Abnormal brown adipose tissue in obese (ob/ob) mice: response to acclimation to cold

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Abstract
Brown adipose tissue mitochondria of the genetically obese (ob/ob) mouse have abnormal ultrastructure and low binding of purine nucleotides; the polypeptide composition of the mitochondrial membranes is relatively normal. Binding of purine nucleotides is a specific site on a polypeptide, of MW 32,000, associated with the thermogenic proton conductance pathway of brown adipose tissue mitochondria. These sites appear to be masked in the ob/ob mouse. Exposure of the ob/ob mouse to cold (4.degree. C) neither increases the binding of purine nucleotides nor changes the ultrastructure of the mitochondria, as it does in lean mice. Acclimation of obese mice to mild cold (14.degree. C), known to improve their cold resistance, induces an almost normal tissue growth, mitochondrial proliferation, and alteration in mitochondrial properties (increase in binding of purine nucleotides; increase in proportion of polypeptides in the region of 32,000; more normal ultrastructure). A defect in brown adipose tissue mitochondria is a contributory cause of the known defect in nonshivering thermogenesis in the ob/ob mouse and thus of obesity in this animal. The defect appears to be in the switching mechanism, mediated by noradrenaline (norepinephrine) that allows an acute thermogenic response to cold. The adaptive mechanism that allows tissue growth and improvement of mitochondrial thermogenic function during acclimation to mild cold is normal and can account for the known improved thermogenic capacity of cold-acclimated ob/ob mice.

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