Introduction : Fat-1 transgenic mice produce [omega]3-Polyunsaturated fatty acids ([omega]3-PUFAs) from [omega]6-Polyunsaturated fatty acids ([omega]6-PUFAs) without a dietary [omega]3-PUFAs supplement, leading to a high accumulation of omega-3 in various tissues. [omega]3-PUFAs show protective effects against various renal injuries and it has recently been reported that [omega]3-PUFAs regulate autophagy. We assessed whether [omega]3-PUFAs attenuated IR-induced acute kidney injury (AKI) and evaluated its associated mechanisms.

Method : C57Bl/6 background fat-1 mice and wild-type mice (wt) were divided into four groups: wt sham (n = 10), fat-1 sham (n = 10), wt IRI (reperfusion 35 min after clamping both the renal artery and vein; n = 15), and fat-1 IRI (n = 15). Kidneys and blood were harvested 24 h after IRI and renal histological and molecular data were collected.

Results : The kidneys of fat-1 mice showed better renal cell survival, renal function, and pathological damage than those of wt mice after IRI. In addition, fat-1 mice showed less oxidative stress and autophagy impairment; greater amounts of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II, Beclin-1, and Atg7; lower amounts of p62; and, higher levels of renal cathepsin D and ATP6E than wt kidneys. They also showed more adenosine monophosphate-activated protein kinase (AMPK) activation, which resulted in the inhibition of phosphorylation of the mammalian target of rapamycin (mTOR).

Conclusions : [omega]3-PUFAs in fat-1 mice contributed to AMPK mediated autophagy activation, leading to a renoprotective response.

CITATION INFORMATION: Choi D., Ham Y., Na K., Lee K., Kim J-.J., Jeong J. Enhancement of Endogenous omega-3 Protect against Ischemia-Reperfusion Renal Injury in Fat-1 Mice Am J Transplant. 2017;17 (suppl 3).

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