Abstract: FR-PO400
Renoprotective Function of Liver Type Fatty Acid Binding Protein (L-FABP) in Diabetic Kidney Disease via Activation of Mitochondrial Function
Session Information
- Diabetic Kidney Disease: Basic - II
October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- Watanabe, Shiika, St. Marianna University School of Medicine, Kawasaki, Japan
- Sugaya, Takeshi, St. Marianna University School of Medicine, Kawasaki, Japan
- Ichikawa, Daisuke, St. Marianna University School of Medicine, Kawasaki, Japan
- Kimura, Kenjiro, Tokyo Takanawa Hospital, Tokyo, Japan
- Shibagaki, Yugo, St. Marianna University School of Medicine, Kawasaki, Japan
- Ikemori, Atsuko, St. Marianna University School of Medicine, Kawasaki, Japan
Background
Tubulointerstitial damage (TID) in diabetic kidney disease (DKD) is one feature of histopathology observed in the diabetic patients with early progressive renal decline. Therefore, TID is a therapeutic target in order to prevent the progression of DKD. Recently, TID in DKD is reported to be associated with renal mitochondrial injury. Renal liver type fatty acid binding protein (L-FABP) has an anti-oxidant effect as a scavenger of reactive oxygen species. However, the interaction between renal L-FABP and mitochondrial function has not been investigated yet. Therefore, the aim of this study is to reveal the renoprotective potential of renal L-FABP via activation of mitochondrial function in streptozotocin-induced DKD.
Methods
To evaluate the role of renal L-FABP, we used human L-FABP chromosomal transgenic (Tg) mice because L-FABP is not expressed in the kidneys of wild-type (WT) mice.
The (Tg) mice and wild-type (WT) mice were divided into two groups: diabetic mice were injected with STZ; control mice were injected with a citrate buffer alone. At 19 weeks after these injections, the mice were killed and the kidney, and urine were isolated for analysis.
Results
The expression of renal L-FABP and the level of urinary L-FABP increased significantly in diabetic Tg mice compared to control Tg mice. Urinary albumin levels, the expression of α-smooth muscle actin in the interstitium and the level of renal oxidative protein were significantly lower in diabetic Tg kidneys compared with diabetic WT kidneys. The expression of mitochondrial superoxide dismutase 2 was significantly higher in diabetic Tg kidneys compared with diabetic WT kidneys. In the diabetic Tg kidneys, the expression of PPARγ co-activator 1α(PGC-1α ) was significantly higher than that of diabetic WT kidneys.
Conclusion
In conclusion, renal L-FABP could activate mitochondrial function by acceleration of mitochondrial biogenesis due to rise of PGC-1α expression, and attenuate renal oxidative stress, and consequently, the renal fibrosis were prevented. Increase in renal L-FABP expression may be a promising treatment against TID in DKD.