The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes

Organisms have evolved to survive rigorous environments and are not prepared to thrive in a world of caloric excess and sedentary behavior. A realization that physical exercise (or lack of it) plays a pivotal role in both the pathogenesis and therapy of type 2 diabetes mellitus (t2DM) has led to the provocative concept of therapeutic exercise mimetics. A decade ago, we attempted to simulate the beneficial effects of exercise by treating t2DM patients with 3 weeks of daily hyperthermia, induced by hot tub immersion. The short-term intervention had remarkable success, with a 1 % drop in HbA1, a trend toward weight loss, and improvement in diabetic neuropathic symptoms. An explanation for the beneficial effects of exercise and hyperthermia centers upon their ability to induce the cellular stress response (the heat shock response) and restore cellular homeostasis. Impaired stress response precedes major metabolic defects associated with t2DM and may be a near seminal event in the pathogenesis of the disease, tipping the balance from health into disease. Heat shock protein inducers share metabolic pathways associated with exercise with activation of AMPK, PGC1-a, and sirtuins. Diabetic therapies that induce the stress response, whether via heat, bioactive compounds, or genetic manipulation, improve or prevent all of the morbidities and comorbidities associated with the disease. The agents reduce insulin resistance, inflammatory cytokines, visceral adiposity, and body weight while increasing mitochondrial activity, normalizing membrane structure and lipid composition, and preserving organ function. Therapies restoring the stress response can re-tip the balance from disease into health and address the multifaceted defects associated with the disease

Effect of temperature and storage time of wheat germ on the oil tocopherol concentration

Wheat germ represents approximately 3% of the grain and it contains 8-14% oil, which is a rich source of tocopherols (vitamin E) and polyunsaturated fatty acids, mainly linoleic acid. The present work shows the influence of temperature (27ºC and 45ºC) and storage time (maximum 35 days) of the wheat germ on the concentration of tocopherol in the oil. Their effect on other quality parameters was also investigated. Results indicated that oil oxidation and free fatty acid formation increased markedly with temperature and storage time. The initial sample contained 3134 µg/g total tocopherol, of which 67% was α-tocopherol and, in a lower proportions, β-tocopherol and Γ-tocopherol (30.5% and 2.4%, respectively). In the temperature range studied, tocopherols decreased as a function of storage time following first-order kinetics. The rate constant k for β-tocopherol increased with temperature. The fatty acid composition was not affected by the storage conditions applied

Nutrition and gastrointestinal microbiota, microbial-derived secondary bile acids, and cardiovascular disease

Purpose of review: The goal is to review the connection between gut microbiota and cardiovascular disease, with specific emphasis on bile acids, and the influence of diet in modulating this relationship. Recent findings: Bile acids exert a much broader range of biological functions than initially recognized, including regulation of cardiovascular function through direct and indirect mechanisms. There is a bi-directional relationship between gut microbiota modulation of bile acid-signaling properties, and their effects on gut microbiota composition. Evidence, primarily from rodent models and limited human trials, suggest that dietary modulation of the gut microbiome significantly impacts bile acid metabolism and subsequently host physiological response(s). Available evidence suggests that the link between diet, gut microbiota, and CVD risk is potentially mediated via bile acid effects on diverse metabolic pathways. However, further studies are needed to confirm/expand and translate these findings in a clinical setting