A new research paper was published in Aging (Aging-US) Volume 15, Issue 11, entitled, “Old-age-induced obesity reversed by a methionine-deficient diet or oral administration of recombinant methioninase-producing Escherichia coli in C57BL/6 mice.”

Obesity increases with aging. Methionine restriction affects lipid metabolism and can prevent obesity in mice. In this new study, researchers Yutaro Kubota, Qinghong Han, Jose Reynoso, Yusuke Aoki, Noriyuki Masaki, Koya Obara, Kazuyuki Hamada, Michael Bouvet, Takuya Tsunoda, and Robert M. Hoffman from AntiCancer Inc., University of California San Diego and Showa University School of Medicine observed C57BL/6 mice double their body weight from 4 to 48 weeks of age and become obese. The team then evaluated the efficacy of oral administration of recombinant-methioninase (rMETase)-producing E. coli (E. coli JM109-rMETase) or a methionine-deficient diet to reverse old-age-induced obesity in C57BL/6 mice. 

“In the present study we tested a low-methionine diet to reverse old-age-induced obesity. [...] E. coli JM109-rMETase was also tested in the present study to reverse old-age-induced obesity.”

Fifteen C57BL/6 male mice aged 12–18 months with old-age-induced obesity were divided into three groups. Group 1 was given a normal diet supplemented with non-recombinant E. coli JM109 cells orally by gavage twice daily; Group 2 was given a normal diet supplemented with recombinant E. coli JM109-rMETase cells by gavage twice daily; and Group 3 was given a methionine-deficient diet without treatment. 

The administration of E. coli JM109-rMETase or a methionine-deficient diet reduced the blood methionine level and reversed old-age-induced obesity with significant weight loss by 14 days. There was a negative correlation between methionine levels and negative body weight change. Although the degree of efficacy was higher in the methionine-deficient diet group than in the E. coli JM109-rMETase group, the present findings suggested that oral administration of E. coli JM109-rMETase, as well as a methionine-deficient diet, are effective in reversing old-age-induced obesity. 

“In conclusion, the present study provides evidence that restricting methionine by either a low-methionine diet or E. coli JM109-rMETase has clinical potential to treat old-age-induced obesity.”

DOI - https://doi.org/10.18632/aging.204783

Corresponding author - Robert M. Hoffman - all@anticancer.com

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Keywords - aging, obesity, methionine restriction, methionine-deficient diet, recombinant methioninase (rMETase), Escherichia coli, microbiome, weight-loss 

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Aging (Aging-US)

Methionine Restriction Reverses Old-age Obesity in Mice

BUFFALO, NY- June 12, 2024 – A new review paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Peripheral vascular dysfunction and the aging brain.”

Aging is the greatest non-modifiable risk factor for most diseases, including cardiovascular diseases (CVD), which remain the leading cause of mortality worldwide. In their new review, researchers Devin Wahl and Zachary S. Clayton from Colorado State University and the University of Colorado note that robust evidence indicates that CVD are a strong determinant for reduced brain health and all-cause dementia with advancing age. 

“CVD are also closely linked with peripheral and cerebral vascular dysfunction, common contributors to the development and progression of all types of dementia, that are largely driven by excessive levels of oxidative stress (e.g., reactive oxygen species [ROS]).”

Emerging evidence suggests that several fundamental aging mechanisms (e.g., “hallmarks” of aging), including chronic low-grade inflammation, mitochondrial dysfunction, cellular senescence and deregulated nutrient sensing contribute to excessive ROS production and are common to both peripheral and cerebral vascular dysfunction. Therefore, targeting these mechanisms to reduce ROS-related oxidative stress and improve peripheral and/or cerebral vascular function may be a promising strategy to reduce dementia risk with aging. Investigating how certain lifestyle strategies (e.g., aerobic exercise and diet modulation) and/or select pharmacological agents (natural and synthetic) intersect with aging “hallmarks” to promote peripheral and/or cerebral vascular health represent a viable option for reducing dementia risk with aging. 

“Therefore, the primary purpose of this review is to explore mechanistic links among peripheral vascular dysfunction, cerebral vascular dysfunction, and reduced brain health with aging. Such insight and assessments of non-invasive measures of peripheral and cerebral vascular health with aging might provide a new approach for assessing dementia risk in older adults.”

DOI - https://doi.org/10.18632/aging.205877

Corresponding authors - Devin Wahl - devin.wahl@colostate.edu, and Zachary S. Clayton - zachary.clayton@colorado.edu

Video short - https://www.youtube.com/watch?v=0gx9DklNZVM

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Keywords - aging, peripheral vascular health, cerebrovascular health, cognitive function, dementia

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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The Aging Brain and Peripheral Vascular Dysfunction

Werner syndrome (WS) is a rare genetic disorder marked by the premature onset of features typically associated with normal aging. This autosomal recessive condition manifests in individuals who generally develop normally until adolescence. As the syndrome progresses, affected individuals are predisposed to age-related diseases much earlier in life. These conditions include cataracts, type 2 diabetes, atherosclerosis, osteoporosis, and various cancers. The underlying cause of Werner syndrome is believed to be mutations in the WRN gene, which encodes a RecQ helicase crucial for DNA repair and replication.

Despite the accelerated aging, cognitive function remains unaffected in individuals with WS, providing a unique model for studying the mechanisms of aging and exploring potential therapeutic interventions. Although extensive research has been conducted, the precise mechanisms underlying these effects remain elusive.

On May 24, 2024, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval published research paper chosen as the cover of Aging’s Volume 16, Issue 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.” Recognizing the limitations of traditional investigative approaches, Aumailley et al. utilized advanced proteomics in their study. Proteomics allows the simultaneous identification and quantification of hundreds of proteins, providing a comprehensive analysis of liver and serum proteome profiles from wild-type and WRN mutant mice at different ages to uncover biological processes influenced by age and genotype.

Full blog - https://aging-us.org/2024/06/werner-syndrome-and-the-power-of-proteomics/

Paper DOI - https://doi.org/10.18632/aging.205866

Corresponding author - Michel Lebel - michel.lebel@crchudequebec.ulaval.ca

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Keywords - aging, proteomics, Werner syndrome, fatty liver, sexual dimorphism, immunoglobulins

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Werner Syndrome and the Power of Proteomics

A traditional, twice-monthly, peer-reviewed, open-access journal covering all areas of research on aging and age-related diseases, including cancer and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome.

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

Methionine Restriction Reverses Old-age Obesity in Mice

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