Low protein diet improves mitochondrial function

[Plasma]

A dietary regimen that is the opposite of the high protein Atkins diet was associated with a longer lifespan and improved mitochondrial function in research conducted with flies at the Buck Institute for Age Research in Novato, California. Reduced functioning of the mitochondria, which are the power plants of the cells, occurs with aging and is associated with such diseases such as type 2 diabetes and Parkinson's disease.

In the October 2, 2009 issue of the journal Cell, Pankaj Kapahi, PhD and colleagues identify the mechanism of the extension of life span observed in flies whose diets were modified by lowering the level of yeast relative to sucrose (the source of carbohydrates in the flies' diets). By examining the expression of genes in restricted flies, Dr Kapahi and his associates found that, although protein synthesis was reduced on a global level, the activity of specific genes involved in the production of energy within the mitochondria increased. According to Dr Kapahi, this activity, which occurs at the level of conversion of RNA to protein, is involved in dietary restriction's protective effects. Flies receiving low protein diets showed increased activity of a protein known as d4EBP, which is part of a signaling pathway called TOR (target of rapamycin) that influences cell growth in response to the availability of nutrients. (Rapamycin, a drug that has many medical uses, was recently shown to increase the lifespan of aged mice.) While flies on a low protein diet experienced a significant extension of lifespan compared to flies whose diets were nonrestricted, knocking out the gene for d4EBP diminished the effect, and restoring d4EBP expression enhanced it.

The findings question the wisdom of popular high protein weight loss diets. "In flies, we see that the long-lived diet is a low protein diet and what we have found here is a mechanism for how that may be working." Dr Kapahi stated.

The study is the first genome-wide investigation of how proteins are translated in dietary restricted organisms. "Our study shows that dietary restriction can enhance mitochondrial function hence offsetting the age-related decline in its performance," Dr Kapahi concluded. "There have been correlative studies that show mitochondria change with dietary restriction; this research provides a causal relationship between diet and mitochondrial function."

http://www.lef.org/newsletter/2009/1013 ... =0#article

Glups !

[Free]

Qui a dit que la muscu était bon pour la santé ?

[Persephone]

L'étude parle surtout d'espérance de vie. C'est différent de l'état de santé.

Mais c'est comme la restriction calorique pour allonger l'espérance de vie: c'est au prix de ne pas avoir de libido, avoir tout le temps froid, flirter avec la dépression, etc.

Là c'est au prix de ne pas avoir de muscle ou très peu, surtout de ne pas pouvoir en prendre, d'avoir un système immunitaire fragile, etc.

[Nutrimuscle-Conseils]

de mémoire, ça concerne des mouches

[icelove]

puis à quoi bon être centenaire ?

[Persephone]

puis à quoi bon être centenaire ?

Ça fait marcher l'industrie de la couche.

[icelove]

de mémoire, ça concerne des mouches

bingo : "in research conducted with flies"

[Alban]

Puisque les mouches vivent plus longtemps quand on remplace une partie de leur protéines par du sucre,

lowering the level of yeast relative to sucrose (the source of carbohydrates in the flies' diets)

Nutrimuscle pourrait proposer du sucre de table, pour ceux qui veulent vivre plus longemps (sic), et continuer à proposer des protéines pour ceux qui veulent du muscle

[Plasma]

C'est parfait ! Je constate avec bonheur que les spécialistes ont fait toutes les réfléxions que je m'étais faites. Me voilà donc rassuré !

[Alban]

Je sais que ça te fera plaisir

Alzheimer's researchers find high protein diet shrinks brain

One of the many reasons to pick a low-calorie, low-fat diet rich in vegetables, fruits, and fish is that a host of epidemiological studies have suggested that such a diet may delay the onset or slow the progression of Alzheimer's disease (AD). Now a study published in BioMed Central's open access journal Molecular Neurodegeneration tests the effects of several diets, head-to-head, for their effects on AD pathology in a mouse model of the disease. Although the researchers were focused on triggers for brain plaque formation, they also found that, unexpectedly, a high protein diet apparently led to a smaller brain. A research team from the US, Canada, and the UK tested four differing menus on transgenic mouse model of AD, which express a mutant form of the human amyloid precursor protein (APP). APP's role in the brain is not fully understood; however it is of great interest to AD researchers because the body uses it to generate the amyloid plaques typical of Alzheimer's. These mice were fed either (1) a regular diet, (2) a high fat/low carbohydrate custom diet, (3) a high protein/low carb version or (4) a high carbohydrate/low fat option. The researchers then looked at the brain and body weight of the mice, as well as plaque build up and differences in the structure of several brain regions that are involved in the memory defect underlying AD.

Unexpectedly, mice fed a high protein/low carbohydrate diet had brains five percent lighter that all the others, and regions of their hippocampus were less developed. This result was a surprise, and, until researchers test this effect on non-transgenic mice, it is unclear whether the loss of brain mass is associated with AD-type plaque. But some studies in the published literature led the authors to put forward a tentative theory that a high protein diet may leave neurones more vulnerable to AD plaque. Mice on a high fat diet had raised levels of plaque proteins, but this had no effect on plaque burden.

Aside from transgenic mice, the pressing question is whether these data have implications for the human brain. "Given the previously reported association of high protein diet with aging-related neurotoxicity, one wonders whether particular diets, if ingested at particular ages, might increase susceptibility to incidence or progression of AD," says lead author, Sam Gandy, a professor at The Mount Sinai School of Medicine in New York City and a neurologist at the James J Peters Veterans Affairs Medical Center in the Bronx NY. The only way to know for sure would require prospective randomised double blind clinical diet trials. According to Gandy, "This would be a challenging undertaking but potentially worthwhile. If there is a real chance that the ravages of AD might be slowed or avoided through healthy eating. Such trials will be required if scientists are ever to make specific recommendations about dietary risks for AD."

[pat g]

C'est pour cela que, par moment, je ne trouve plus mon pot de prot

[Plasma]

Je sais que ça te fera plaisir

C'est pas une question de "faire plaisir".

C'est essayer de comprendre un tout petit peu les choses et de garder une certaine ouverture. C'est aussi trouver pourquoi une étude est bidon quand elle l'est. Je te remercie pour l'étude. Bon, c'est sur des souris transgéniques et apparemment le mécanisme n'est pas clair. Il y aussi des études qui indiquent que certains lipides sont mauvais pour le cerveau et idem pour les glucides. Une vieille chatte n'y retrouverait pas ses petits.