Why does dietary restriction increase lifespan?

A study in the worm C. elegans suggests that regulating mitochondrial function by dietary restriction or genetic method can increase lifespan. The findings, available in this month's online edition of the journal Cell Metabolism, may lead to new drug targets for promoting healthy aging.

This work is conducted by researchers from Harvard T.H. Chan School of Public Health in collaboration with researchers from Duke University Medical Center.

Mitochondria are organelles found in the cytoplasm of every eukaryotic cell. The specialized organelles are best known for their role in energy production. All cells need energy to perform essential activities, such as growth, division, metabolism, and protein synthesis. Chemical energy is mainly stored in molecules like carbohydrates and fatty acids. Mitochondria metabolize or break down carbohydrates and fatty acids to generate energy to meet the cell's need. So, mitochondria are often referred to as the "power house" of eukaryotic cells.

In most cells, mitochondria continually change shape through the processes of fusion and fission, allowing the mitochondrial network to constantly remodel itself. This is the so-called mitochondrial dynamics, which affects mitochondrial function and quality. When mitochondrial dynamics is disrupted, cellular dysfunction happens, and even cell death occurs. Mitochondria are seen as an arbiter in the balance between cell life and death. Aging is associated with a decline in mitochondrial function, but the underlying mechanisms have not been fully understood.

For the current study, Dr. William Mair, associate professor of genetics and complex diseases at Harvard T.H. Chan School of Public Health, and coworkers employed C. elegans to investigate the relationship between mitochondrial network remodeling and longevity. To manipulate mitochondrial network remodeling in cells, the researchers restricted the worms' diet. They discovered that this type of dietary restriction increased the lifespan of the worms by maintaining mitochondrial network homeostasis and by modulating fatty acid metabolism. Besides, using a genetic method to mimic the effect of dietary restriction, the researchers found that genetic manipulation of the key metabolic regulator AMPK also promoted longevity in C. elegans.

AMPK, short for AMP-activated protein kinase, is an important enzyme, conserved from yeast to human. This enzyme is a master regulator of cellular and organismal metabolism in eukaryotes. It also modulates the transactivation of nuclear genes involved in mitochondrial biogenesis and function.

Collectively, these data suggest that dietary restriction and AMPK manipulation may promote healthy aging by modulating mitochondrial networks. The study sheds light on why dietary restriction increases lifespan. Identifying the underlying mechanisms will aid in the development of preventative and therapeutic strategies for aging-related disorders, according to Dr. Weir.

Consistent evidence has shown that dietary restriction or fasting possesses health-enhancing and anti-aging effects. For example, fasting leads to reduced weight loss and lower blood pressure and cholesterol in a variety of animal models. But why fasting induces so many benefits still remains largely unknown. A challenge for the future is to explore the association between mitochondrial networks and fasting-induced benefits, and to develop genetic and pharmacological interventions for aging-related disorders by modulating mitochondrial networks.
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