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Diabetes and Antidiabetic Therapy: Control of Glucose
Published in Richard J. Sundberg, The Chemical Century, 2017
The purpose of insulin control is integration of energy demand versus availability. A key mediator is AMP-activated protein kinase (AMPK). A falling energy status is reflected as a decreasing ATP level. AMPK then activates both ATP-forming catabolism and down-regulates ATP-consuming anabolic processes. AMPK also interacts with the hypothalamus to connect energy status and appetite. This is achieved through the hormonal polypeptides ghrelin and leptin. AMPK also plays a key role in the relationship between exercise and energy status. Exercise dramatically increases ATP utilization. During exercise, AMPK promotes conversion of triglycerides to fatty acids and balances fatty acid metabolism with glucose to insure adequate glucose levels in the brain. Fatty acid utilization increases with duration of exercise and exercise capacity and endurance is increased by training. AMPK upregulates mitochondrial metabolic capacity in response to regular exercise.
Mechanisms of Nanotoxicity to Cells, Animals, and Humans
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Belinda Wong Shu Ee, Puja Khanna, Ng Cheng Teng, Baeg Gyeong Hun
Apart from the mTOR pathway, the level of cellular energy is also an important pathway that regulates autophagy. One of the cell's energy sensors is the 5’-AMP-activated protein kinase (AMPK). Low ATP/AMP ratio under poor growth conditions leads to AMPK activation, which promotes TSC2 phosphorylation and the formation of TSC1/TSC2 complex. This complex also inhibits Rheb and mTOR, followed by autophagy activation (Inoki et al. 2003; Huang and Manning 2008). In mouse podocyte cells exposed to TiO2 NPs, an increase in the levels of LC3-II/LC3-I ratio, p62, and Beclin 2 was observed, proving that AMPK and mTOR are involved in autophagy activation (Zhang et al. 2016a).
Carbohydrate intake and training efficacy – a randomized cross-over study
Published in Journal of Sports Sciences, 2018
Florian Beaudouin, Frederic Joerg, Anette Hilpert, Tim Meyer, Anne Hecksteden
Much of the research in this direction has focused on genetic factors which are estimated to account for about 50 percent of interindividual variability in training response (Bouchard et al., 1999, 2011; Gaskill et al., 2001). On the other hand, a considerable number of modifiable moderators of training efficacy have been previously described (e.g. nutritional factors, training status, sleep, psychological stress, habitual physical activity) (Fullager et al., 2015; Hecksteden et al., 2015; Mann et al., 2014). For many of these modifiable moderators the underlying mechanism is an attenuation of exercise-induced perturbation of cellular homeostasis, which is in turn the starting point of adaptive processes. The principal physiological mechanism is well studied for carbohydrate availability. In particular, it has been shown that the intensity-dependent activation of AMP-activated protein kinase (AMPK), a key energy-deficiency sensor in human cells (Hardie, Ross, & Hawley, 2012), is blunted when glucose availability is high (Akerstrom et al., 2006; Civitarese, Hesselink, Russell, Ravussin, & Schrauwen, 2005; Roepstorff et al., 2005; Wojtaszewski et al., 2003). AMPK is involved in signaling pathways leading to endurance-type adaptations in skeletal muscle. It plays a key role in mitochondrial biogenesis, GLUT-4-translocation and oxidation of non-esterified fatty acids (Austin & St. Pierre, 2012; Hardie, 2004; Kemp et al., 1999; Röckl, Witczak, & Goodyear, 2008).
The protective mechanism underlying total flavones of Dracocephalum (TFD) effects on rat cerebral ischemia reperfusion injury
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Peng Wu, Xu-sheng Yan, Yu Zhang, Dong-sheng Huo, Wei Song, Xin Fang, He Wang, Zhan-jun Yang, Jian-xin Jia
AMP-activated protein kinase (AMPK), a serine threonine kinase, is a key metabolic and stress sensor/effector that is activated under conditions of nutrient deprivation, vigorous exercise or heat shock (Turnley et al. 1999). AMPK plays an important role in oxidative stress and apoptosis in the central nervous system (Deng et al. 2016; Li and McCullough 2010; Manwani and McCullough 2013). Jung et al. (2004) showed that overexpression of active AMPK enhanced oxidative stress and induced apoptosis in mouse neuroblastoma cells through NF-κB activation.
The protective mechanism underlying total flavones of Dracocephalum (TFD) effects on rat cerebral ischemia reperfusion injury
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Peng Wu, Xu-sheng Yan, Yu Zhang, Dong-sheng Huo, Wei Song, Xin Fang, He Wang, Zhan-jun Yang, Jian-xin Jia
AMP-activated protein kinase (AMPK), a serine threonine kinase, is a key metabolic and stress sensor/effector that is activated under conditions of nutrient deprivation, vigorous exercise or heat shock (Turnley et al. 1999). AMPK plays an important role in oxidative stress and apoptosis in the central nervous system (Deng et al. ; Li and McCullough 2010; Manwani and McCullough 2013). Jung et al. (2004) showed that overexpression of active AMPK enhanced oxidative stress and induced apoptosis in mouse neuroblastoma cells through NF-κB activation.