Abstract
SummaryCalorie restriction (CR) has been repeatedly shown to prevent cancer, diabetes, hypertension, and other age‐related diseases in a wide range of animals, including non‐human primates and humans. In rodents, CR also increases lifespan and is a powerful tool for studying the aging process. Recently, it has been reported in mice that dietary fat plays an important role in determining lifespan extension with 40% CR. In these conditions, animals fed lard as dietary fat showed an increased longevity compared with mice fed soybean or fish oils. In this paper, we study the effect of these dietary fats on structural and physiological parameters of kidney from mice maintained on 40% CR for 6 and 18 months. Analyses were performed using quantitative electron microcopy techniques and protein expression in Western blots. CR mitigated most of the analyzed age‐related parameters in kidney, such as glomerular basement membrane thickness, mitochondrial mass in convoluted proximal tubules and autophagic markers in renal homogenates. The lard group showed improved preservation of several renal structures with aging when compared to the other CR diet groups. These results indicate that dietary fat modulates renal structure and function in CR mice and plays an essential role in the determination of health span in rodents.
Highlights
Aging can be defined as a time-dependent degenerative process caused by accumulated damage that leads to cell dysfunction, tissue failure, and Accepted for publication 10 January 2016 death (Campisi, 2013)
Mice sequentially lost weight in the CRS compared to the control (CON) group and there were no differences between calorie restriction (CR) groups at either 6 or 18 months (Table 1)
A similar result was found for serum urea levels, which were decreased in the CRS group at both time periods
Summary
Aging can be defined as a time-dependent degenerative process caused by accumulated damage that leads to cell dysfunction, tissue failure, and Accepted for publication 10 January 2016 death (Campisi, 2013). The action of free radicals (many of them produced at the mitochondria) may contribute to aging, the mechanisms through which this occurs are still not entirely known. Several hallmarks have been proposed to explain the molecular and physiological basis of aging and mitochondrial dysfunction seems to play a central role in this process (Lopez-Otın et al, 2013; GonzalezFreire et al, 2015). The mechanisms by which CR operates are not completely understood, it is often assumed that the anti-aging action of CR is partially based on its ability to suppress oxidative stress and maintain the cellular redox status to provide optimal cell signaling processes and normal gene expression (Chung et al, 2013). CR has been proposed to induce biogenesis of efficient mitochondria (Lopez-Lluch et al, 2008)
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