Effects of dried natto diet on the transcript levels of the peroxisome proliferator-activated receptor-γ, coactivator-1α and -1ß, and nuclear receptor corepressor 1 genes in laying hens.

The effects of natto, a fermented soybean food, on transcript levels of hen peroxisome proliferator-activated receptor-γ (PPARG), PPARG coactivator-1α and -1ß (PPARGC1A and PPARGC1B), and nuclear receptor corepressor 1 (NCOR1) were investigated using real-time polymerase chain reaction in white leghorn (Julia strain) hens. Twenty-one- and 34-week-old hens were fed a basic or 3% dried natto-supplemented diet for 8 weeks. In the 21- and 34-week-old hens fed the natto-supplemented diet, hepatic PPARGC1B and NCOR1 transcript levels and adipose and hepatic PPARG transcript levels were significantly lower, respectively, than those in the control group. Furthermore, 34- and 42-week-old hens were fed a basic diet supplemented with 3% of the protein/fiber-enriched fraction (PFB) or 0.6% of the fat-enriched fraction (FAT) of natto, respectively, for 8 weeks. Adipose PPARG transcript levels were higher in the FAT diet group and significantly lower in the PFB diet group than in the control group. However, both FAT and PFB diet groups showed significantly lower hepatic PPARG transcript levels than did the control group. These results suggest that dried natto influences the transcript levels of PPARG, PPARGC1B, and NCOR1, and the FAT and PFB of natto influence the adipose and hepatic PPARG transcript levels in hens.

Catalase deficiency renders remnant kidneys more susceptible to oxidant tissue injury and renal fibrosis in mice.

BACKGROUND: Catalase is one of the important antioxidant enzymes regulating the levels of intracellular hydrogen peroxide and hydroxyl radical. The effect of catalase deficiency on progressive renal fibrosis has not been fully elucidated. METHODS: Homozygous acatalasemic mutant mice (C3H/AnLCs(b)Cs(b)) and control wild-type mice (C3H/AnLCs(a)Cs(a)) were subjected to 5/6 nephrectomy. The functional and morphological alterations of the remnant kidneys, including tubulointerstitial fibrosis, epithelial to mesenchymal transition (EMT), peroxidation, antioxidant enzyme activity, and gene expression of EMT-related molecules were compared between the two groups at 6, 12, and 18 weeks after 5/6 nephrectomy. RESULTS: The 5/6 nephrectomy resulted in albuminuria, decreased renal function, and tubulointerstitial fibrosis with accumulation of type I and type IV collagens in the remnant kidneys of both mouse groups. However, the degree of these changes was significantly higher in acatalasemic mice after 5/6 nephrectomy as compared with wild-type mice until week 18. EMT, a crucial phenotypic alteration of tubular epithelial cells, was observed in acatalasemic mice by electron microscopy and was associated with upregulation of EMT-related alpha-smooth muscle actin (alpha-SMA), transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor (CTGF), and fibroblast specific protein-1 (FSP-1) gene expression. Significant increases in the tubulointerstitial deposition of lipid peroxidation products, including 4-hydroxy-2-nonenal and urinary excretion of 8-hydroxy-2'- deoxyguanosine were observed in the acatalasemic mice after 5/6 nephrectomy as compared with the wild-type mice. Glomerular sclerosis developed after tubulointerstitial injury in acatalasemic mice. The level of catalase activity remained low in the remnant kidneys of acatalasemic mice until week 18 without compensatory up-regulation of glutathione peroxidase or superoxide dismutase (SOD) activity. Finally, supplementation of a SOD mimetic tempol did not prevent peroxidation and tubulointerstitial fibrosis in the acatalasemic remnant kidneys. CONCLUSION: These findings indicate that acatalasemia exacerbates renal oxidant tissue injury and sensitizes remnant kidneys to EMT and progressive renal fibrosis. This study suggests a central role for catalase in the defense against oxidant-mediated renal fibrosis.