The research has focused on low-calorie diets and whether there is any relationship between this type of diet and healthy aging. For this, the scientists involved undertook to examine the energy sensing processes in animals. In this case they turned to the nematode worm Caenorhabditis elegans. This worm has been used in several anatomical studies, such as shaping immune responses.
Previous research using C. elegans had shown that limiting food intake (“caloric restriction”) seems to improve so-termed metabolic dysfunction, which seems to be linked to healthy aging.
The recent experiment has advanced this further, showing that in addition to caloric restriction certain parts of the central nervous system could be used to stimulate the same effect as the low-calorie diet, without the need for eating habits to be changed. Specifically the study focused on a molecule termed “AMP-activated protein kinase.” This molecule functions acts as a molecular fuel gauge and it detects energy levels.
One thing that AMP-activated protein kinase does is to slowdown the the activity of a protein termed CRTC-1. This protein is found in neurons and, through varying the production of a neurotransmitter, it affects the activity of mitochondria (which control and produce energy in cells.).
By playing around with AMP-activated protein kinase, the researchers were able to override its ability to influence the metabolism. This, in turn, affected longevity in tissues (making the aging process healthier.)
In short, it would seem that the aging process is influenced by what animals perceive they were eating than what they actually eat. The implications, should the results be one day reproducible in people, is that manipulating the energy-sensing metabolic pathway could trigger people to perceive that their cells are in a low-energy state, even when they are eating normally. This may then influence age-related diseases like cancer.
The findings have been published in the science journal Cell. The research paper is titled “Neuronal CRTC-1 Governs Systemic Mitochondrial Metabolism and Lifespan via a Catecholamine Signal.”
