Mechanisms of cardiac dysfunction in metabolic syndrome
| Project/Area Number |
18590761
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Gunma University |
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Principal Investigator |
YOKOYAMA Tomoyuki Gunma University, Faculty of Medicine, professor (70312890)
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| Co-Investigator(Kenkyū-buntansha) |
KURABAYASHI Masahiko GUNMA UNIVERSITY, Graduate School of Medicine, professor (00215047)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,740,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥240,000)
Fiscal Year 2007: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2006: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | obesity / stearoyl-CoA desaturase-1 / fatty acid / pressure overload / Suppressor of cytokine signal-3 / メタボリックシンドローム / N-epsilon-(hexanol) lysine / 酸化ストレス / Suppressor of cytokine signal-3 / 心筋細胞 |
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| Research Abstract |
1) Increased stearoyl-CoA desaturase-1 (SCD-1) expression in obese rat heart enhances to myocardial lipid accumulation and metabolic abnormality
Although SCD1 is expressed in various tissues including heart, SCDI involvement in cardiovascular disease is poorly understood. We therefore examined the expression of cardiac SCD1 in obese rats which were induced by a sucrose-rich diet. Using Real-time PCR, SCD1 mRNAs expression was significantly increased in rat heart after sucrose-rich diet. We also detected protein expression of SCD1 up-regulation in cardiomyocytes by immunohistochemistry. To establish a relationship between SCD1 and lipid metabolism, we prepared SCD1 overexpressed cardiac myocytes using adenovirus. SCD1-overexpression significantly increased accumulation of triglyceride in myocytes by 30% and decreased fatty acid oxidation by 58%. In conclusions, our results demonstrated for the first time that SCD1 expression was up-regulated in visceral obese rat hearts and SCD1-overexpr
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ession led to excessive lipid accumulation and deterioration of fatty acid oxidation.
2) Acute pressure overload up-regulates, but chronic pressure overload down-regulates Suppressor of cytokine signal-3 (SOCS-3) expression in rat heart
Recent study showed that SOCS-3 was rapidly induced by angiotensinII (Ang1T) in heart and modulated AngII signaling. However, role of SOCS-3 in cardiovascular diseases has not been known. We therefore examined expression of SOCS-3 mRNA in pressure overloaded rat heart. One day after aortic banding, SOCS-3 mRNA expression in heart was markedly increased by Northern blotting. Interestingly, SOCS-3 expressions in rats 2 and 4 weeks after banding were significantly decreased in comparison with sham rats. Further, 24 hours exposure to isolated neonatal rat ventricular myocytes with AngII, TNFa or leptin induced distinct SOCS-3 mRNA expression, but continuous exposure of theses growth factors for 48 to 72 hours diminished SOCS-3 expression time-dependently. We conclude that acute pressure overload up-regulates SOCS-3 expression in cardiac myocytes, and SOCS-3 may inhibit signaling of growth factors as negative feedback system. However, chronic pressure overload down-regulates SOCS-3 expression. Less
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Report
(3 results)
Research Products
(12 results)
