The glycogen synthase kinase-3β (GSK-3β) gene has been implicated in Alzheimer's disease (AD). Polymorphisms in this gene are plausible modulators of brain function. However, little is known about the potential role of the GSK-3β rs334558 polymorphism, which has been associated with ...
The catalytic role of the cofactor phosphate moiety at the active site of glycogen phosphorylase has been the subject of many investigations including solution-state high-resolution 31P-NMR studies. In this study the pyridoxal phosphate moiety in both the inactive and active forms of microcrystalline...
Summary In fish, exhaustive exercise stress differs from steady-state aerobic exercise in causing (1) a depletion of glycogen, creatine phosphate (CP) and ... CM Wood - 《J.exp.biol》 被引量: 522发表: 1991年 Reliability, reproducibility and validity of the individual anaerobic threshold Acid...
Very low levels of insulin (or a low ratio of insulin to counterregulatory hormones) are necessary to prevent ketoacidosis; as insulin levels increase, further gluconeogenesis and glycogen metabolism are sequentially switched off. Because just small amounts of insulin are needed to prevent ketosis, ...
In addition to causing insertional mutations due to viral gene integration, epigenetic alterations and inducing chronic immunological dys- function are all methods by which these viruses turn hepatocytes into cancerous ones. While expanding our knowl- edge of the illness, identifying ...
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AMPK also increases glucose uptake via GLUT4 translocation, reducing the rate of glycogen synthesis, and shifting glucose metabolism toward lactate production in skeletal muscle cells[29], decreasing hepatic expression of molecules involved in gluconeogenesis such as phosphoenolpyruvate carboxykinase (PEPCK) ...
function and adversely affect clinical outcome. Nutritional therapy has been proposed as a means to correct PCM and thereby improve clinical outcomes. The rationale for aggressive nutritional therapy in patients with advanced liver disease is based on promising but nascent clinical trials and the ...
Heart, skeletal muscle, and liver are the target organs of glycogen accumulation. In the heart, the enzyme defect causes progressive lysosomal glycogen accumulation that thickens the myocytes and myocardial walls, impairs diastolic relaxation (diastolic dysfunction), and irreversibly damages myocytes, ...
Our results support a mechanism where inhibition of axonal trafficking is initiated at the plasma membrane by soluble low molecular weight Aβ species and is exacerbated by fibrils. Since trafficking inhibition does not coincide with the loss of mitochondrial function, restoration of axonal transport ...