Abstract

This study was designed to determine whether genetic defect in the efficiency of ATP synthesis existed in the NIDDM-prone BHE/cdb rat and to determine whether these defect caused the development of glucose intolerance. Thyroxine treatment provided an excellent clue as to the nature of the genetic defects in this rat. The characteristics of hyperthyroid and control Sprague-Dawley(SD) and BHE/cdb rats were studied. Hyperthyroisdism was induced through the addition of thyroxine$(T_4)$ to the diet(2mg/kg of diet). Active proton conductances and passive proton conductances were tested. Mitochondria from hyperhyroid BHE/cdb rats were less efficient in active proton conductances than mitochondria from hyperthyroid SD rats. It showed that decreased efficiency of ATP synthesis in the BHE/cdb rat was probably related to defects inactive proton conductance, indicating aberrant $F_{0}ATPase$. The levels of $F_{1}F_{0}ATPase$ activity were tested. Mitochondria from hyperhyroid BHE/cdb rats were less active than mitochondria from hyperthyroid SD rats. This may be an attribute of aberrant $F_{1}F_{0}ATPase$ and may contribute to the BHE/cdb strain's characteristic of reduced ATP synthesis efficiency. Glucose tolerances were tested. BHE/cdb rats were profoundly affected by thyroxine, whereas SD rats were less so. It showed that the diabetes phenotype in BHE/cdb rats was related to defects in thyroxine-induced uncoupling. These results showed the decreased efficiency of ATP synthesis due to genetic defects in $F_{1}F_{0}ATPase$ had relevance to the characteristic of impaired glucose tolerance in the NIDDM-prone BHE/cdb rat.

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