Seminar in Biological Mechanisms of Aging and Cancer/Deregulated Nutrient Sensing

An attempt at a graphical abstract outlining the regulatory effects of Pten on the P13K/Akt/FOXO pathway that influences metabolism and longevity in the model organism, as shown by the research of Oretega-Molina, et. al (2012).

In the hallmarks of aging review, written by López-Otín et. al, there is an extensive summary of the nine hallmarks of aging, which are categorized based on various cellular occurrences that contribute to aging. Nutrient sensing is a cellular process within an organism that ensures proper levels of nutrition for optimal metabolic function. Over time this cellular process that monitors and regulates nutrition will become damaged and unable to function properly. Metabolic activities stress and damage cells over time due to oxidative stress, ER stress, and mitochondrial dysfunction. Thus, the hallmark of aging known as deregulated nutrient sensing, describes the process by which these deregulated nutrient sensing pathways, which are intended to deal with the checks and balances of nutrition, can dramatically alter metabolism in that particular organism. Drastic changes in metabolism often result in obesity, diabetes, other metabolic diseases, and aging.

Through research conducted by Ortega-Molina, A. et. al, it becomes clear how strict regulation of a nutrient sensing pathway leads to longevity in the model organism. In this study Ortega-Molina et. al, explore the overall effects of the moderate over-expression of a tumor suppressor gene known as Pten in a transgenic mouse model. They wanted to understand how this tumor suppressor gene could influence these transgenic mice, other than lowering the incidence of cancer. Therefore, in the transgenic mouse model they genetically modified the mice to slightly over express the Pten gene, which would express two times more than the wild-type control mice. Overall, this over expression of Pten caused a nutrient sensing pathway known as P13K/Akt/FOXO to be down-regulated. This had tremendous effects on the overall metabolism on the transgenic mice and resulted in hyperactive adipose tissue, increased energy expenditure, decreased insulin resistance and decreased metabolic damage. All of these results essentially created a greater regulation of this pathway and caused the transgenic mice to live longer than the wild-type control mice. Overall, it was concluded that altering this pathway that would otherwise become deregulated over time and cause metabolic damage, in fact extended life span in the model organism. --Amberg11 (discuss • contribs) 01:03, 6 March 2017 (UTC)