Gamblebauer1250

Inhibition of AMPK activity and PGC-1β expression diminished the anti-steatotic effect of NTP in hepatocytes. JNK inhibition could also be associated with NTP-mediated inhibition of lipid accumulation, but we did not find the association between AMPK and JNK. These results suggest that NTP inhibits lipid accumulation by maintaining mitochondrial function in hepatocytes via AMPK activation, or by inhibiting JNK.Skeletal muscle is the largest metabolic organ in the human body and is able to rapidly adapt to drastic changes during exercise. Histone acetyltransferases (HATs) and histone deacetylases (HDACs), which target histone and non-histone proteins, are two major enzyme families that control the biological process of histone acetylation and deacetylation. Balance between these two enzymes serves as an essential element for gene expression and metabolic and physiological function. Genetic KO/TG murine models reveal that HDACs possess pivotal roles in maintaining skeletal muscles' metabolic homeostasis, regulating skeletal muscles motor adaptation and exercise capacity. HDACs may be involved in mitochondrial remodeling, insulin sensitivity regulation, turn on/off of metabolic fuel switching and orchestrating physiological homeostasis of skeletal muscles from the process of myogenesis. Moreover, many myogenic factors and metabolic factors are modulated by HDACs. HDACs are considered as therapeutic targets in clinical research for treatment of cancer, inflammation, and neurological and metabolic-related diseases. This review will focus on physiological function of HDACs in skeletal muscles and provide new ideas for the treatment of metabolic diseases.Maintenance of cerebral blood vessel integrity and regulation of cerebral blood flow ensure proper brain function. The adult human brain represents only a small portion of the body mass, yet about a quarter of the cardiac output is dedicated to energy consumption by brain cells at rest. Due to a low capacity to store energy, brain health is heavily reliant on a steady supply of oxygen and nutrients from the bloodstream, and is thus particularly vulnerable to stroke. Stroke is a leading cause of disability and mortality worldwide. By transiently or permanently limiting tissue perfusion, stroke alters vascular integrity and function, compromising brain homeostasis and leading to widespread consequences from early-onset motor deficits to long-term cognitive decline. While numerous lines of investigation have been undertaken to develop new pharmacological therapies for stroke, only few advances have been made and most clinical trials have failed. Overall, our understanding of the acute and chronic vascular responses to stroke is insufficient, yet a better comprehension of cerebrovascular remodeling following stroke is an essential prerequisite for developing novel therapeutic options. In this review, we present a comprehensive update on post-stroke cerebrovascular remodeling, an important and growing field in neuroscience, by discussing cellular and molecular mechanisms involved, sex differences, limitations of preclinical research design and future directions.Soon after its discovery in the 18th century, oxygen was applied as a therapeutic agent to treat severely ill patients. Lack of oxygen, commonly termed as hypoxia, is frequently encountered in different disease states and is detrimental to human life. However, at the end of the 19th century, Paul Bert and James Lorrain Smith identified what is known as oxygen toxicity. The molecular basis of this phenomenon is oxygen's readiness to accept electrons and to form different variants of aggressive radicals that interfere with normal cell functions. The human body has evolved to maintain oxygen homeostasis by different molecular systems that are either activated in the case of oxygen under-supply, or to scavenge and to transform oxygen radicals when excess amounts are encountered. Research has provided insights into cellular mechanisms of oxygen homeostasis and is still called upon in order to better understand related diseases. Oxygen therapy is one of the prime clinical interventions, as it is life saving, readily available, easy to apply and economically affordable. However, the current state of research also implicates a reconsidering of the liberal application of oxygen causing hyperoxia. Increasing evidence from preclinical and clinical studies suggest detrimental outcomes as a consequence of liberal oxygen therapy. In this review, we summarize concepts of cellular mechanisms regarding different forms of disturbed cellular oxygen homeostasis that may help to better define safe clinical application of oxygen therapy.

To investigate the time-course of changes in knee-extensors muscle mass, architecture and function in response to plyometric training (PLT) performed on a novel training device, the Tramp-Trainer. This machine consists in a trampoline connected to an inclined sledge which allows the performance of repeated jumps while the subject is sitting on a chair.

Eight healthy males (173.6 ± 4.7 cm, 69.7 ± 13.5 kg, 25.3 ± 4.6 years) underwent 6 weeks of bilateral PLT on the tramp-trainer machine. Training was performed three times per week (between 120 and 150 bounces per session). read more Knee-extensor maximum voluntary torque (MVT) and power, quadriceps femoris (QF) volume (VOL), cross-sectional area from the 20% to the 60% of femur length and CSA

, together with vastus lateralis (VL) architecture (fascicle length, Lf, and pennation angle, PA) were assessed after 2, 4, and 6 weeks of PLT.

All results are presented as changes versus baseline values. MVT increased by 17.8% (week 2,

< 0.001) and 22.2% (week 4,

CSA

and QF VOL cannot fully explain the increment in muscle power, it is likely that other factors (such as adaptations in neural drive or tendon mechanical properties) may have contributed to such fucntional changes.

PLT induced rapid increases in muscle volume, fascicle length, pennation angle, torque and power in healthy younger adults. Notably, changes in VL VOL and Lf were detectable already after 2 weeks, followed by increases in knee extensors VOL and power from week 4 of PLT. Since the increase in CSA mean and QF VOL cannot fully explain the increment in muscle power, it is likely that other factors (such as adaptations in neural drive or tendon mechanical properties) may have contributed to such fucntional changes.