Document Type

Journal Article

Publisher

Scientific Research Publishing

School

School of Medical Sciences/Centre of Excellence in Alzheimer's Disease Research and Care

RAS ID

21732

Comments

Originally published as: Martins, I. J. (2016). Anti-aging genes improve appetite regulation and reverse cell senescence and apoptosis in global populations. Advances in Aging Research, 5(1), 9-26. Original article available here

Abstract

Appetite regulation by nutritional intervention is required early in life that involves the anti-aging gene Sirtuin 1 (Sirt 1) with Sirt 1 maintenance of other cellular anti-aging genes involved in cell circadian rhythm, senescence and apoptosis. Interests in anti-aging therapy with appetite regulation improve an individual’s survival to metabolic disease induced by gene-environment interactions by maintenance of the anti-aging genes connected to the metabolism of bacterial lipopolysaccharides, drugs and xenobiotics. Interventions to the aging process involve early calorie restriction with appetite regulation connected to appropriate genetic mechanisms that involve mitochondrial biogenesis and DNA repair in neurons. In the aging process as the anti-aging genes are suppressed as a result of transcriptional dysregulation chronic disease accelerations and connected to insulin resistance, non-alcoholic fatty liver disease (NAFLD) and neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Interests in the gene-environment interaction indicate that the anti-aging gene Sirt 1 that regulates food intake has been repressed early in the aging process in various global populations. The connections between Sirt 1 and other anti-aging genes such as Klotho, p66Shc (longevity protein) and Forkhead box proteins (FOXO1/ FOXO3a) have been associated with programmed cell death and alterations in these anti-aging genesregulate glucose, lipid and amyloid beta metabolism that are important to various chronic diseases.

DOI

10.4236/aar.2016.51002

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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