作者: CHANDRA MOHAN , PAUL J. GEIGER , SAMUEL P. BESSMAN
DOI: 10.1016/B978-0-12-152830-0.50006-2
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摘要: Publisher Summary This chapter discusses the intracellular site of action insulin involving mitochondrial Krebs cycle. To begin with, there is at present no coherent model that accounts, through process partial phosphorylation or dephosphorylation enzymes other proteins, for all manifold actions on cells. It known stimulates uptake glucose most effectively in fat cells which mitochondria are close to plasma membrane. Also, much evidence has accumulated show reverses net catabolism protein, glycogen, and promotes their build up storage. Furthermore, incorporation into protein primarily those pyruvate carbons converted glutamic acid Insulin a far greater stimulatory effect methylene succinate than carboxyl carbons. can be attributed fact 2 3 either reenter cycle as acetyl-CoA remain second third opportunity glutamate by transamination α-KG.