Mitochondrial genotype associated with longevity

Tanaka, Masashi; Gong, Jian; Zhang, Jin; Yoneda, Makoto; Yagi, Kazuichi

doi:10.1016/s0140-6736(05)78211-8

Cited by 289 publications

(254 citation statements)

References 5 publications

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“…Indeed, our observations are in agreement with suggestions that germline removal promotes longevity in part by modulating insulin signaling and lipid metabolism (Hansen et al, 2013), and with expectations that naturally occurring variation in mitochondrial function and metabolism specifically affects male aging (Zeh and Zeh, 2005;Camus et al, 2012). Moreover, mitochondrialnuclear genetic interactions tied to aging are likely to include nuclear-encoded genes associated with reproduction-induced mortality (Tanaka et al, 1998;De Benedictis et al, 1999;Rand et al, 2006;Clancy, 2008;Zhu et al, 2014). A recent study found that interactions between genes spanning the mitochondrial and nuclear genomes were associated with components of male reproductive aging via direct effects on ejaculate weight and indirect effects on the size of eggs produced by females (Immonen et al, 2016).…”

Section: Discussionsupporting

confidence: 90%

Reproductive activity triggers accelerated male mortality and decreases lifespan: genetic and gene expression determinants in Drosophila

Branco¹,

Schilling

Silkaitis

et al. 2016

Heredity

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Reproduction and aging evolved to be intimately associated. Experimental selection for early-life reproduction drives the evolution of decreased longevity in Drosophila whereas experimental selection for increased longevity leads to changes in reproduction. Although life history theory offers hypotheses to explain these relationships, the genetic architecture and molecular mechanisms underlying reproduction-longevity associations remain a matter of debate. Here we show that mating triggers accelerated mortality in males and identify hundreds of genes that are modulated upon mating in the fruit fly Drosophila melanogaster. Interrogation of genome-wide gene expression in virgin and recently mated males revealed coherent responses, with biological processes that are upregulated (testis-specific gene expression) or downregulated (metabolism and mitochondria-related functions) upon mating. Furthermore, using a panel of genotypes from the Drosophila Synthetic Population Resource (DSPR) as a source of naturally occurring genetic perturbation, we uncover abundant variation in longevity and reproduction-induced mortality among genotypes. Genotypes displayed more than fourfold variation in longevity and reproduction-induced mortality that can be traced to variation in specific segments of the genome. The data reveal individual variation in sensitivity to reproduction and physiological processes that are enhanced and suppressed upon mating. These results raise the prospect that variation in longevity and age-related traits could be traced to processes that coordinate germline and somatic function.

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Section: Discussionsupporting

confidence: 90%

Reproductive activity triggers accelerated male mortality and decreases lifespan: genetic and gene expression determinants in Drosophila

Branco¹,

Schilling

Silkaitis

et al. 2016

Heredity

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“…Using a quantitative polymerase chain reaction (PCR) method, a 1997 study by Kato et al 131 found a significantly higher ratio of deleted to wild-type mitochondrial DNA (mtDNA) in the cerebral cortex of patients with bipolar disorder compared to agematched controls. After 3 years, Kato et al also reported a significantly higher rate of the 5178C mtDNA genotype, known to be associated with an increased risk and earlier onset of both Alzheimer's and Parkinson's disease, 132 in bipolar patients compared to controls. 133 In addition, bipolar patients with the 5178C genotype exhibited significantly lower brain pHi than patients with the 5178A genotype, 133 which suggests a possible connection between abnormal mtDNA and the reduced pH levels consistently reported in bipolar patients (Table 3).…”

Section: Connection To Other Findings In Bipolar Researchmentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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Magnetic resonance spectroscopy (MRS) affords a noninvasive window on in vivo brain chemistry and, as such, provides a unique opportunity to gain insight into the biochemical pathology of bipolar disorder. Studies utilizing proton ( 1 H) MRS have identified changes in cerebral concentrations of N-acetyl aspartate, glutamate/glutamine, choline-containing compounds, myo-inositol, and lactate in bipolar subjects compared to normal controls, while studies using phosphorus ( 31 P) MRS have examined additional alterations in levels of phosphocreatine, phosphomonoesters, and intracellular pH. We hypothesize that the majority of MRS findings in bipolar subjects can be fit into a more cohesive bioenergetic and neurochemical model of bipolar illness that is both novel and yet in concordance with findings from complementary methodological approaches. In this review, we propose a hypothesis of mitochondrial dysfunction in bipolar disorder that involves impaired oxidative phosphorylation, a resultant shift toward glycolytic energy production, a decrease in total energy production and/or substrate availability, and altered phospholipid metabolism. Molecular Psychiatry (2005) 10, 900-919.

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“…The frequency of the Mt5178A genotype, a genetic marker of mitochondrial haplogroup D, is significantly higher in Japanese centenarians than in the general population (Alexe et al 2007;Tanaka et al 1998) and it is reported that individuals with Mt5178A (mitochondrial haplogroup D) are less susceptible to lifestyle-related adult-onset diseases, for example hypertension (Kokaze et al 2007), diabetes (Wang et al 2001), metabolic syndrome ), myocardial infarction (Mukae et al 2003;Takagi et al 2004), and cerebrovascular diseases (Ohkubo et al 2002), than those with Mt5178C. Mt5178 C/A polymorphism is, moreover, also reported to be associated with blood pressure (Kokaze et al 2004a(Kokaze et al , 2007, serum lipid levels (Kokaze et al 2001(Kokaze et al , 2003a, fasting plasma glucose levels and glucose tolerance (Kokaze et al 2005a), serum uric acid levels (Kokaze et al 2006), intraocular pressure (Kokaze et al 2004b), hematological data (Kokaze et al 2005b), and serum protein fraction levels (Kokaze et al 2002(Kokaze et al , 2003b, and its interaction with smoking habits is associated with serum triglyceride levels (Kokaze et al 2003a), intraocular pressure (Kokaze et al 2004b), red blood cell counts (Kokaze et al 2005b), and serum protein fraction levels (Kokaze et al 2003b).…”

Section: Introductionmentioning

confidence: 95%

“…Mitochondrial DNA 5178 cytosine/adenine (Mt5178 C/A) polymorphism (also known as NADH dehydrogenase subunit 2237 leucine/methionine (ND2-237 Leu/Met) polymorphism) is reportedly associated with longevity in the Japanese population (Tanaka et al 1998). The frequency of the Mt5178A genotype, a genetic marker of mitochondrial haplogroup D, is significantly higher in Japanese centenarians than in the general population (Alexe et al 2007;Tanaka et al 1998) and it is reported that individuals with Mt5178A (mitochondrial haplogroup D) are less susceptible to lifestyle-related adult-onset diseases, for example hypertension (Kokaze et al 2007), diabetes (Wang et al 2001), metabolic syndrome ), myocardial infarction (Mukae et al 2003;Takagi et al 2004), and cerebrovascular diseases (Ohkubo et al 2002), than those with Mt5178C.…”

Section: Introductionmentioning

confidence: 99%

Longevity-associated mitochondrial DNA 5178 C/A polymorphism and its interaction with cigarette consumption are associated with pulmonary function in middle-aged Japanese men

et al. 2007

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Pulmonary function is a crucial factor associated with longevity. Mitochondrial DNA 5178 cytosine/ adenine (Mt5178 C/A) polymorphism is reported to be associated with longevity in the Japanese population. We have previously reported that Mt5178 C/A polymorphism is widely associated with physiological and biochemical status. The objective of this study was to investigate whether Mt5178 C/A polymorphism is associated with pulmonary function. The subjects were 463 Japanese men (mean age ± SD 54.0 ± 7.6 years). Genotyping of Mt5178 C/A was performed by polymerase chain reaction-restriction fragment length polymorphism. A cross-sectional study of the relationship between genotype and spirometric data, namely forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV 1 ), was conducted. Among younger subjects (age <55 years), FVC and FEV 1 were significantly higher for men with Mt5178A than for those with Mt5178C. Interaction between Mt5178 C/A polymorphism and smoking habits in FEV 1 /FVC ratio was observed. Cigarette consumption (pack-years of smoking) was significantly and negatively associated with FEV 1 / FVC ratio for men with Mt5178C. Among older subjects (age ‡55 years), FEV 1 /FVC ratio was significantly lower for current smokers with Mt5178C than for never smokers with Mt5178C or for never smokers with Mt5178A. Mt5178 C/A polymorphism and its interaction with cigarette consumption may be associated with pulmonary function in Japanese men.

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Mitochondrial genotype associated with longevity

Cited by 289 publications

References 5 publications

Reproductive activity triggers accelerated male mortality and decreases lifespan: genetic and gene expression determinants in Drosophila

Reproductive activity triggers accelerated male mortality and decreases lifespan: genetic and gene expression determinants in Drosophila

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

Longevity-associated mitochondrial DNA 5178 C/A polymorphism and its interaction with cigarette consumption are associated with pulmonary function in middle-aged Japanese men

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