Antiaging, longevity and calorie restriction

Morley, John E.; Chahla, Elie; Alkaade, Saad

doi:10.1097/mco.0b013e3283331384

Cited by 36 publications

(29 citation statements)

References 71 publications

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“…CR does not promote longevity in all species and is not proven so far to do so in humans (Shanley and Kirkwood, 2006). Studies with monkeys often lacked sufficient number of individuals and the amount of food intake might have been inappropriate as the amount of calories fed to the CR group were comparable to the amount available in the wild; thus, not representing a true CR (Banks et al, 2003;Morley et al, 2009). Several studies confirmed the crucial role of sirtuins, NAD + -dependent deacetylases, in the CR-dependent deceleration of aging.…”

Section: Role Of Insulin Sensitivity and Calorie Restriction In Agingmentioning

confidence: 99%

“…In general, CR increases the amount of ATP generated via respiration, stimulates mitochondrial biogenesis, and leads to reduced levels of ROS (Nisoli et al 2005;Guarente 2008). Still, the underlying mechanisms of CR on aging are controversially debated (Morley et al, 2009). CR does not promote longevity in all species and is not proven so far to do so in humans (Shanley and Kirkwood, 2006).…”

Section: Role Of Insulin Sensitivity and Calorie Restriction In Agingmentioning

confidence: 99%

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Impaired quality control of mitochondria: Aging from a new perspective

Weber

Reichert

2010

Experimental Gerontology

103

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Section: Role Of Insulin Sensitivity and Calorie Restriction In Agingmentioning

confidence: 99%

Section: Role Of Insulin Sensitivity and Calorie Restriction In Agingmentioning

confidence: 99%

Impaired quality control of mitochondria: Aging from a new perspective

Weber

Reichert

2010

Experimental Gerontology

103

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“…Visceral adiposity and ectopic lipid accumulation are linked with morbidity and all-cause mortality in aged mammals (15,16). Despite evidence indicating that CR improves regional adiposity, metabolic parameters, and inflammatory status in obese older adults (17–19), it remains unclear whether CR is feasible and/or appropriate in nonobese older adults (20,21). Moreover, dietary interventions that restrict calorie intake are often difficult to maintain (22).…”

mentioning

confidence: 99%

17α-Estradiol Alleviates Age-related Metabolic and Inflammatory Dysfunction in Male Mice Without Inducing Feminization

Stout

Steyn

Jurczak

et al. 2016

GERONA

102

116

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Aging is associated with visceral adiposity, metabolic disorders, and chronic low-grade inflammation. 17α-estradiol (17α-E2), a naturally occurring enantiomer of 17β-estradiol (17β-E2), extends life span in male mice through unresolved mechanisms. We tested whether 17α-E2 could alleviate age-related metabolic dysfunction and inflammation. 17α-E2 reduced body mass, visceral adiposity, and ectopic lipid deposition without decreasing lean mass. These declines were associated with reductions in energy intake due to the activation of hypothalamic anorexigenic pathways and direct effects of 17α-E2 on nutrient-sensing pathways in visceral adipose tissue. 17α-E2 did not alter energy expenditure or excretion. Fasting glucose, insulin, and glycosylated hemoglobin were also reduced by 17α-E2, and hyperinsulinemic-euglycemic clamps revealed improvements in peripheral glucose disposal and hepatic glucose production. Inflammatory mediators in visceral adipose tissue and the circulation were reduced by 17α-E2. 17α-E2 increased AMPKα and reduced mTOR complex 1 activity in visceral adipose tissue but not in liver or quadriceps muscle, which is in contrast to the generalized systemic effects of caloric restriction. These beneficial phenotypic changes occurred in the absence of feminization or cardiac dysfunction, two commonly observed deleterious effects of exogenous estrogen administration. Thus, 17α-E2 holds potential as a novel therapeutic for alleviating age-related metabolic dysfunction through tissue-specific effects.

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“…Calorie restriction (CR) as the oldest and most robust dietary intervention provides many health benefits and has been used for health promotion among different races, religions, and regions worldwide (Morley, Chahla, & Alkaade, 2010). Although the relationship between CR and health benefits has been empirically demonstrated (Walford, Harris, & Gunion, 1992), the mechanisms underlying this process are multifactorial and still under intensive investigation.…”

Section: Introductionmentioning

confidence: 99%

Ketone body 3‐hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina

et al. 2017

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SummaryCalorie restriction (CR) being the most robust dietary intervention provides various health benefits. D‐3‐hydroxybutyrate (3HB), a major physiological ketone, has been proposed as an important endogenous molecule for CR. To investigate the role of 3HB in CR, we investigated potential shared mechanisms underlying increased retinal 3HB induced by CR and exogenously applied 3HB without CR to protect against ischemic retinal degeneration. The repeated elevation of retinal 3HB, with or without CR, suppressed retinal degeneration. Metabolomic analysis showed that the antioxidant pentose phosphate pathway and its limiting enzyme, glucose‐6‐phosphate dehydrogenase (G6PD), were concomitantly preserved. Importantly, the upregulation of nuclear factor erythroid 2 p45‐related factor 2 (Nrf2), a regulator of G6PD, and elevation of the tricarboxylic acid cycle's Nrf2 activator, fumarate, were also shared. Together, our findings suggest that CR provides retinal antioxidative defense by 3HB through the antioxidant Nrf2 pathway via modification of a tricarboxylic acid cycle intermediate during 3HB metabolism.

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Antiaging, longevity and calorie restriction

Cited by 36 publications

References 71 publications

Impaired quality control of mitochondria: Aging from a new perspective

Impaired quality control of mitochondria: Aging from a new perspective

17α-Estradiol Alleviates Age-related Metabolic and Inflammatory Dysfunction in Male Mice Without Inducing Feminization

Ketone body 3‐hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina

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