained sedentary. Dexa was administered during the last 10 days (1 mg · kg(-1) per day i. p.). After 70 days, an intraperitoneal glucose tolerance test (ipGTT) was performed. Protein levels of IRS-1, AKT, and PKC-α in the tibialis anterior (TA) muscle were identified using Western blots. Dexa treatment increased blood glucose and the area under the curve (AUC) of ipGTT. Training attenuated the hyperglycemia and the AUC induced by Dexa. Dexa reduced IRS-1 (- 16%) and AKT (- 43%) protein level with no changes in PKC-α levels. Moreover, these effects on IRS-1 and AKT protein level were prevented in trained animals. These results show for the first time that aerobic exercise prevented reductions of IRS-1 and AKT level induced by Dexa in the TA muscle, suggesting that aerobic exercise is a good strategy to prevent Dexa-induced peripheral insulin resistance.

In rat alveolar bone repair, meloxicam did not affect VEGF expression but downregulated VEGFR expression, which may cause a delay in the bone repair/remodeling process.

This study investigated whether exercise training (T) could prevent the insulin resistance, oxidative stress and hypertension induced by dexamethasone (Dexa) treatment. Rats underwent a T period where they were either submitted to a running protocol (8weeks) or kept sedentary. After this T period, the animals underwent a Dexa treatment (1mg/kg/day, i.p., 10days), concomitant with training. An ipGTT was performed at the end of the experimental period and the area under the glucose curve (AUC) was calculated. Arterial pressure (AP) was measured. Reduced/oxidized glutathione ratio (GSH/GSSG) and lipid peroxidation were also determined in the skeletal muscle. Western blot analysis was performed to identify PKCα protein expression in the tibialis anterior (TA) muscle. Dexa increased AP (23 mmHg) and T attenuated this increase by 11%. Dexa decreased the GSH/GSSG ratio by 44% and increased the lipid peroxidation by 55% in sedentary groups, and T blocked these alterations. Dexa reduced the PKC‐α protein expression by 45%, which was prevented by T. Accordingly, T attenuated the increases in the AUC, whose values were 39% higher in sedentary ones. Therefore T is effective in regulating physiological antioxidant systems and glucose uptake, which could contribute to prevent hypertension and insulin resistance induced by Dexa.