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607 results on '"Uzu, Takashi"'

15. Replication study for the association of 3 SNP loci identified in a genome-wide association study for diabetic nephropathy in European type 1 diabetes with diabetic nephropathy in Japanese patients with type 2 diabetes

Author

Maeda, Shiro, Imamura, Minako, Kurashige, Mahiro, Araki, Shinichi, Suzuki, Daisuke, Babazono, Tetsuya, Uzu, Takashi, Umezono, Tomoya, Toyoda, Masao, Kawai, Koichi, Imanishi, Masahito, Hanaoka, Kazushige, Maegawa, Hiroshi, Uchigata, Yasuko, and Hosoya, Tatsuo

Published
2013
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21. Calorie restriction enhances cell adaptation to hypoxia through Sirt1-dependent mitochondrial autophagy in mouse aged kidney

Author

Kume, Shinji, Uzu, Takashi, Horiike, Kihachiro, Chin-Kanasaki, Masami, Isshiki, Keiji, Araki, Shin-ichi, Sugimoto, Toshiro, Haneda, Masakazu, Kashiwagi, Atsunori, and Koya, Daisuke

Subjects
Cell physiology -- Reorganization and restructuring -- Health aspects -- Physiological aspects -- Research, Autophagy (Cytology) -- Research -- Physiological aspects -- Health aspects, Kidneys -- Medical examination -- Research -- Physiological aspects -- Health aspects, Mitochondria -- Properties -- Research -- Physiological aspects -- Health aspects, Low-calorie diet -- Health aspects -- Research -- Physiological aspects, Hypoxia -- Physiological aspects -- Research, Company organization, Company restructuring/company reorganization, Health care industry
Abstract

Mitochondrial oxidative damage is a basic mechanism of aging, and multiple studies demonstrate that this process is attenuated by calorie restriction (CR). However, the molecular mechanism that underlies the beneficial effect of CR on mitochondrial dysfunction is unclear. Here, we investigated in mice the mechanisms underlying CR-mediated protection against hypoxia in aged kidney, with a special focus on the role of the NAD-dependent deacetylase sirtuin 1 (Sirt1), which is linked to CR-related longevity in model organisms, on mitochondrial autophagy. Adult-onset and long-term CR in mice promoted increased Sirt1 expression in aged kidney and attenuated hypoxia-associated mitochondrial and renal damage by enhancing BCL2/adenovirus E1B 19-kDa interacting protein 3-dependent (Bnip3-dependent) autophagy. Culture of primary renal proximal tubular cells (PTCs) in serum from CR mice promoted Sirt1-mediated forkhead box O3 (Foxo3) deacetylation. This activity was essential for expression of Bnip3 and p27Kip1 and for subsequent autophagy and cell survival of PTCs under hypoxia. Furthermore, the kidneys of aged [Sirt1.sup.±] mice were resistant to CR-mediated improvement in the accumulation of damaged mitochondria under hypoxia. These data highlight the role of the Sirt1-Foxo3 axis in cellular adaptation to hypoxia, delineate a molecular mechanism of the CR-mediated antiaging effect, and could potentially direct the design of new therapies for age- and hypoxia-related tissue damage., Introduction Increasing age causes progressive postmaturational deterioration of tissues and organs, leading to impairment of tissue functioning, increased vulnerability to challenges, and death. The kidney is a typical target organ [...]

Published
2010
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24. Structural and functional changes in the kidneys of high-fat diet-induced obese mice

Author

Deji, Naoko, Kume, Shinji, Araki, Shin-ichi, Soumura, Mariko, Sugimoto, Toshiro, Isshiki, Keiji, Chin-Kanasaki, Masami, Sakaguchi, Masayoshi, Koya, Daisuke, Haneda, Masakazu, Kashiwagi, Atsunori, and Uzu, Takashi

Subjects
Metabolic syndrome X -- Research, Metabolic syndrome X -- Health aspects, Kidney diseases -- Risk factors, Ketogenic diet -- Health aspects, Biological sciences
Abstract

Metabolic syndrome has been reported to be associated with chronic kidney disease, but the mechanisms remain unclear. Although feeding of a high-fat diet (HFD) to C57BL/6 mice is reported to induce systemic metabolic abnormalities and subsequent renal injuries, such as albuminuria, similar to human metabolic syndrome, alterations in HFD-induced renal injuries have not been fully elucidated in detail. We therefore investigated the structural and functional changes in the kidneys of C57BL/6 mice on a HFD. Six-week-old mice were fed a low-fat diet (LFD; 10% of total calories from fat) or a HFD (60% fat) for 12 wk. Mice fed a HFD showed significant increases in body weight, systolic blood pressure, plasma insulin, glucose, and triglycerides compared with those on a LFD. Accompanying these systemic changes, mice on a HFD showed albuminuria, an increase in glomerular tuft area, and mesangial expansion. These systemic and renal alterations in mice on a HFD were prevented by body weight control with the dietary restriction of feeding a HFD. Furthermore, mice on a HFD showed renal patho-physiological alterations including renal lipid accumulation, an increased accumulation of type IV collagen in glomeruli, an increase in macrophage infiltration in the renal medulla, an increase in urinary 8-hydroxy-2'-deoxyguanosine excretion, and impaired sodium handling. In conclusion, this study suggests that local metabolic alterations in the kidney play important roles in the development of renal injury associated with metabolic syndrome in addition to systemic metabolic changes and an increase in body weight. metabolic syndrome; dietary restriction; lipotoxicity; inflammation; salt-sensitive hypertension

Published
2009

41. Replication Study for the Association Between Four Loci Identified by a Genome-Wide Association Study on European American Subjects With Type 1 Diabetes and Susceptibility to Diabetic Nephropathy in Japanese Subjects With Type 2 Diabetes

Author

Maeda, Shiro, Araki, Shin-ichi, Babazono, Tetsuya, Toyoda, Masao, Umezono, Tomoya, Kawai, Koichi, Imanishi, Masahito, Uzu, Takashi, Watada, Hirotaka, Suzuki, Daisuke, Kashiwagi, Atsunori, Iwamoto, Yasuhiko, Kaku, Kohei, Kawamori, Ryuzo, and Nakamura, Yusuke

Published
2010
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