Abstract
To assess the effect of 4 weeks of high fat-high fructose feeding on whole body composition, energy balance, specific markers of oxidative stress and inflammation, and insulin sensitivity in the liver of middle-aged rats, rats (1 year) were fed a diet rich in saturated fatty acids and fructose (HFF rats), mimicking the “Western diet”, and compared with rats of the same age that were fed a low fat diet (LF rats). HFF rats exhibited a significant increase in the gain of body weight, energy, and lipids compared to LF rats. HFF rats also showed hepatic insulin resistance, together with an increase in plasma triglycerides, cholesterol, and tumor necrosis factor alpha. Hepatic lipids, triglycerides and cholesterol were higher in HFF rats, while a significant decrease in Stearoyl-CoA desaturase activity was found in this tissue. A marked increase in the protein amount of complex I, concomitant to a decrease in its contribution to mitochondrial respiration, was found in HFF rats. Lipid peroxidation and Nitro-Tyrosine content, taken as markers of oxidative stress, as well as NADPH oxidase activity, were significantly higher in HFF rats, while the antioxidant enzyme catalase decreased in these rats. Myeloperoxidase activity and lipocalin content increased, while peroxisome proliferator activated receptor gamma decreased in HFF rats. The present results provide evidence that middle-aged rats show susceptibility to a short-term “Western diet”, exhibiting altered redox homeostasis, insulin resistance, and early mitochondrial alterations in the liver. Therefore, this type of dietary habits should be drastically limited to pursue a “healthy aging”.
Highlights
In the last 20 years, gerontological research has produced significant progresses in the comprehension of the phenomenon of aging, opening the prospective that the symptoms and functional consequences of aging can be delayed, reduced, or perhaps eliminated [1]
One group of rats was euthanized at the beginning of the experiment for determination of initial values of body composition, while the other two groups were fed a high fat-high fructose (HFF) or low-fat diet (LF) for 4 weeks
Plasma concentrations of TNF-α were assessed as marker of systemic inflammation, and the results show that TNF-α was significantly increased in HFF rats compared to LF after 4 weeks of dietary treatment (Figure 1F)
Summary
In the last 20 years, gerontological research has produced significant progresses in the comprehension of the phenomenon of aging, opening the prospective that the symptoms and functional consequences of aging can be delayed, reduced, or perhaps eliminated [1]. It has been shown that the consumption of a high fat-high sugar diet, a common lifestyle factor especially in Western countries, may add to aging to alter cellular function [2,3]. Many studies have been performed on diet-induced impairment of liver function in animal models [4,5]. Middle-age, an earlier stage of the aging process, is a life phase in which animals are more exposed to develop diet-induced insulin resistance and liver dysfunction [6,7], few data are available on the impact of western diets on physiological responses at middle age [7,8,9], despite the fact that obesity is more. Among the organs that are more prone to oxidative damage, the liver is deeply involved in the onset of metabolic disorders, including insulin resistance [12], due to its major role in the regulation of systemic lipid and glucose homeostasis [13,14]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
