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| Item Type: | Article |
|---|---|
| Title: | Decreased hepatic gluconeogenesis in transgenic rats with increased circulating angiotensin-(1-7) |
| Creators Name: | Bilman, V., Mares-Guia, L., Nadu, A.P., Bader, M., Campagnole-Santos, M.J., Santos, R.A.S. and Santos, S.H.S. |
| Abstract: | The renin-angiotensin (Ang) system (RAS) plays an important role in the control of glucose metabolism and glycemia. Several studies demonstrated that the effects of angiotensin-(1-7) are mainly opposite to the actions of biological angiotensin II. Recent studies have demonstrated that rats with increased circulating angiotensin-(1-7), acting through the G protein coupled receptor Mas, have enhanced glucose tolerance and insulin sensitivity, presenting improved metabolic parameters. However, there is no data regarding the role of angiotensin-(1-7)-Mas axis in hepatic glycemic metabolism. In the present study, the gluconeogenesis and glycogenolysis was investigated in Sprague-Dawley (SD) and in TGR(A1-7)3292 (TGR) rats which present approximately twofold increase in plasma Ang-(1-7) levels compared to SD. The pyruvate administration in fasted rats showed a decreased synthesis of glucose in TGR compared to the SD rats, pointing to a downregulation of gluconeogenesis. Supporting this data, the mRNA evaluation of gluconeogenic enzymes showed a significant reduction in phosphoenolpyruvate carboxykinase reinforced by a significantly diminished expression of hepatocyte nuclear factor 4{alpha} (HNF-4{alpha}), responsible for the regulation of gluconeogenic enzymes. In conclusion our data show that the improved glucose metabolism induced by Ang-(1-7) could be due, at least in part, to a downregulation of hepatic gluconeogenesis. |
| Keywords: | Angiotensin I, Gluconeogenesis, Liver, Peptide Fragments, Animals, Rats |
| Source: | Peptides |
| ISSN: | 0196-9781 |
| Publisher: | Elsevier |
| Volume: | 37 |
| Number: | 2 |
| Page Range: | 247-251 |
| Date: | October 2012 |
| Official Publication: | https://doi.org/10.1016/j.peptides.2012.08.002 |
| PubMed: | View item in PubMed |
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