Obesity May Accelerate the Aging Process

Salvestrini, Valentina; Sell, Christian; Lorenzini, Antonello

doi:10.3389/fendo.2019.00266

Cited by 176 publications

(168 citation statements)

References 210 publications

(255 reference statements)

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“…Additionally, an increasing body of knowledge is suggesting that obesity may speed up the aging process by inducing senescence. [33][34][35] Women displayed an 80% increased likelihood of having excess body weight compared to men in this present study. In contrast to high income countries, women living in lower and middle income countries bear a disproportionate burden of obesity.…”

Section: Discussionsupporting

confidence: 41%

Obesity Epidemic in Urban Tanzania: A Public Health Calamity in an already Overwhelmed and Fragmented Health System.

Pallangyo¹,

Mgopa²,

Mkojera³

et al. 2019

Preprint

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Background Worldwide, the epidemiological and demographic transitions have resulted in nutrition shift characterized by an increased consumption of sugar-sweetened beverages and energy-dense fast food products. In just over 3 decades, overweight and obesity rates have nearly tripled to currently affecting over a third of the global population. Notwithstanding the ever present under-nutrition burden, sub Saharan Africa (SSA) is witnessing a drastic escalation of overweight and obesity. We aimed to explore the prevalence and associated factors for obesity among residents of Dar es Salaam city in Tanzania.Methods Participants from this study were recruited during a community screening conducted in Dar es Salaam. Sociodemographic and clinical data were gathered using a structured questionnaire during enrollment. Dietary habits, anthropometric measurements and blood pressure were assessed. All statistical analyses utilized STATA v11.0 software. Pearson Chi square and Student’s T-test were used to compare categorical and continuous variables respectively. Linear logistic regression analyses were used to assess for factors associated with BMI≥25. All tests were 2-sided and p<0.05 was used to denote a statistical significance.Results A total of 6691 participants were enrolled. The mean age was 43.1 years and males constituted 54.2% of all participants. Over two-thirds of participants were alcohol consumers and 6.9% had a positive smoking history. Eighty eight point three percent of participants were underactive, 4.7% had a history of diabetes mellitus and 18.1% were known to have elevated blood pressure. Overweight and obesity were observed in 34.8% and 32.4% of participants respectively. Among overweight and obese participants, 32.8% had a misperception of having a healthy weight. Age≥40, female sex, a current working status, habitual breakfast skipping, poor water intake, high soft drink consumption, regular fast food intake, low vegetable and fruit consumption, alcohol consumption and elevated blood pressure were found to be independent associated factors for obesity.Conclusion A sizeable proportion of participants were overweight or obese. Concomitantly, the rates of physical inactivity and unhealthy eating are disproportionately high. In view of this, community-based and multilevel public health strategies to promote and maintain healthy eating and physical activity require an urgent step-up in urban Tanzania.

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Section: Discussionsupporting

confidence: 41%

Obesity Epidemic in Urban Tanzania: A Public Health Calamity in an already Overwhelmed and Fragmented Health System.

Pallangyo¹,

Mgopa²,

Mkojera³

et al. 2019

Preprint

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“…Moreover, obesity in mid-life has been shown to accelerate aging mechanisms and induce phenotypes more commonly observed in older mammals [6][7][8][9][10][11][12]. These observations have led many to postulate that obesity may represent a mild progeria syndrome [13][14][15][16][17]. Although it is well established that dietary interventions, including calorie restriction, can reverse obesity-related metabolic sequelae, many of these strategies are not well tolerated in older patients due to concomitant comorbidities [2,18].…”

mentioning

confidence: 99%

Health benefits attributed to 17α-estradiol, a lifespan-extending compound, are mediated through estrogen receptor α

Mann

Hadad

Nelson-Holte

et al. 2020

Preprint

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Aging is the greatest risk factor for most chronic diseases. Metabolic dysfunction underlies several chronic diseases, which are further exacerbated by obesity. Dietary interventions can reverse metabolic declines and slow aging processes, although compliance issues remain paramount due to adverse effects on quality of life.17α-estradiol treatment improves metabolic parameters and slows aging in male mice. The mechanism by which 17α-E2 elicits benefits remain unknown, which has led speculation that an uncharacterized receptor is involved. Herein, we show that 17α-estradiol and 17β-estradiol elicit similar genomic binding and transcriptional activation of ERα and that the ablation of ERα in male mice completely attenuates the beneficial effects of 17α-estradiol. Our findings also suggest that 17α-E2 acts primarily through the liver and/or hypothalamus to elicit benefits, and that 17α-E2 also improves metabolic parameters in male rats. Collectively, these data suggest ERα is a relevant drug target for mitigating chronic diseases in male mammals. KEYWORDS17α-estradiol, aging, estrogen receptor, hypothalamus, liver, metabolism, obesity Aging is the leading risk factor for most chronic diseases, many of which are associated with declines in metabolic homeostasis [1]. Metabolic detriments associated with advancing age are further exacerbated by obesity [2,3], which has risen substantially in the older population (> 65 years) over the past several decades [4,5]. Moreover, obesity in mid-life has been shown to accelerate aging mechanisms and induce phenotypes more commonly observed in older mammals [6][7][8][9][10][11][12]. These observations have led many to postulate that obesity may represent a mild progeria syndrome [13][14][15][16][17]. Although it is well established that dietary interventions, including calorie restriction, can reverse obesity-related metabolic sequelae, many of these strategies are not well tolerated in older patients due to concomitant comorbidities [2,18]. Compliance issues across all age groups also remain a paramount hurdle due to calorie restriction adversely affecting mood, thermoregulation, and musculoskeletal mass [19]. These adverse health outcomes demonstrate the need for pharmacological approaches aimed at curtailing metabolic perturbations associated with obesity and aging.17α-estradiol (17α-E2) is one of the more recently studied compounds to demonstrate efficacy for beneficially modulating obesity-and age-related health outcomes. The NIA Interventions Testing Program (ITP) found that long-term administration of 17α-E2 extends median lifespan of male mice in a dose-dependent manner [20,21]. Our group has been exploring potential mechanisms by which 17α-E2 may improve healthspan and extend lifespan in a sex-specific manner. We have found that 17α-E2 administration reduces food intake and regional adiposity in combination with significant improvements in a multitude of systemic metabolic parameters in both middle-aged obese and old male mice without inducing deleterious effects [22][23...

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“…Obesity increases systemic inflammation and oxidative stress, and also affects cellular senescence and aging [42,43]. Adipocytokines, including adiponectin and visfatin, have previously been implicated in aging, longevity, and age-related diseases [44,45].…”

Section: Discussionmentioning

confidence: 99%

Visfatin Induces Senescence of Human Dental Pulp Cells

Park

Jang

et al. 2020

Cells

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Dental pulp plays an important role in the health of teeth. The aging of teeth is strongly related to the senescence of dental pulp cells. A novel adipokine, visfatin, is closely associated with cellular senescence. However, little is known about the effect of visfatin on the senescence of human dental pulp cells (hDPCs). Here, it was found that in vivo visfatin levels in human dental pulp tissues increase with age and are upregulated in vitro in hDPCs during premature senescence activated by H2O2, suggesting a correlation between visfatin and senescence. In addition, visfatin knockdown by small interfering RNA led to the reduction in hDPC senescence; however, treatment with exogenous visfatin protein induced the senescence of hDPCs along with increased NADPH consumption, which was reversed by FK866, a chemical inhibitor of visfatin. Furthermore, visfatin-induced senescence was associated with both the induction of telomere damage and the upregulation of senescence-associated secretory phenotype (SASP) factors as well as NF-κB activation, which were all inhibited by FK866. Taken together, these results demonstrate, for the first time, that visfatin plays a pivotal role in hDPC senescence in association with telomere dysfunction and the induction of SASP factors.

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Obesity May Accelerate the Aging Process

Cited by 176 publications

References 210 publications

Obesity Epidemic in Urban Tanzania: A Public Health Calamity in an already Overwhelmed and Fragmented Health System.

Obesity Epidemic in Urban Tanzania: A Public Health Calamity in an already Overwhelmed and Fragmented Health System.

Health benefits attributed to 17α-estradiol, a lifespan-extending compound, are mediated through estrogen receptor α

Visfatin Induces Senescence of Human Dental Pulp Cells

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