Nutritional Benchmarking: A Top Priority
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 10, Issue 1
Abstract
In the world of nutritional science, more and more studies have been performing for the last years with interesting results; nevertheless, at the moment outcomes of these studies do not provide consistent benchmarks that may use to build a nutritional plan or to lead further researches. Contrasting evidence represents an important drawback in this field creating a confusing background; indeed, these conflictual aspects concern the majority of topics in nutritional science. When attention is focused on total daily caloric intake, protein daily intake and daily carbohydrate (CHO)/ fat ratio, it is possible to observe a great discordance of evidence. As regards total daily caloric intake, recent evidence shows that a daily reduction of 20-30% of caloric intake may significantly increase life span; in particular, this increased longevity seems to be confirmed in animal models whereas in humans long-term studies are not present at the moment to confirm this hypothesis [1-3]. Considering that actual dietary guidelines suggest approximately 2000 kcal/die diet for a man of ~70 kg, a reduction of 20-30% of daily caloric intake would be represented by a nutritional plan of ~1400 kcal/d for a man of ~70 kg [4-6]. Several mechanisms have been proposed to explain this evidence, and the reduction of mitogen stimuli caused at least partly by decreased hormonal levels, such as insulin, insulin-growth factor 1 (IGF-1), and testosterone appears to play a pivotal role [78]. This decrease in hormonal production affects also negatively the activity of mitogen pathways, such as mammalian target of rapamycin (mTOR) signalling pathway activated by insulin and FOXO a key checkpoint gene in the insulin-IGF-1 signaling pathway upregulated by CR[9]. Furthermore, caloric restriction (CR) seems to mimic physical exercise activating biological pathways which are stimulated by physical exercise, such as AMP-activated protein kinase (AMPK) signalling pathways, and to increase sirtuin levels [10] . In particular, the ability of sirtuins to influence metabolism and potentially life span is believed to revolve around the ability of sirtuin family members to function as protein deacetylases. Evidence suggests that mitochondrial biogenesis is regulated at least in part by proliferator-activated receptor coactivator-1a (PGC-1a), a transcriptional coactivator of peroxisome proliferator- activated receptor-y (PPARy) as well as other transcription factors [11] . It was therefore of considerable interest when it was shown that PGC-1a was in fact a deacetylation target of Sirt1 and that mechanism regulated PGC-1a activity [12].
Authors and Affiliations
Massimiliano Sansone, Andrea Sansone, Elena Gangitano, Mariagrazia Romano, Silvia Seraceno, Francesco Romanelli
Keywords
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- EP ID EP591849
- DOI 10.26717/BJSTR.2018.10.001893
- Views 166
- Downloads 0
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