The Jacob-Monod model for the regulation of enzymic activity has been used in the analysis of some types of metabolic disease. Three lesions have been considered: (l)loss of allosteric inhibition of phosphofructokinase by citrate in the condition of lipomatosis; (2) failure of covalent modification of triglyceride lipase from inactive to active forms in the condition of triglyceride storage disease, and (3) failure of repression of HMG-CoA reductase by a mutant low-density lipoprotein in a new variant* of familial hypercholesterolaemia. Defects in enzymic regulation are contrasted with catalytic defects (the inborn errors); the major difference being an accumulation of a normal metabolic end-product of an unregulated pathway, rather than accumulation of an unusual intermediary metabolite as in the inborn errors.

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