Abstract
When starving rats were prevented from mobilizing their fat stores by the antilipolytic agent 3, 5-dimethylisoxazole the following adaptive changes in hepatic metabolism occurred:1In fasting rats more urea was produced following dimethylisoxazole as indicated by a two-fold rise in plasma urea levels. Livers from such animals produced more urea when isolated and perfused without added substrates. Plasma urea levels were similarily elevated in fasting adrenalectomized rats. The increase in amino acid metabolism is not mediated, therefore, by the action of adrenal cortical hormones. An increase in urea formation following dimethylisoxazole was absent in fed animals which do not rely upon lipolysis to secure a sufficient supply in energy yielding substrates. It is considered, therefore, to represent an adaptive response to the shortage in substrates for energy metabolism arising when lipolysis is inhibited in starving rats.2Livers from starving rats which had received dimethylisoxazole produced more glucose than those of corresponding controls when perfused without added substrate. Similarily liver slices taken from these rats did incorporate more bicarbonate carbon into glucose when incubated in vitro. It is concluded from these results that gluconeogenesis from endogenous substrates has been stimulated. Adrenalectomized rats were unable to form additional glucose from endogenous amino acids and fatal hypoglycemia resulted when fasting adrenalectomized rats were injected with dimethylisoxazole.3Although more glucose is formed in livers of fasting rats treated with dimethylisoxazole, the capacity of such livers to utilize alanine for gluconeogenesis did not increase to a major degree. It is concluded that glucose formed in addition in livers of treated animals is derived from endogenous substrates. These are made available to gluconeogenesis by an increased proteolysis resulting in an elevated deamination of amino acids, and an increase in urea formation.
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