Dietary restriction and the pursuit of effective mimetics

Selman, Colin

doi:10.1017/s0029665113003832

Cited by 37 publications

(46 citation statements)

References 152 publications

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“…Exactly how they generate the health benefits remains open for debate, however CR results in promoted oxidative stress resistance, enhanced autophagy, and a generalized shift from carbohydrate to fat metabolism, all of which could be essential components of the beneficial effects (Selman, 2014;Speakman and Mitchell, 2011). As described previously, our experiments showed that worms treated with rBTI showed increased oxidative stress resistance.…”

Section: Rbti Decreases Glycolysis Increased Lipolysis and Induced supporting

confidence: 75%

“…We hypothesized that rBTI elicits its beneficial effects by mimicking CR, and CR has been linked to increased AMP:ATP ratio, respiration and transient ROS signal (Masoro, 2005;Selman, 2014). As reported by others (Boveris and Chance, 1973;Kemp et al, 2003), increased AMP could induce respiration, and ROS generation is increased by respiration, as inevitable by-product of respiration.…”

Section: Rbti Increases Amp:atp Ratio and Respiration Induces A Tranmentioning

confidence: 82%

“…Several such compounds, including rapamycin, metformin and resveratrol, have been identified as potential CR mimetics. Although these compounds show similar effects, they act through different genes to elicit corresponding effects on the lifespan (Blagosklonny, 2007;Mouchiroud et al, 2010;Selman, 2014). Here, we hypothesized that rBTI could elicit its beneficial effects by mimicking CR.…”

Section: Introductionmentioning

confidence: 99%

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rBTI extends Caenorhabditis elegans lifespan by mimicking calorie restriction

Cui

Wang

et al. 2015

Experimental Gerontology

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Section: Rbti Decreases Glycolysis Increased Lipolysis and Induced supporting

confidence: 75%

Section: Rbti Increases Amp:atp Ratio and Respiration Induces A Tranmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

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rBTI extends Caenorhabditis elegans lifespan by mimicking calorie restriction

Cui

Wang

et al. 2015

Experimental Gerontology

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“…DR 25 had no effect on hepatic protein levels of PGC-1a, TFAM, and OXPHOS complexes skeletal muscle mitochondria. We highlight tissue-specific differences in the critical factor that may help explain the unresponsiveness of particular organisms to 68 DR-induced longevity is genetic background [1], [7], [18], [19]. For example, the 69 effect of DR on survival in DBA/2 mice has been a source of debate for many years, 70 with DR reported to extend [20], [21], have no effect [22], or shorten lifespan [14].…”

mentioning

confidence: 99%

Disentangling the effect of dietary restriction on mitochondrial function using recombinant inbred mice

Mulvey

Sands

Salin

et al. 2017

Molecular and Cellular Endocrinology

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TejJ114 (see Figure 1 for schematic outlining our original predictions). 0.1mM EGTA, 0.2% BSA (pH 7.4)), as set out in protocols previously described [58]. 208The muscle was subsequently rinsed three times in 1ml of fresh isolation buffer, and Results 318Mitochondrial oxygen consumption rates (OCR) within isolated liver 319 mitochondria under all conditions studied ( Fig. 2A) were unaffected by 10 months of 320 40% DR in strain TejJ89 relative to AL controls. A similar lack of a DR effect on 321 hepatic respiratory capacities was observed in strain TejJ48 (Fig. 2B). In contrast, 322DR in strain TejJ114 (Fig. 2C) under DR (Fig. S2H). 345Total hepatic protein levels of PGC-1α (Fig. 5A), a key transcriptional co-346 activator linked to mitochondrial metabolism and biogenesis, was unaltered by 347 treatment or strain, with both nuclear (Fig. 5B) and cytoplasmic (Fig. 5C) PGC-1α 348 levels likewise unaffected. Similarly, mitochondrial transcription factor A (TFAM), a 349 key activator of mitochondrial transcription, was unaffected by DR or strain (Fig. 5D). 350We then examined various OXPHOS complexes within liver, but again observed no we then went on to investigate whether DR induced mitonuclear protein imbalance and UPR mt by firstly calculating the ratio of nuclear encoded SDHB to mitochondrially 355 encoded MTCO1 as previously described [45]. We observed no effect of either 356 treatment or strain on mitochondrial nuclear imbalance ( Fig. 6A-C). No differences 357were observed between either treatment groups or strains in the mitochondrial 358 chaperone HSP60 (Fig. 6D), but a significant reduction in hepatic HSP90 (Fig. 6E) 359was observed in strain TejJ114 under DR (t=2.267, p=0.045) relative to AL controls. 360In order to determine whether mitochondrial dysfunction in strain TejJ114 was 361 specific to liver, we also examined a number of mitochondrial parameters in isolated 362 skeletal muscle from these same mice. No treatment or strain-specific differences in 363 mitochondrial OCR were observed ( Fig. 7A-E skeletal muscle were unaffected by treatment and strain (Figure S3D-F; Fig. 10A), as 373 was also the case in heart ( Fig. S3G-I; Fig. 10B). Discussion 375The phenotypic plasticity of the mitochondria is crucial to allow energetic

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“…First identified in rats and mice at the beginning of the last century, restricting food intake in rodents prolonged longevity (McDonald & Ramsey, 2010). Ever since, except for a few exceptions (Selman, 2014;Speakman & Hambly, 2007), food restriction has increased the life span of all organisms tested (Fontana et al, 2010;Mair & Dillin, 2008;Trepanowski, Canale, Marshall, Kabir, & Bloomer, 2011).…”

Section: Dr and The Nutrient-sensing Networkmentioning

confidence: 99%