Abstract
Caloric restriction (CR) represents a powerful intervention for extending healthspan and lifespan in several animal models, from yeast to primates. Additionally, in humans, CR has been found to induce cardiometabolic adaptations associated with improved health. In this study, we evaluated in an aged and obese rat model the effect of long-term (6 months) caloric restriction (−40%) on the oxidative/inflammatory balance in order to investigate the underlining mechanisms. In plasma, we analyzed the oxidative balance by photometric tests and the adiponectin/tumor necrosis factor-α-induced gene/protein 6 (TSG-6) levels by Western blot analysis. In the white adipose tissue, we examined the protein levels of AdipoR1, pAMPK, NFκB, NRF-2, and glutathione S-tranferase P1 by Western blot analysis. Our results clearly showed that caloric restriction significantly improves the plasmatic oxidative/inflammatory balance in parallel with a major increase in circulating adiponectin levels. Additionally, at the level of adipose tissue, we found a positive modulation of both anti-inflammatory and antioxidant pathways. These adaptations, induced by caloric restriction, with the achievement of normal weight, suggest that inflammatory and redox imbalance in obese aged rats appear to be more linked to obesity than to aging.
Highlights
Obesity prevalence is constantly growing worldwide in all age groups and represents a serious publichealth problem, given its close correlation with several chronic diseases [1,2]
We evaluated theevaluated plasmatic plasmatic protein levels of tumor necrosis factor-α-induced gene/protein 6 (TSG-6), a multifunctional protein associated with inflammation
To analyze the oxidative imbalance linked to obesity detected at the plasma level, we evaluated two important cytoplasmatic antioxidant enzymes, SOD1 and GSTP1, in adipose tissue
Summary
Obesity prevalence is constantly growing worldwide in all age groups and represents a serious publichealth problem, given its close correlation with several chronic diseases [1,2]. Lines of evidence from several studies have shown that obesity adversely affects health status and life span through cellular processes in a manner similar to aging, and the link between these processes appears to be adiponectin [3,4]. This adipokine, mainly secreted from adipocytes, modulates a number of metabolic processes and represents a key molecule in maintaining the functionality of many organs [22]; it is involved in the development and progression of several obesity-related malignancies such as breast cancer [23,24]. Since the use of old animals is very important to phenocopy the systemic aging context, we used an elderly and obese rat model, a useful model that mimics the weight gain due to aging that occurs in humans
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