Η μείωση της πρωτεΐνης στη διατροφή βελτιώνει την υγεία και παρατείνει τη διάρκεια ζωής

Σύμφωνα με νέα ερευνητικά ευρήματα, η μείωση της ποσότητας πρωτεΐνης στη διατροφή παράγει μια σειρά από ευνοϊκά αποτελέσματα για την υγεία, συμπεριλαμβανομένης της επιμήκυνσης της διάρκειας ζωής, και αυτά τα αποτελέσματα εξαρτώνται από μια μεταβολική ορμόνη που προέρχεται από το ήπαρ που ονομάζεται Fibroblast Growth Factor 21.

Μια ενιαία ορμόνη κατευθύνει τις αντιδράσεις του σώματος στη δίαιτα χαμηλή σε πρωτεΐνη.

Τα ποντίκια ζουν περισσότερο και χάνουν βάρος ενώ τρώνε περισσότερο όταν υπάρχει η ορμόνη FGF21.

Μία μόνο ορμόνη φαίνεται να είναι υπεύθυνη για την παράταση της διάρκειας ζωής που παράγεται από μια δίαιτα χαμηλή σε πρωτεΐνες.

Μια νέα μελέτη από το Pennington Biomedical Research Center, που δημοσιεύτηκε πρόσφατα στο περιοδικό Επικοινωνίες για τη φύσηδιαπίστωσε ότι η μείωση της ποσότητας πρωτεΐνης στη διατροφή παρήγαγε μια σειρά από ευνοϊκά αποτελέσματα για την υγεία, συμπεριλαμβανομένης της επιμήκυνσης της διάρκειας ζωής, και ότι αυτά τα αποτελέσματα εξαρτώνται από μια μεταβολική ορμόνη που προέρχεται από το ήπαρ που ονομάζεται Αυξητικός Παράγοντας Ινοβλαστών 21 (FGF21).

[{” attribute=””>acid intake contributes to this beneficial effect. Several recent studies indicate that diets that are low in protein, but not so low that they produce malnutrition, can improve health. Conversely, overconsumption of high-protein diets has been linked to increased mortality in certain age groups.

A few years ago, Pennington Biomedical’s Neurosignaling Laboratory discovered that the metabolic hormone FGF21 was a key signal linking the body to the brain during protein restriction. Without this signal, young mice failed to change their feeding behavior or metabolism when placed on a low-protein diet.

“Our data suggest that FGF21 talks to the brain, and that without this signal the mouse doesn’t ‘know’ that it is eating a low-protein diet. As a result, the mouse fails to adaptively change its metabolism or feeding behavior,” said Christopher Morrison, Ph.D., Professor and Director of the Neurosignaling Lab.

Christopher Morrison and Cristal Hill

Christopher Morrison, Ph.D. and Cristal M. Hill, Ph.D.

The group’s newest work, led by postdoctoral researcher Cristal M. Hill, Ph.D., demonstrates that low-protein diets produce beneficial metabolic effects in aged mice, improving metabolic health, reducing frailty, and extending lifespan. These beneficial effects were also apparent when protein intake was reduced in middle-aged mice, even protecting against the detriments of obesity. Importantly, these beneficial effects were lost in mice that lacked FGF21, suggesting that its action in the brain is critical for the increase in health and lifespan.

“We previously showed that FGF21 acts in the brain to improve metabolic health in young mice fed a low-protein diet. These new data extend this work by demonstrating that FGF21 also improves metabolic health and extends lifespan. Collectively, these data provide clear evidence that FGF21 is the first known hormone that coordinates feeding behavior and metabolic health to improve lifespan during protein restriction,” Dr. Hill said.

However, Dr. Hill said several questions remain. It’s unclear exactly how these observations will translate to aging humans, but the hope is that this work will uncover novel molecular and neural pathways that can be leveraged to improve health in people.

“This groundbreaking research has important implications for extending the health and lifespan of people. If scientists can better understand how diets and nutritional hormones like FGF21 act to extend lifespan, these discoveries could offset many of the health issues that occur in middle age and later,” said Pennington Biomedical Executive Director John Kirwan, Ph.D.

Reference: “FGF21 is required for protein restriction to extend lifespan and improve metabolic health in male mice” by Cristal M. Hill, Diana C. Albarado, Lucia G. Coco, Redin A. Spann, Md Shahjalal Khan, Emily Qualls-Creekmore, David H. Burk, Susan J. Burke, J. Jason Collier, Sangho Yu, David H. McDougal, Hans-Rudolf Berthoud, Heike Münzberg, Andrzej Bartke and Christopher D. Morrison, 7 April 2022, Nature Communications.
DOI: 10.1038/s41467-022-29499-8

This work was supported by the National Institutes of Health grants R01DK105032, R01DK121370, R01DK123083, and F32DK115137. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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