Abnormal Myocardial Energy-Production State in Mitochondrial Cardiomyopathy and Acute Response to L-Arginine Infusion - C-11 Acetate Kinetics Revealed by Positron Emission Tomography -

Arakawa, Kazuhisa; Kudo, Takashi; Ikawa, Masamichi; Morikawa, Norihiro; Kawai, Yasuyuki; Sahashi, Ko; Lee, Jong–Dae; Kuriyama, Masaru; Miyamori, Isamu; Okazawa, Hidehiko; Yoneda, Makoto

doi:10.1253/circj.cj-10-0044

Cited by 28 publications

(27 citation statements)

References 31 publications

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“…Diabetes or impaired glucose tolerance affects the majority of the m.3243A>G carriers (Frederiksen et al 2009) and, indeed, the present study extends previous findings by suggesting that glucose intolerance may reflect in insulin resistance in the myocardium in these patients (Arakawa et al 2010;Lodi et al 2004). In patients with type 2 diabetes FFA release from fat tissue is high and, even during euglycemic hyperinsulinemia, cardiac glucose uptake is 25 % lower and FFA availability is 46 % higher than those in controls (Nuutila et al 1992;Rijzewijk et al 2009).…”

Section: Discussionsupporting

confidence: 85%

“…In addition, a recent study including six patients showed a 27 % decrease in [ 11 C]acetate kinetics suggesting a low citric acid cycle and myocardial oxidation activity. The authors suggested that an increased glucose uptake and anaerobic glycolysis would partly compensate the ATP production deficiency (Arakawa et al 2010). In this work we characterized myocardial glucose uptake in patients harbouring the m.3243A>G mutation.…”

Section: Introductionmentioning

confidence: 94%

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Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA

Lindroos

Pärkkä

Taittonen

et al. 2015

J of Inher Metab Disea

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Mitochondrial mutations impair glucose oxidation and increase glucose uptake in cell cultures and lead to cardiomyopathy in patients. Here we characterize cardiac glucose uptake in 14 patients with the m.3243A > G mutation in mitochondrial DNA. The 14 patients with m.3243A > G and 13 controls were similar in age, physical activity and body mass index. Ten patients had diabetes. Left ventricular glucose uptake per tissue mass (LVGU) was measured with 2-[(18) F]fluoro-2-deoxyglucose positron emission tomography during euglycemic hyperinsulinemia. Cardiac morphology and function were assessed with magnetic resonance imaging. We found that the LVGU was 25% lower in the patients than that in the controls (P = 0.029). LVGU was inversely correlated with mutation heteroplasmy, glycated haemoglobin and fasting lactate in patients. The seven patients with mutation heteroplasmy ≥ 49% had 44% lower LVGU than the seven patients with heteroplasmy < 49%. This difference remained significant after adjustment for concurrent free fatty acid concentration or glycated haemoglobin or glucose uptake in skeletal muscle or all (p < 0.048 [All]). Patients with m.3243A > G had a lower stroke volume and a higher heart rate than the controls, whereas cardiac output and work were similar. Myocardial glucose uptake is not increased but decreased with a threshold effect pattern in patients with the m.3243A > G mutation. The glucose hypometabolism adds to the impaired cardiac energetics and likely contributes to the progression of the mitochondrial cardiomyopathy.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 94%

Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA

Lindroos

Pärkkä

Taittonen

et al. 2015

J of Inher Metab Disea

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“…14, 15 In the current issue of the Journal, Arakawa et al also demonstrate, using 11 C-acetate-PET, that L-Arg administration rescues the impaired TCA-cycle metabolism without a correlation to MBF in patients with mitochondrial cardiomyopathy carrying A3243G (mechanism (b)). 6 Although further…”

Section: Article P 2702mentioning

confidence: 94%

“…6 The 11 C-acetate-PET was used to noninvasively evaluate the metabolic rate of the tricarboxylic acid (TCA) cycle, myocardial efficiency and myocardial blood flow (MBF) (Figure). 7, 8 As reported in this issue of the Journal, they found suppressed TCA-cycle kinetics and, paradoxically, increased myocardial efficiency at baseline in their patient group compared with the control group.…”

Section: Article P 2702mentioning

confidence: 99%

“…7, 8 As reported in this issue of the Journal, they found suppressed TCA-cycle kinetics and, paradoxically, increased myocardial efficiency at baseline in their patient group compared with the control group. 6 The TCA cycle generates NADH, which is converted to ATP in normal mitochondrial respiratory chains (ie, aerobic metabolism), from glycolysis and fatty acid metabolism (Figure). Deteriorated TCA-cycle activity indicates impaired respiratory chains and enhanced anaerobic metabolism in patients with mitochondrial cardiomyopathy.…”

Section: Article P 2702mentioning

confidence: 99%

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Energy States in Mitochondrial Cardiomyopathy

Ikawa

Yoneda

Tanaka

2010

Circ J

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Nanomedicine Approaches for Advanced Diagnosis and Treatment of Atherosclerosis and Related Ischemic Diseases

Boakye‐Yiadom

et al. 2020

Adv Healthcare Materials

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Cardiovascular diseases (CVDs) remain one of the major causes of mortality worldwide. In response to this and other worldwide health epidemics, nanomedicine has emerged as a rapidly evolving discipline that involves the development of innovative nanomaterials and nanotechnologies and their applications in therapy and diagnosis. Nanomedicine presents unique advantages over conventional medicines due to the superior properties intrinsic to nanoscopic therapies. Once used mainly for cancer therapies, recently, tremendous progress has been made in nanomedicine that has led to an overall improvement in the treatment and diagnosis of CVDs. This review elucidates the pathophysiology and potential targets of atherosclerosis and associated ischemic diseases. It may be fruitful to pursue future work in the nanomedicine‐mediated treatment of CVDs based on these targets. A comprehensive overview is then provided featuring the latest preclinical and clinical outcomes in cardiovascular imaging, biomarker detection, tissue engineering, and nanoscale delivery, with specific emphasis on nanoparticles, nanostructured scaffolds, and nanosensors. Finally, the challenges and opportunities regarding the future development and clinical translation of nanomedicine in related fields are discussed. Overall, this review aims to provide a deep and thorough understanding of the design, application, and future development of nanomedicine for atherosclerosis and related ischemic diseases.

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Abnormal Myocardial Energy-Production State in Mitochondrial Cardiomyopathy and Acute Response to L-Arginine Infusion - C-11 Acetate Kinetics Revealed by Positron Emission Tomography -

Cited by 28 publications

References 31 publications

Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA

Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA

Energy States in Mitochondrial Cardiomyopathy

Nanomedicine Approaches for Advanced Diagnosis and Treatment of Atherosclerosis and Related Ischemic Diseases

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