La réduction des protéines dans le régime alimentaire améliore la santé et prolonge la durée de vie

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Selon les résultats d’une nouvelle recherche, la réduction de la quantité de protéines dans l’alimentation produit une série de résultats favorables pour la santé, y compris une extension de la durée de vie, et ces effets dépendent d’une hormone métabolique dérivée du foie appelée facteur de croissance des fibroblastes 21.

Une seule hormone dirige les réponses du corps à un régime pauvre en protéines.

Les souris vivent plus longtemps et perdent du poids tout en mangeant plus lorsque l’hormone FGF21 est présente.

Une seule hormone semble être responsable de l’extension de la durée de vie produite par un régime pauvre en protéines.

Une nouvelle étude du Pennington Biomedical Research Center, publiée récemment dans le journal Nature Communicationsa révélé que la réduction de la quantité de protéines dans le régime alimentaire produisait une série de résultats favorables pour la santé, y compris une extension de la durée de vie, et que ces effets dépendaient d’une hormone métabolique dérivée du foie appelée facteur de croissance des fibroblastes 21 (FGF21).

Il est reconnu depuis longtemps que réduire la quantité de nourriture consommée améliore la santé et prolonge la durée de vie, et l’on s’intéresse de plus en plus à la possibilité que la réduction des protéines ou des acides aminés 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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