Low-grade chronic inflammation and superoxide anion production by NADPH oxidase are the main determinants of physical frailty in older adults

Baptista, Grégory; Dupuy, Anne‐Marie; Jaussent, Audrey; Durant, R.; Ventura, E.; Sauguet, Pauline; Picot, Marie‐Christine; Jeandel, Claude; Cristol, Jean Paul

doi:10.3109/10715762.2012.692784

Cited by 37 publications

(27 citation statements)

References 34 publications

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“…For example, the increased oxidative stress that has been observed in frail older adults has been hypothesized to arise from mitochondrial dysfunction (Villamena and Zweier 2004). Consistent with this hypothesis is the study by Baptista et al (2012) showing that superoxide anion production was increased in white blood cells of frail older adults. Recently, it was also shown in blood that, lower mtDNA copy number, a marker that reveals mitochondrial depletion, energy reserves, and oxidative stress is associated with frailty (Ashar et al 2015).…”

Section: Introductionsupporting

confidence: 63%

A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse

et al. 2017

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Frailty is a geriatric syndrome that is an important public health problem for the older adults living in the USA. Although several methods have been developed to measure frailty in humans, we have very little understanding of its etiology. Because the molecular basis of frailty is poorly understood, mouse models would be of great value in determining which pathways contribute to the development of frailty. More importantly, mouse models would be critical in testing potential therapies to treat and possibly prevent frailty. In this article, we present data showing that Sod1KO mice, which lack the antioxidant enzyme, Cu/Zn superoxide dismutase, are an excellent model of frailty, and we compare the Sod1KO mice to the only other mouse model of frailty, mice with the deletion of the IL-10 gene. Sod1KO mice exhibit four characteristics that have been used to define human frailty: weight loss, weakness, low physical activity, and exhaustion. In addition, Sod1KO mice show increased inflammation and sarcopenia, which are strongly associated with human frailty. The Sod1KO mice also show alterations in pathways that have been proposed to play a role in the etiology of frailty: oxidative stress, mitochondrial dysfunction, and cell senescence. Using Sod1KO mice, we show that dietary restriction can delay/prevent characteristics of frailty in mice.

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Section: Introductionsupporting

confidence: 63%

A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse

et al. 2017

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“…44 However, because of their evanescent nature, they are difficult to measure directly in humans. 45 Superoxide anion overproduction was noted in isolated white blood cells of frail older adults, which further confirmed the association between oxidative stress and frailty. 45 Superoxide anion overproduction was noted in isolated white blood cells of frail older adults, which further confirmed the association between oxidative stress and frailty.…”

Section: Reactive Oxygen Species and Frailtysupporting

confidence: 53%

Oxidative Stress and Frailty

Hsiung

Hsu

et al. 2014

Aging

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“…A number of observational studies have associated markers of oxidative stress or inflammation with measures of frailty such as slow gait speed. (71, 72) These studies have suggested that adiposity induces oxidative stress and thus grip strength(73) and that inflammation is associated with reduced grip strength and reduced walking speed in older subjects with the highest body fat percentage. (74) But it is also known that inflammation only partially explains observed mobility limitations.…”

Section: Discussionmentioning

confidence: 99%

Obesity and Physical Frailty in Older Adults: A Scoping Review of Lifestyle Intervention Trials

Starr

McDonald

Bales

2014

Journal of the American Medical Directors Association

152

105

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Many frail older adults are thin, weak, and undernourished; this component of frailty remains a critical concern in the geriatric field. However, there is also strong evidence that excessive adiposity contributes to frailty by reducing the ability of older adults to perform physical activities and increasing metabolic instability. Our scoping review explores the impact of being obese on physical frailty in older adults by summarizing the state of the science for both clinical markers of physical function and biomarkers for potential underlying causes of obesity-related decline. We used the five-stage methodological framework of Arksey and O’Malley to conduct a scoping review of randomized trials of weight loss and/or exercise interventions for obesity (BMI ≥ 30 kg/m2) in older adults (aged > 60 yrs), examining the outcomes of inflammation, oxidative stress, and lipid accumulation in muscle, as well as direct measures of physical function. Our initial search yielded 212 articles; exclusion of cross-sectional and observational studies, cell culture and animal studies, disease-specific interventions, and articles published before 2001 led to a final result of 21 articles. Findings of these trials included the following major points: The literature consistently confirmed benefits of lifestyle interventions to physical function assessed at the clinical level. Generally speaking, weight loss alone produced a greater effect than exercise alone and the best outcomes were achieved with a combination of weight loss and exercise, especially exercise programs that combined aerobic, resistance, and flexibility training. Weight loss interventions tended to reduce markers of inflammation and/or oxidative damage when more robust weight reduction was achieved and maintained over time, whereas exercise did not change markers of inflammation. However, participation in a chronic exercise program did reduce the oxidative stress induced by an acute bout of exercise. Weight loss interventions consistently reduced lipid accumulation in the muscle; however, in response to exercise, three studies showed an increase and two a decrease in muscle lipid infiltration. In summary, this scoping review identified strong clinical evidence that weight reduction and/or exercise interventions can improve physical function and biomarkers of physical dysfunction among overweight/obese older adults, supporting the suggestion that excessive adiposity contributes to physical frailty. However, the evidence also suggests a complexity of metabolic influences, both systemically and within muscle, which has not been elucidated to date. Considerable further study is needed to examine the mechanisms by which lifestyle interventions influence physical frailty before the net impact of such interventions can be fully understood.

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Low-grade chronic inflammation and superoxide anion production by NADPH oxidase are the main determinants of physical frailty in older adults

Abstract: Physical frailty in older people is associated with superoxide anion overproduction by NADPH oxidase and low-grade chronic inflammation.

Cited by 37 publications

References 34 publications

A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse

A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse

Oxidative Stress and Frailty

Obesity and Physical Frailty in Older Adults: A Scoping Review of Lifestyle Intervention Trials

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