Energy restriction (ER), without malnutrition, increases maximum life span and retards the development of a broad array of pathophysiological changes in laboratory rodents. The mechanism responsible for the retardation of aging by ER is, however, unknown. One proposed explanation is a reduction in energy expenditure (EE). Reduced EE may increase life span by decreasing the number of oxygen molecules interacting with mitochondria, thereby lowering reactive oxygen species (ROS) production. As a step toward testing this hypothesis, it is important to determine the effect of ER on EE.
OBJECTIVE: To determine whether there is a difference in risk-factor improvement for coronary heart disease (CHD) between the intra-abdominal fat (IF) and subcutaneous fat (SF) obesity phenotypes after weight loss. RESEARCH METHODS AND PROCEDURES: Subjects included 55 mildly obese women (body mass index, 25 to 36 kg/m(2); age range, 34 to 63 years) who had at least two of three CHD risk factors [systolic blood pressure (SBP), >140 mm Hg; total cholesterol (TC), >220 mg/dL; fasting plasma glucose, >110 mg/dL).
OBJECTIVE: To determine whether "low-intensity" exercise (walking) and "high-intensity" exercise (aerobic dance), when added to a weight loss diet, have different effects on coronary heart disease (CHD) risk factors and physical fitness. RESEARCH METHODS AND PROCEDURES: Ninety obese women were divided into diet only (DO), diet plus walking (DW), and diet plus aerobic dance (DA) groups. DXA was used to evaluate segmental body composition. Leg-extension strength and maximal oxygen uptake (VO2max) were the indicators of physical fitness.
Diminished mitochondrial oxidative phosphorylation and aerobic capacity are associated with reduced longevity. We tested whether resveratrol (RSV), which is known to extend lifespan, impacts mitochondrial function and metabolic homeostasis. Treatment of mice with RSV significantly increased their aerobic capacity, as evidenced by their increased running time and consumption of oxygen in muscle fibers.
American Journal of Physiology. Endocrinology and Metabolism
Adiponectin, a physiologically active polypeptide secreted by adipocytes, shows insulin-sensitizing, anti-inflammatory, and antiatherogenic properties in rodents and humans. To assess the effects of chronic hyperadiponectinemia on metabolic phenotypes, we established three lines of transgenic mice expressing human adiponectin in the liver.
Caloric restriction (CR) extends lifespan in most animals, but the mechanisms underlying this phenomenon are the subject of much debate. We investigated the association between longevity and resting metabolic rate (RMR) in Indian stick insects (Carausius morosus) by (i) determining the appropriate scaling coefficient for calculating mass-corrected RMR of insects throughout development, (ii) quantifying the response of RMR to diet history, and (iii) correlating RMR in multiple life-history stages with adult and total lifespan.
We have previously shown that autophagy is required for chronological longevity in the budding yeast Saccharomyces cerevisiae. Here we examine the requirements for autophagy during extension of chronological life span (CLS) by calorie restriction (CR). We find that autophagy is upregulated by two CR interventions that extend CLS: water wash CR and low glucose CR. Autophagy is required for full extension of CLS during water wash CR under all growth conditions tested.
Studies in mutant, gene knock-out and transgenic mice have demonstrated that growth hormone (GH) signalling has a major impact on ageing and longevity. Growth hormone-resistant and GH-deficient animals live much longer than their normal siblings, while transgenic mice overexpressing GH are short lived. Actions of GH in juvenile animals appear to be particularly important for life extension and responsible for various phenotypic characteristics of long-lived hypopituitary mutants.