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Glucose fasting state

The cyde is central to the oxidation of any fuel that yields acetyl CoA, induding glucose, fritty acids, ketone bodies, ketogenic amino acids, and alcohol There is no hormonal control of the cyde, as activity is necessary irrespective of the fed or fasting state. Control is exerted by the energy status of the cell. [Pg.179]

During the fasting state, the energy needs of the liver are provided by fatty acid catabolism ( 3-oxidation), which spares further glucose for export to peripheral tissues. [Pg.63]

The glucocorticoids have important dose-related effects on carbohydrate, protein, and fat metabolism. The same effects are responsible for some of the serious adverse effects associated with their use in therapeutic doses. Glucocorticoids stimulate and are required for gluconeogenesis and glycogen synthesis in the fasting state. They stimulate phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and glycogen synthase and the release of amino acids in the course of muscle catabolism. [Pg.880]

The net results of these actions are most apparent in the fasting state, when the supply of glucose from gluconeogenesis, the release of amino acids from muscle catabolism, the inhibition of peripheral glucose uptake, and the stimulation of lipolysis all contribute to maintenance of an adequate glucose supply to the brain. [Pg.880]


See other pages where Glucose fasting state is mentioned: [Pg.338]    [Pg.753]    [Pg.177]    [Pg.649]    [Pg.546]    [Pg.106]    [Pg.169]    [Pg.178]    [Pg.68]    [Pg.74]    [Pg.212]    [Pg.50]    [Pg.144]    [Pg.3]    [Pg.61]    [Pg.393]    [Pg.534]    [Pg.38]    [Pg.40]    [Pg.905]    [Pg.338]    [Pg.395]    [Pg.654]    [Pg.224]    [Pg.80]    [Pg.141]    [Pg.169]    [Pg.182]    [Pg.123]    [Pg.226]    [Pg.444]    [Pg.475]    [Pg.585]    [Pg.585]    [Pg.221]    [Pg.248]    [Pg.349]    [Pg.349]    [Pg.339]    [Pg.550]    [Pg.44]    [Pg.32]    [Pg.132]    [Pg.1264]    [Pg.1272]   
See also in sourсe #XX -- [ Pg.9 , Pg.170 , Pg.172 ]




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