Jamie whyte salk

This work provides insight into potential new therapies for mitochondrial and metabolic diseases in humans. When Evans and collaborators studied these mice, they found that the longevity-promoting endocrine hormone FGF21 was highly active, even though these mice display hallmarks of accelerated aging. To explain this paradox, the team found that FGF21 actually assists stressed mitochondria and reprograms the metabolic state of these mice.

In the paper, Evans and collaborators describe how FGF21 appears to switch tissues with important metabolic functions from burning sugar to burning fat—which is easier fuel for the dysfunctional mitochondria to process.

In young but rapidly aging mice, high-fat diet feeding right ramps up heat production and metabolic activity relative to cooler mice fed a normal chow diet left. Click here for a high-resolution image.

The new observation has the potential to impact human health in multiple ways, says Evans. Elevated FGF21 levels have previously been observed in people with mitochondrial diseases, so increasing dietary fat intake could potentially ease their symptoms by helping the hormone reduce the strain on the mitochondria. Johan W.

Olefsky , Handle: RePEc:nat:nature:vyid More about this item Statistics Access and download statistics. Corrections All material on this site has been provided by the respective publishers and authors. Louis Fed.

Help us Corrections Found an error or omission? RePEc uses bibliographic data supplied by the respective publishers. The air sacs white in the alveoli on the left, which were taken from a normal mouse, have expanded fully, indicating the animal could breath normally. Those on the right have failed to expand, because the mouse suffered from a new respiratory syndrome discovered by Salk scientists.

Unlike type 2 pneumocytes, which mature rapidly in infants given steroid hormone, the type 1 cells failed to respond to steroid treatment and the mice died due to the inability of their lungs to function. However, mice treated with the medications propylthiouracil or methimazole, normally given to people with thyroid disease, recovered from the disorder and their type 1 cells matured normally.

The genetic make up of mice and humans is very similar, so the researchers are optimistic that their findings will eventually lead to new treatments for infants with RDS. He cautioned, however, that the thyroid drugs used in the study are only approved for adults, and that their use in infants would have to be explored with caution.

However, because their properties are well known there is clear potential for their use in infants.