Sprague-Dawley rats were injected for 16 d with long-acting insulin, and energy balance was calculated using the comparative carcass technique. Two experiments were carried out with females (starting weights 150 and 90 g respectively), and one with males (starting weight 150 g). In a fourth experiment, cytochrome c oxidase (EC 1.9.3.1) activity was measured as an indicator of the capacity for substrate oxidation. 2. Insulin increased weight gain by up to 57% (P less than 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P less than 0.01 for all studies). The excess weight gained by the insulin-treated rats was predominantly due to fat deposition. 3. Energy expenditure, calculated as the difference between metabolizable intake and carcass energy gain, was expressed on a whole-body basis, or relative to either metabolic body size (kg body-weight0.75) or fat-free mass. Insulin consistently raised energy expenditure, regardless of the method of expression, but this change reached statistical significance in only two of the nine comparisons. 4. Cytochrome c oxidase activity was not affected by insulin treatment in either interscapular brown adipose tissue or gastrocnemius muscle. In liver, total enzyme activity (U/tissue) was increased from 2928 (SE 162) in the controls to 3940 (SE 294) in the treated group (P less than 0.02), but specific activity (U/mg protein) was unchanged. 5. It is concluded that, despite causing substantial hyperphagia, insulin treatment only slightly increases energy expenditure in rats. The costs of increased tissue deposition may account for this change.
