关键词: 能量代谢, 高温暴露, 代谢率, 氧化应激, 解偶联蛋白, 黑线仓鼠

Abstract: The adaptive regulation of animal energy metabolism affects life history characteristics such as growth, development, reproduction, and aging. Metabolic rate and tissue mitochondrial respiration rate are related to free radical levels, which are important factors influencing the aging of the organism. In this study, we investigated the intrinsic link among energy metabolism, tissue respiration rates of major metabolically active organs, free radical levels, and antioxidant capacity in response to high ambient temperature. We used as a model species striped hamsters (Cricetulus barabensis) that were previously acclimated to room temperature (21 ℃) and warm temperature (32.5 ℃) for 4 weeks and then were acutely exposed to extremely high temperature (37 ℃) for 48 h. The energy intake, metabolic rate, body temperature, mitochondrial respiration rate, and uncoupling protein (UCP) gene (ucp) expression of brown adipose tissue (BAT), liver and skeletal muscle were measured. The levels of protein carbonyl and malondialdehyde (MDA), and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were also determined. The results showed that the acclimation to 32.5℃ and acute exposure to 37℃ resulted in significant reductions in gross and digestive energy intake, basal metabolic rate, and non-shivering thermogenesis. Cytochrome c oxidase (COX) activity was reduced after acclimation to 32.5℃ by 84.2%, 50.0%, and 56.6% in BAT, liver, and muscle, respectively. The liver COX activity decreased further by 23.3% after exposure to 37℃, but COX activity in BAT and muscle was not significantly changed. The acute exposure to 37℃ deceased BAT ucp1 expression by 89.5%, liver ucp2 by 76.2%, and muscle ucp3 by 58.8% in the hamster previously acclimated to 21℃, but it had no significant effect on the gene expression in the hamsters previously acclimated to 32.5℃. Acclimation to 32.5℃ significantly decreased MDA levels in heart, lung, kidney, and muscle, but not in liver and brain, and it significantly increased protein carbonyl levels in the kidney only. Acute exposure to 37℃ significantly reduced protein carbonyl levels in liver and heart, but it had no significant effect on MDA levels in all tissues. In addition, acclimation to 32.5℃ significantly reduced SOD activity in liver and muscle, but did not affect heart, lung, kidney, or brain; and it decreased GSH-Px activity in heart, lung, and kidney, but increased GSH-Px activity in muscle, and had no effect in liver. These findings suggest that (1) the effects of acute exposure to high temperatures on energy metabolism and mitochondrial respiration rate are related to habitat ambient temperature, with the animals at lower ambient temperature being more affected by high temperature; (2) after being acclimated to the warm and acutely exposed to high temperature, the metabolic rate of the organism and mitochondria respiratory decreased, while the liver, heart, lung, kidneys, skeletal muscle, and brain do not show considerable oxidative stress and damage, being inconsistent with the‘free radical hypothesis’ .

Key words: Energy metabolism, High-temperature exposure, Metabolic rate, Oxidative stress, Uncoupling protein, Striped hamsters