Energy balance in rats given chronic hormone treatment

Abstract

1. 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 oxidasc (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 < 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P < 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 < 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.