“Evidence is accumulating that eating in a 6-hour period and fasting for 18 hours can trigger a metabolic switch from glucose-based to ketone-based energy, with increased stress resistance, increased longevity, and a decreased incidence of diseases, including cancer and obesity.”
Highlights
• SWS suppression during nighttime sleep leads to a significant increase in salivary melatonin.
• Elevated melatonin appears to play a key role in glucose tolerance changes after disturbed sleep.
• Melatonin’s effect on morning glucose tolerance depends on its secretion timing.
• Durations of REM sleep and nocturnal awakenings appear to play an important role in melatonin secretion and glucose tolerance.
• Glucose tolerance is associated with the total duration of undisturbed sleep and the length of REM sleep rather than the amount of SWS.
https://www.sciencedirect.com/science/article/abs/pii/S1389945719316405
“Mitochondria are fascinating structures of the cellular compartments that generate energy to run the cells. However, inherent disorders of mitochondria due to diabetes can cause major disruption of metabolism that produces huge amount of reactive oxygen species (ROS). Here we study the elevated level of ROS provoked by high glucose (HG) environment triggered mitochondrial dysfunction, inflammatory response and apoptosis via stress signalling pathway in keratinocytes. Our results demonstrated that elevated glucose level in keratinoctes, increase the accumulations of ROS and decrease in cellular antioxidant capacities.”
High glucose augments ROS generation regulates mitochondrial dysfunction and apoptosis via stress signalling cascades in keratinocytes. – PubMed – NCBI
“Caloric restriction was effective in decreasing body and fat weights, total cholesterol and LDL. These effects were totally or partially reversed after 30 days of refeeding (groups GRL). During liver perfusion, the high glucose output of the GRs was further enhanced by adrenaline (1 μM), but not by lactate infusion. In contrast, in groups G6L, G12 L, G6RL and G12RL glycogenolysis (basal and adrenaline-stimulated glucose output) was low and gluconeogenesis from lactate was significant. A twofold increase in liver content of PKA in group G6R suggests that liver sensitivity to glucagon and adrenaline was higher because of caloric restriction, resulting in enhanced glucose output.”
—a systematic review and meta-analysis | European Journal of Clinical Nutrition