FGF21 is one of the targets for potential pharmaceutical intervention to modestly slow aging that has emerged from the past decades of research into calorie restriction. Evidence suggests that there are significant differences between mice and humans in levels of FGF21 in response to aging and calorie restriction, however. A fair amount of this research is focused on obesity as a condition, rather than or in addition to aging, as FGF21 appears to be involved in the mechanisms that determine weight gain in response to diet. The paper noted here suggests that FGF21 has quite different behavior in these two circumstances. This and the general tenor of other research from the past few years combines to make this is a much less attractive area of work for anyone intending to build novel calorie restriction mimetic therapies.
Pharmacological treatment with FGF21 ameliorates age-related metabolic disorders such as insulin resistance, dyslipidemia, and obesity in rodents, and pilot studies in humans indicate that treatment with an FGF21-analog has beneficial effects on hyperlipidemia and body weight. Sustained increases in FGF21 levels attained by transgenic overexpression of FGF21 extend the lifespan of
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