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Abstract
Communities eating a western-like diet, rich in fat, sugar and significantly deprived
of fibers, share a relevant increased risk of both metabolic and cancerous diseases.
Even more remarkable is that a low-fiber diet lacks some key components—as phytates
and inositols—for which a mechanistic link has been clearly established in the pathogenesis
of both cancer and metabolic illness. Reduced bioavailability of inositol in living
organisms could arise from reduced food supply or from metabolism deregulation. Inositol
deregulation has been found in a number of conditions mechanistically and epidemiologically
associated to high-glucose diets or altered glucose metabolism. Indeed, high glucose
levels hinder inositol availability by increasing its degradation and by inhibiting
both myo-Ins biosynthesis and absorption. These underappreciated mechanisms may likely
account for acquired, metabolic deficiency in inositol bioavailability.
In older women and men, greater intakes of dietary calcium, potassium, and total fluid reduce the risk of kidney stone formation, while supplemental calcium, sodium, animal protein, and sucrose may increase the risk. Recently, phytate has been suggested to play a role in stone formation. To our knowledge, no prospective information on the role of dietary factors and risk of kidney stone formation is available in younger women. We prospectively examined, during an 8-year period, the association between dietary factors and the risk of incident symptomatic kidney stones among 96 245 female participants in the Nurses' Health Study II; the participants were aged 27 to 44 years and had no history of kidney stones. Self-administered food frequency questionnaires were used to assess diet in 1991 and 1995. The main outcome measure was an incident symptomatic kidney stone. Cox proportional hazards regression models were used to adjust simultaneously for various risk factors. We documented 1223 incident symptomatic kidney stones during 685 973 person-years of follow-up. After adjusting for relevant risk factors, a higher dietary calcium intake was associated with a reduced risk of kidney stones (P =.007 for trend). The multivariate relative risk among women in the highest quintile of intake of dietary calcium compared with women in the lowest quintile was 0.73 (95% confidence interval, 0.59-0.90). Supplemental calcium intake was not associated with risk of stone formation. Phytate intake was associated with a reduced risk of stone formation. Compared with women in the lowest quintile of phytate intake, the relative risk for those in the highest quintile was 0.63 (95% confidence interval, 0.51-0.78). Other dietary factors showed the following relative risks (95% confidence intervals) among women in the highest quintile of intake compared with those in the lowest quintile: animal protein, 0.84 (0.68-1.04); fluid, 0.68 (0.56-0.83); and sucrose, 1.31 (1.07-1.60). The intakes of sodium, potassium, and magnesium were not independently associated with risk after adjusting for other dietary factors. A higher intake of dietary calcium decreases the risk of kidney stone formation in younger women, but supplemental calcium is not associated with risk. This study also suggests that some dietary risk factors may differ by age and sex. Finally, dietary phytate may be a new, important, and safe addition to our options for stone prevention.
Cells regulate the biophysical properties of their membranes by coordinated synthesis of different classes of lipids. Here, we identified a highly dynamic feedback mechanism by which the budding yeast Saccharomyces cerevisiae can regulate phospholipid biosynthesis. Phosphatidic acid on the endoplasmic reticulum directly bound to the soluble transcriptional repressor Opi1p to maintain it as inactive outside the nucleus. After the addition of the lipid precursor inositol, this phosphatidic acid was rapidly consumed, releasing Opi1p from the endoplasmic reticulum and allowing its nuclear translocation and repression of target genes. Thus, phosphatidic acid appears to be both an essential ubiquitous metabolic intermediate and a signaling lipid.
[2
]Department of Surgery “Pietro Valdoni”, Sapienza University of Rome, Via Antonio Scarpa
14, 00161 Rome, Italy;
alessandra.cucina@
123456uniroma1.it
[3
]Department of Medical Sciences, IPUS-Institute of Higher Education, 5250 Chiasso,
Switzerland;
vunfer@
123456gmail.com
[4
]Policlinico Umberto I, viale del Policlinico 155, 00161 Rome, Italy
Licensee MDPI, Basel, Switzerland. This article is an open access article distributed
under the terms and conditions of the Creative Commons Attribution (CC BY) license
(
http://creativecommons.org/licenses/by/4.0/).
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