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Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

Watanabe, Tomoyuki ; Saotome, Masao ; Nobuhara, Mamoru ; Sakamoto, Atsushi ; Urushida, Tsuyoshi ; Katoh, Hideki ; Satoh, Hiroshi ; Funaki, Makoto ; Hayashi, Hideharu

Experimental Cell Research, 01 May 2014, Vol.323(2) [Tạp chí có phản biện]

ISSN: 0014-4827 ; E-ISSN: 1090-2422 ; DOI: 10.1016/J.YEXCR.2014.02.027

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  • Nhan đề:
    Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance
  • Tác giả: Watanabe, Tomoyuki ; Saotome, Masao ; Nobuhara, Mamoru ; Sakamoto, Atsushi ; Urushida, Tsuyoshi ; Katoh, Hideki ; Satoh, Hiroshi ; Funaki, Makoto ; Hayashi, Hideharu
  • Chủ đề: 60 Applied LIFE Sciences ; Cardiovascular Diseases ; Glucose ; Hydrogen Peroxide ; Insulin ; Lipids ; Metabolites ; Mitochondria ; Oxygen ; Pathogenesis ; Porphyrins ; Uptake ; Biology
  • Là 1 phần của: Experimental Cell Research, 01 May 2014, Vol.323(2)
  • Mô tả: Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ{sub m}) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H{sub 2}O{sub 2}), they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ{sub m} depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H{sub 2}O{sub 2}-induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ{sub m} depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin-resistance. • Inhibition of DRP or ROS failed to improve palmitate-induced insulin-resistance. • Mitochondrial dysfunction by lipid metabolites would induce insulin-resistance.
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 0014-4827 ; E-ISSN: 1090-2422 ; DOI: 10.1016/J.YEXCR.2014.02.027

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