Calorie restriction delays cardiac senescence and improves cardiac function in obese diabetic rats
- PDF / 1,007,663 Bytes
- 9 Pages / 595.276 x 790.866 pts Page_size
- 49 Downloads / 195 Views
Calorie restriction delays cardiac senescence and improves cardiac function in obese diabetic rats Naoki Makino1 · Toyoki Maeda1 Received: 16 July 2020 / Accepted: 2 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract The aims of this study were to investigate the impact of caloric restriction (CR) on cardiac senescence in an animal model of diabetes and examine the signal transduction mechanisms for changes in cell survival as well as cardiac function. Male 8-week-old Otsuka Long-Evans Tokushima fatty (OLETF) diabetic rats were divided into 2 groups: a group fed ad libitum (AL), and a group fed with CR (30% energy reduction). Long-Evans Tokushima Otsuka (LETO) non-diabetic rats were used as controls. LETO rats were divided into 3 groups: a high fat diet (HFD) group with a 22% increase in caloric intake, a CR group, and a group fed AL. At 40 weeks of age, the telomere length was significantly shorter in the heart tissue of HFD rats but was not altered by CR in experimental rats with or without CR, however, telomerase activity in both strains of CR rats was significantly elevated. Protein expression of IGF-1, Sirt 1 and phospho-FoxO1 was increased in both CR groups. Echocardiography showed that CR preserved LV diastolic function with a significantly shorter E-wave deceleration time and a greater E/A ratio compared with the AL groups. These findings suggest that CR protocol increased telomerase activity without changing of telomere length, enhanced autophagy and improved LV diastolic function in animal model of diabetes rats. It is finally suggested that those impacts may be important for the maintenance of normal cardiac function and for delayed cardiac aging. Keywords Telomere · Calorie restriction · Diabetes · Autophagy · Diastolic function · Signal transduction
Introduction Caloric restriction (CR) in primates, delays the onset of some age-related diseases such as cancer, atherosclerosis, diabetes, neurodegeneration and respiratory failure [1, 2] so-called ‘Extension of healthy longevity’. At the metabolic level, CR leads to improved insulin sensitivity and reduced fasting blood glucose, protecting from age-dependent metabolic syndrome and diabetes [2]. Human CR also reduces risk factors for cardiovascular disease and cancer [3], but has been reported to adversely affect bone mineral density and muscle mass [4, 5]. The exact mechanism by which CR functions is currently being debated, but the most common theory is that DNA damage decreases with decreasing metabolism [6]. A well-documented link between telomere * Naoki Makino [email protected] 1
Division of Cardiology and Clinical Gerontology, Department of Internal Medicine, Beppu Hospital, Kyushu University, 4546 Tsurumihara, Beppu 874‑0838, Japan
shortening and aging suggests a possible role for telomere dynamics in the systemic effects of CR. One mechanism for the beneficial effects of CR is attenuation of mitochondrial dysfunction in different disease conditions [7]. Several studies have now demonstrated th
Data Loading...
