atment of BTBR *ob/ob* mice with honokiol appear to be relatively consistent. Furthermore, the large reduction in glomerular inflammation we observed in these mice demonstrates that SIRT3 has a potent anti-inflammatory effect on the diabetic kidney that has never been reported before. Glomerular hypertrophy has been identified as a characteristic feature of diabetic glomerular injury in experimental models and in humans. This is accompanied by the inability of podocytes to maintain complete coverage of the glomerular filtration surface area, which results in podocyte hypertrophic stress, leading to podocyte detachment^[@CR35]^. Podocytes are critical players in maintaining the integrity of the glomerular filtration barrier, and podocyte injury and loss have been identified as the initial event in the development of proteinuria and glomerular lesions, ending in glomerulosclerosis. The evidence indicates that the podocyte is the earliest target of diabetic injury, and indeed podocyte number correlates with albuminuria, and glomerular podocyte density appears to be one of the best predictors of albuminuria and disease progression^[@CR36]^. In this study, the anti-albuminuric effect of honokiol was associated with an amelioration of the defective expression of podocyte proteins and a reduction in podocyte loss in BTBR *ob/ob* mice. Increasing evidence indicates that the disruption of mitochondrial bioenergetics in podocytes is crucial for dictating the development and progression of DN^[@CR37]--[@CR39]^, and recent findings have provided novel correlations between podocyte mitochondrial morphology and the progression of DN^[@CR40],[@CR41]^. Here, treatment with honokiol improved podocyte mitochondrial abnormalities in diabetic mice and also restored the expression of PGC-1α, a known modulator of mitochondrial homeostasis, thereby reinforcing the hypothesis that increasing SIRT3 activity is crucial in the preservation of mitochondrial integrity^[@CR42],[@CR43]^. According to a recent study^[@CR44]^, it is conceivable