Researchers at the Salk Institute found a diet high in fat may provide benefits for human patients suffering with mitochondrial disease.
A study reported in the Proceedings of the National Academy of Sciences investigated mice populations born with thousands of mutations in their mitochondrial DNA, and revealed how a hormone normally associated with longevity may aid in metabolic homeostasis in early years.
Ronald Evans, Director of Salk’s Gene Expression Laboratory, claimed the work could pave the way for new clinical interventions for those suffering with obesity and other metabolic disorders.
“These findings help us understand the link between diet, health and aging, and they give us the potential to dissect these connections in a molecular way that could lead to therapeutics,” the author of the new study published June 29, 2015 said.
Mice with the metabolic disease normally display the usual traits of ageing, such as thinning hair, poor hearing, heart problems and infertility, according to bioidentical hormone doctors. However, when scientists studied the mice, they found that the longevity-promoting endocrine hormone FGF21 was highly active, even though the mice showed the classic hallmarks of accelerated aging.
“FGF21 is classically thought of as an anti-aging gene, turned on by exercise or fasting and suspected to extend lifespan,” says Christopher Wall, first author of the new paper and a graduate student in the Evans lab at the time of the study. “Yet these mice ultimately age prematurely, despite having high levels of this hormone.”
To resolve this paradox, researchers found that the FGF21gene reprogrammed the metabolic condition of the mice, and altered tissues with crucial metabolic functions from burning sugar for fuel to burning fat instead. This change aided their metabolism as fat is an easier fuel for the damaged mitochondria to process.
The observation means that increasing dietary fat intake could ease some sufferer’s symptoms, or using drugs which stressed the mitochondria could activate beneficial metabolic shift in patients living with a metabolic disorder.
Michael Downes, a senior staff scientist at Salk, believes that “can manipulate this dynamic in different ways” to investigate further “the interaction between FGF21 and dietary fat in human patients.”