ABSTRACT
Abstract AIMS Previously, we verified that overtrained mice upregulated the TRB3 levels, its association with Akt, and the hepatic concentrations of glycogen. It is known that APPL1 can limit the interaction between TRB3 and Akt, playing an important role in the glucose homeostasis. Thus, we verified the effects of three overtraining protocols on the hepatic levels of APPL1 and APPL2. METHODS Rodents were divided into control (CT), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up) and overtrained by running without inclination (OTR). The hepatic contents of APPL1 and APPl2 were measured by the immunoblotting technique. RESULTS Significant elevation of APPL1 observed in the OTR/down and OTR/up groups, as well as the tendency of increase (p=0.071) observed in the OTR group. CONCLUSION These results indicate that this particular protein is likely to participate in the glucose homeostasis previously observed in response to these OT protocols.(AU)
Subject(s)
Animals , Male , Mice , Adaptation, Physiological/physiology , Adaptor Proteins, Signal Transducing/metabolism , Hemostasis/physiology , Insulin/metabolism , Liver/physiology , Resistance Training , Mice, Inbred C57BLABSTRACT
Objective To determine the role of APPL1,an adaptor protein,played in pancreatic β-cell.Methods APPL1 was overexpressed in INS-1 cells with adenovirus encoding APPL1.Western blot was conducted to measure protein cxprcssion.Propidium iodide/Hoechst staining was used to determine the cell apoptosis.Insulin secretion was measured by ELISA.Results Exposure of INS-1 cells to 20 mmol/L glucose or 30U/ml interleukin-1 β plus 20 ng/ml TNF-α 48 h induced β-cell apoptosis (P＜0.01) and impaired 2 h glucosestimulated insulin secretion (P＜ 0.01).Overexpression of APPL1 in INS-1 decreased cell apoptosis by 34.16％-42.79％ (P＜0.01) and increased glucose-induced insulin secretion by 1.39-2.20 folds compared with control groups (P＜0.05).Conclusion APPL1 decreases β-cell apoptosis and increases glucose-stimulated insulin secretion,and thus protects β-cell against high glucose or cytokines-induced dysfunction.