In the liver of genetically diabetic mice (db/db) a rise of CoA and alterations in the structure of its moiety (an increase in CoA/short-chain fatty acyl-CoA and CoA/long-chain fatty acyl-CoA ratios) were found being one of the hyperlipogenesis-providing factors. A rise of the content of CoA in diabetes was caused by the activation of its biosynthesis from vitamin-containing precursors; an increase in the deposition of the latter in panthotenate-protein complexes was also noted. Panthetine and 4'-phosphopanthotenate administration to diabetic animals returned to normal the level of total and free CoA and the ratios of separate components in the structure of coenzyme moiety, and the content of CoA precursors (phosphopantheteine and dephospho-CoA) in the liver.
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