Why the study?
Does Angiotensin (1-7) improve fatty acid composition in rats with STZ-induced diabetic nephropathy?
Does Angiotensin (1-7) improve fatty acid composition in rats with STZ-induced diabetic nephropathy?
Angiotensin (1-7) modulates fatty acid composition and attenuates diabetes-induced changes in renal cortical tissue in a rat model of diabetic nephropathy.
Ang (1-7) may modulate renal fatty acids in diabetic rats; hypothesis-generating and leaves open clinical translation.
Diabetes mellitus is often associated with altered fatty acids composition. This study was designed to investigate the role of angiotensin (Ang) (1-7)/Mas receptor in improving fatty acids composition in streptozotocin (STZ)-induced diabetic nephropathy (DN) in rats. Rats treated with STZ (50 mg/kg, i.p. once) developed DN after 8 weeks. Fatty acid composition was estimated in renal cortical tissue by gas chromatography. Treatment with Ang (1-7), A-779, and Ang (1-7) plus A-779 was given from week 4 to week 8. Diabetic rats exhibited a significant increase in levels of saturated fatty acids and a significant decrease in levels of polyunsaturated fatty acids (PUFAs). Treatment with Ang (1-7) significantly attenuated these diabetes-induced changes. In diabetic rats, prior administration of A-779 significantly attenuated the increase in PUFAs produced by Ang (1-7); however, for saturated fatty acids, A-779 significantly blocked the decrease in palmitic acid only. Our study, for the first time, documented that endogenous Ang (1-7) modulates fatty acid composition in rats. Further, treatment with Ang (1-7) significantly attenuated diabetes-induced changes in fatty acids composition. This may be an additional mechanism implying the renoprotective role of Ang (1-7) in diabetic rats.
No takes yet. Share an insight, caveat, or question.
Singh et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: